Paul Rushe – Data Interpretation

TUTORIAL 1: ECG 04/01/18

Make sure to say what is wrong in the ECG before giving the dx

ECG
- Comes down to depolarization of cardiac muscle
o Na channels opening=depolarization
- Action Potential of cardiac muscle
o Phase 0 = rapid depolarization
o Phase 1: early repolarization
o Phase 2 – plateau phase
o Phase 3 – rapid repolarization
o Phase 4 – resting phase
General Info
- SA node – pacemaker – is where the impulse should
start
- Runs down along tracts to AV node (at borders of
ventricles & atria) à then goes down to the R & L
bundle branches à bundle of His
- SA node: 60-100/min – main pacemaker of the heart
- AV junction – 40-60/min
o Not actually a pacemaker – but acts to delay the impulse
o Surrounding tissue contains pacemaker cells
- Purkinje fibers – 20-40 /minute
o Can act as pacemakers but only if supposed to if there’s an issue above

ECG:
- Idea is to measure direction of electrical current put out by the heart itself
- ECG looks this in different directions or planes between 2 poles - positive and negative
- When electrical current travels toward negative pole
à waveform deflects downward and when the
electrical current travels toward the positive pole à
waveform deflects upwards
- P – QRS – T
- 12 leads in general
- 3 limb leads (leads I/II/III) bipolar leads
o Should all produce a positive deflection in
general
o Useful for looking @ cardiac axis – how heart
is positioned
o Lead II/III useful for inferior MI
o Leads I, II, III on the left typically of an ECG
o Lead II is the rhythm strip and is typically
repeated on the bottom
- 3 augmented leads
o aVr – normal negative – no specific view of the heart
o aVL – normally positive , looks at lateral heart wall
o aVF –normally positive, looks at the inferior heart wall
- 6 chest leads –
o Unipolar throughout – plane is one-way
§ (All others are going vertically – so these are going straight through the heart i.e.
they run along the horizontal plane of the heart)
o V1 – septal area of the heart
o V2 – V3 – anterior aspect & some
septal
o V4 – anterior aspect of the heart
o V5 – lateral wall
o V6 – inferior/lateral wall
Limb Leads
- I – lateral left ventricle
- II – interior portion of the left ventricle
- III – inferior portion of the left ventricle
- aVR – square root of squat? (ignore!)
- aVL – lateral left ventricle
- aVF – inferior portion of the left ventricle
Pre-cordial leads
- V1 – septal
- V2 – antero-septal
- V3 – antero-septal
- V4- anterior
- V5 – lateral left ventricle
- V6 – lateral left ventricle

Waveforms
- P wave: atrial depolarization
- QRS: ventricle depolarization
- T wave: ventricular repolarization
- U wave: unknown

P wave
- Atrial depolarization – comes from SA node
- What we use to look for normal rhythms
- Normal sinus = always a P wave preceding a QRS
o A-fib or atrial flutter – lose p wave b/c its coming from another focus
- Should be 0.06-0.12sec in length (<3 small squares- each small square is 0.04)
o If it is bigger than 3 small squares there is something else going on in the area
- About 2-3mm in height
Abnormal P waves:
- Peaked/notched = COPD/emboli –
o Something placing a strain on the heart (enlarged lungs putting pressure back onto the
heart/atria – so the peak contracts upwards)
- Absent = rhythm arising somewhere besides SA node
- Varying = varying sites of conduction
PR interval
- Represents the current passing through the atria & into the bundles/ventricles
- Most important thing about it is its duration
- Measure from the start of the P wave to the start of the QRS complex
- Should be between 3-5 small boxes (0.12-0.20 secs)
- Abnormal
o Short PR interval – indicates rhythm starts somewhere else (pacemaker etc)
o Prolonged PR interval– conduction delay through atria or AV junction (digoxin toxicity)
QRS complex:
- Ventricular depolarization or intraventricular conduction time
- Made up of
o Q wave = first negative deflection after P wave
o R wave = first + deflection after P or Q wave
o S wave = the first negative deflection after the R wave
o This is important because they may not always be there
- Abnormal
o Lack of p wave in front of it – think abnormal rhythm (a-fib or rhythm arising elsewhere
besides SA node)
o Notched R wave – bundle branch block
o Lack of QRS indicates issue at AV node (heart block)
ST segment
- Extremely important
- Essential to recognize what’s normal & not normal
- Should be more or less isoelectric (not deviated up or down)
- From the end of the S wave to the beginning of the T wave
- Abnormal
o ST segment depression
§ Depression of the segment
• Think ischemia or digoxin toxicity
§ May be in your non-ST elevation MI (NSTEMI)
o ST elevation
§ >1mm or more above the baseline
§ Indicates myocardial damage
§ Elevation + (chest pain +/- raised troponin) = ST elevation MI
§ Just because you have ST elevation on ECG doesn’t mean they are having an MI
(need 2 of 3 concurrent leads for STEMI!)
T wave
- Shows repolarization
 - Usually up the way in I/II/V3-6 à the other leads are all variable
- Can also show some abnormalities
o tall tented T waves (bigger than QRS itself)
§ You need to know this phrase
§ Indicates hyperkalemia or can also be a sign of myocardial ischemia
o Inversion of T wave à ischemia! (In 1/11/V3-V6)
§ Look for the tick sign
QT interval
- Measurement of ventricular depolarization & repolarization
- Extends from beginning of Q wave to the end of the T wave
- Not a fixed measurement
o Varies according to age/sex/heart rate
- Normal = between 0.36msec to 0.44msec
- Important because abnormalities à increased risk of arrhythmias
o Prolongation
§ Huge numbers of drugs associated with prolongation
• Anti-arrhythmias - amiodarone/sotalol
• Anti-depressants - fluoxetine
• Anti psychotics – haloperidol
§ Familial syndrome
o Shortened – increased Ca/Digoxin

How to approach – stepwise approach

- What is rhythm?
o Idea is to tell if this s regular or irregular (does it contract regularly)
o Look at the p wave! – If this is there all the time then its generally a regular rhythm
o Irregular? – How to tell
§ Piece of paper & a biro
§ Align along R lines
§ Mark where they are for 2/3 QRS complexes
§ Then move piece of paper across
§ If regular = same distance between them all
§ Don’t forget to look at P wave here as well – if its not present – chances are its
irregular?
o Can have a sinus rhythm and then have a regular rhythm
- What is the rate?
o Simple in general
o Use a 6 second strip – watch out for variants in this
o 1 small horizontal block = 0.04 second
o 5 small horizontal blocks = 1 large block = 0.2 seconds
o 5 large horizontal blocks = 1 second
o Normal strip = 30 large horizontal blocks = 6 seconds
o To calculate rate
§ Use 300 as your base (if regular)
§ There are 300 large square in 1 minute (300 x 200msec)
§ To calculate divide 300 by the # of squares between the p waves or the QRS
complexes
§ HR = 300/ (# of squares b/w the complexes) = 300/4 squares = 75 BPM
o Bradycardia < 60 BPM? (or 50?)
o Tachycardia > 100 BPM
o For irregular rhythms
§ Use the 6 second strip
• ECG usually in increments = 15 large boxes = 3 seconds
• Therefore 6 second strip = 30 boxes
• 6 x 10 = 1 minute
§ Add up number of complexes in 6 second
§ Multiply that number by 10
§ Gives rate over a minute
§ HR = # of QRS complexes x 10 = BPM (7 x 10 = 70 BPM)
- P wave
o Glance at all the lines – most important at the bottom line (long strip of lead II)
o Is there a p wave present – if so, for every complex?
o Are there any abnormalities?
§ Are they all the same size/duration?
- QRS
o Complex for every P wave? Same size & duration?
 o What size is QRS complex (normal is 0.06-0.20 seconds)
- ST
o Simple – any depression/elevation
o Is it isoelectric throughout
o Don’t just look at one lead – must look at them all!!
o If there is elevation – what area of the heart is involved??
- T waves
o Are they present?
o Do they match QRS complex in terms of there deviation (is there any inversion)
- Finally, into intervals
o PR – measure from start of P to start of QRS
§ Prolonged PR interval
- Looks @ other abnormalities
o Ideally should calculate QT
o Look for ectopics
o Any visible abnormalities
Simple process
- Rhythm, rate, P wave, QR, ST, T wave, PR interval, others

TUTORIAL 2: ECG 2 12/01/18

Recap
- Inferior leads: II, III, avF
- Lateral leads: I, aVL, V5, V6
- Anterior leads: V1, V2, V3, V4
- Rate and rhythm: bottom line
o If its regular: 300/# of boxes from 1 QRS to another
- Sinus: for every P wave there is a QRS complex
o If not regular à sinus arrhythmia
Sinus arrhythmia
- Often normal
- Seen in athletes & commonly in children
- Occasionally associated w/ infarction /HICP(raised ICP)/Digoxin usage
o Raised ICP: Papilledema, increased BP, decreased HR
- Needs careful examination of ECG
- Very basic
o Inspiration à increased blood à decreased vagal tone à increased HR & closer complexes
o Opposite occurs in expiration
o Therefore regular arrhythmia/sinus = p wave always present - & otherwise normal
Tachyarrhythmias
- Now start making subdivision
- Approach – follow system
- Even if you get rhythm wrong – you have approach right
- Divide inta supraventricular & ventricular in general
- Often also determined by the words
o Narrow complex tachy – SVT
§ QRS is narrow bc rhythm arises above AV

§
§ Increased heart
o Broad complex tachy = VT
§ AV/ventricles are pacemaker à broad QRS complex

§
 -
Sinus tachycardia
- Will be regular – for every P, there is a QRS
- Normal response to pain, exercise, anxiety, fever, or fear
- Compensatory mechanism in shock, anemia, respiratory distress, sepsis
- Heart conditions themselves – CCF/Pericarditis
- Secondary to medications/stimulants (atropine/caffeine)
What should be on the ECG
- Rhythm, rate, P wave, QRS (who big is QRS), ST (raised, elevated, isolectric), T wave, PR interval,
others
- make sure to check everything – may see a big thing but miss a small thing!
Is sinus tachy dangerous?
- Can be abnormal if it occurs when not supposed to be
Atrial arrhythmias
- Cardiac rhythm disturbance
- Again there is no need for this exam to understand fully why it occurs – maybe own personal
knowledge
- Basic fact is that cells outside the A node start to contract & produce current
- SA node is 60-100BPM
- Causes
o Stimulants
o Cardiac issues – cardiomypathy/MI
o Cor pulmonale
o Abnormal TFTs – high
o Most common – digoxin
- No P wave (this comes from SA so if rhythm not from here then there is no P wave)
Atrial tachycardia
- Can appear stimulus to sinus at times – another pacemaker cell contracting
- More rapid 150-200 (sinus tachy typ 100-120)
- P wave often on top of the T wave & the PR interval is often short
- Rhythm is usually regular àunless there is a block at AV
- P wave always regular i.e. the atrial wave
Atrial tachycardia with block
- Something stops an impulse going through to the ventricles
- P waves are regular but fast & you lose a QRS complex
- Regular atrial & ventricular rhythm
- Its always in a multiple (2:2/3:1) = 2 p waves per QRS complex
- Can appear very similar to A flutter
A flutter
- Regular rhythm – in terms that the amount of boxes between the QRS doesn’t change
- Sawtooth pattern
 o If this can get fast & it gets narrower and narrower – the sawtooth pattern can be difficult to
see
- Another SV tachycardia
- Unlike A. fib = regularly irregular
- Rapid but regular atrial contraction – usually >250bpm
- Saw tooth pattern
- There is usually a block – as in the AV (remember limited conduction) wont allow the current
through – 2:1 – 3:1, etc
- Rhythm =
o Atrial – regular
o Ventricular – If a regular block = regular rhythm
o Ventricular – irregular (usually in exams) hence regularly irregular
- Rate: usually very fixed (300/150/100)
- P wave: classic saw toothed appearance
- QRS = normal length
Treatment
- Carotid sinus pressure
o By applying pressure to carotid sinus you can stimulate the AV & SA nodes via vagal
stimulation> this will be reduce the frequency of discharge from the SA node, & increase the
time of conduction across the AV node
o Thus by applying pressure to the carotid sinus you can
• Reduce the rate of some arrhythmias
• Completely stop some arrhythmias
§ It will have no effect on ventricular tachycardias – thus can help you differentiate
Atrial fib vs Atrial flutter

- A fib – atria are irregular & ventricles are irregular – so its irregularly irregular
o Both atria & ventricles contract @ different times
o Be careful – watch irregular irregular rhythm – some t waves look like p waves
- A flutter – atria is irregular but ventricles are regular – so its irregularly regular
o Atria contracts @ different time but ventricles contract & same time
- 1st word talking about atria, 2nd word talking about ventricles
A fib
- Asynchronous activity in the atria
- “Quiver effect”
- Lose P waves as a result
- QRS complexes are irregular
- Irregularly irregular – there is nothing corresponding b/w the atria & ventricles
- Atria contract @ one time, the ventricles contract @ another
- Causes
o Alcohol, post MI, hyperthyroidism, medications (anti-arrhythmic), pneumonia, sepsis, mitral
valve disease
- Treat
 o Rate control & rhythm control
o Beta blocker is rate control, CCB
o Rhythm control – give anticoagulate before cardioconversion (unless they are
hemodynamic unstable, also do an echo)
o Treat the cause

-
Broad complex
Wide complex tachycardias
- Ventricular tachycardia
- Supraventricular tachycardia & ICD – RBBB, LBBB, RRIVCD
- Wolf-Parkinson White tachycardias
- Pacemaker tachycardias
- Hyperkalemia
- Torsades des pointes
Ventricular tachycardia
- Dangerous rhythm
- Patient can be either stable or unstable when you see this rhythm
o Do they have a pulse or do they not have a pulse
- It is essential to say which they are or to check which they are as this will determine management
- Causes
o Myocardial ischemia, MI, CAD, valvular heart disease, heart failure, cardiomyopathy,
electrolyte imbalances such as hypokalemia, drug intoxication (digoxin (Lanoxin),
procainamide, quinidine, cocaine)
- Features
o No atrial rhythm or rate can be seen – pacemaker coming from ventricles
o The QRS is often relatively regular
o QRS is wide (>0.12)
o T wave may or may not be present – usually in the opposite direction
- Divides into 2 types on ECG
o Monomorphic – QRS is uniform
o Polymorphic – QRS is not uniform
- Management
o O2, cardiac
o 2 IV cannulas, O2, cardiac monitor, take bloods
o if causing
 - Note: adenosine makes you feel worse before you get better – chest tightness etc
- If unstable à shock!
Torsades de point
- Form of polymorphic VT (compare the 2)
- QRS complexes wind around the baseline
- Can go up & down
- High risk of going into VF if not controlled
- Think of things that can prolong the QT
o Amiodarone etc
- Treatment: give magnesium sulfate!
o Reverse underlying cause, if unstable à shock
Ventricular Fibrillation
- No pattern, no coordination
- No atrial rate, cant figure out the ventricular rate
- Almost all the same causes of VT
- No recognizable pattern
- No coordination between contraction
- You cant figure out the ventricular rate or the atrial rate
- Cardiac arrest à get shocking
- Treatment - ACLS
o IV cannulas, bloods to check for reversible causes of cardiac arrest
o Adrenaline, amiodarone
Asystole
- Rhythm of death
- No electrical activity, no Cardiac Output
- Not shockable
- Be very careful not refined v-fib?

TUTORIAL 3: Blocks 19/01/18

Review
- If rate too quick
o Give adenosine – makes you feel really sick, warn patient
- ST depression causes
 o Ischemia
o Strain
o Medications – digoxin
- If you see ST elevation make sure you look for reciprocal ST depression
- Leads
o Inferior leads: II, III, avF
o Lateral leads: 1, aVL, V5, V6
o Anterior leads: V1, V2, V3, V4
Heart blocks
- AV heart block results from an interruption in the conduction of impulses between the atria &
ventricles
o Either block in the atria or in the ventricles
- AV block can be total or partial or it may delay conduction
o Most likely place is AV
- The block can occur @ AV node, the bundle of His, or the bundle branches
- Clinically
o How many impulses are completely blocked
o How slow the ventricular rate is as a result
o Does the block affect the heart
- Slow ventricular rate
o Decrease CO
o ? symptoms
- causes of heart blocks
o permanent
§ aging
§ congental
§ MI
§ Cardiomyopathy
§ Cardiac sx
o Temporary
§ MI
§ Digoxin toxicity
§ Acute myocarditis
§ CCB
§ Beta blockers
o Lyme disease
- Remember block & incremental worsening of each one
- Understand, recognize, need the way we’ve spelt it out however
1st degree AV block
- Rate rhythm P wave, QRS
- PR interval – this is abnormal!
- PR extended to >0.2
o Normal PR interval
§ Measure from the start of the pwave to the start of the QRS complex
§ Should be b/w 3-5 small boxes (0.12-0.20 secs)
- Don’t treat! – treat the symptoms!
2nd degree AV block
- Divides into 2 types
- Need to be able to recognize difference
- Clinically essential for the patient
o Type 1 = Wenchebach phenomenon (Mobitz I)
§ PR interval gradually prolongs further – then drops QRS
§ Every 3 beats you get a dropped QRS – atria contracts – t
§ Cyclical rhythm
§ *** look up
§ No tx if you are asymptomatic
§ Symptomatic – atropine may improve AV node conduction
§ Temporary pacemaker may required for long term relief of symptoms until the
rhythm resolve
o Type 2 (Mobitz II)
§ Non cyclical
§ PR is constant
§ PR may be prolonged but may be the same length all the time
§ Sudden p wave followed by no QRS
§ This may be constant as in 2:1 or 3:1 or it may be completely random
§ Atrial = regular/ventricular = irregular
 § Likely to be far more symptomatic – not always though
§ Type II 2nd degree AV block commonly requires placement of a pacemaker
§ Temporary pacemaker may be used until a permanent pacemaker can be placed
3rd degree AV block
- No pattern – no link b/w p wave & QRS
- Atria & ventricles are completely out of sync
- Needs treatment
- AV block occurs when impulses from atria are completely blocked @ AV node & can’t be conducted to
ventricles
- Ventricular rate is so slow, 3rd AV block presents as life threatening situation bc CO can drop
dramatically
- Looking for complete dissociation
- Both atria & ventricles conduct regularly but there is no connect b/w them
- P wave/WRS regular – however, there is no synchronicity
- There is generally no real connection
- Atrial rate is faster than ventricular – generally
- QRS is usually normal – depending on where contraction originations it may become widened

Bundle branch block

- where impulse gets through AV
- problem instead arises in the bundle branches
- where would you expect to see issues arise on the ECG
o QRS complex!
- QRS is lengthened in BBB (widened)
Right BBB
- Normal heart – depolarization of septum occurs form right to left
- In RBB this still happens but bc RBB is blocked, then the right ventricle doesn’t depolarize @ same
time as left
- Left ventricular depolarization continues as normal & produces a normal R & a normal S wave
- After this happens, right ventricle then depolarizes & causes a second R wave
- V1 – creates an M shaped QRS – because the R wave is positive, S is negative (R1 is also positive)
o This is known as an RSR pattern – there is an up R then a down S & another up R
- V6 – creates W shaped QRS – b/c its opposite

-
LBBB
- opposite to RBB
- now thing M sign is in V6
 - need
o QRS > 0.12
o Broad R waves V6 w/ no Q waves
o Broad S waves in V1

-
Summary or blocks
- 1st degree
o prolonged PR regular – don’t tx
- 2nd degree
o type 1 – progressively prolonging PR
§ may or may not tx – atropine/pacemaker
o type 2
§ always tx w/ pacemaker
§ cyclical drop in QRS
- 3rd degree
o just at AV
o no synchronization
o always tx
- BBB
o right BBB
§ M in V1 & W in V6
o Left BBB
§ prolonged RS in V1 & M in V6
§ be wary of – can’t interpret MI in this
- QRS shouldn’t be greater than 3 small boxes! – if widened – then something wrong!
Tachycardia
- QRS is narrow
o Regular
§ Sinus tach, SVT, aflutter
o Irregularly
§ Afib, MAT, aflutter, VAR conduction
- QRS is wide >3 boxes wide
o Regular rhythm
§ VTach, sinus tach w/ aberrancy, SVT w/ BBB/WPW
o Irregular rhythm
§ Afib w/ BBB, afib w/ pre-excitation, Vfib
Monomorphic V –tach - tombstones
- Rate regular
- Rhythm R wave to ra wayve
- P wave – fotne not seen/present
- Causes
o Mi, ischemia, CAD, valvular heart disease, HF, cardiomyopathy, electrolyte imbalances such
as hypokalemia, drug intox (digoxin (lanoxin), procainamide, quinidine, cocaine)
- Polymorphic – variation in shapes
- Unstable
o Synchronized DC cardioversion
o If pulseless- tx like v fib
- Stable
o IV antiarrhytmic
§ Amiodarone
§ Procainamide
§ Sotalol
§ Recurrent episodes à ICD
Torsades de pointes
- Tx w/ magnesium sulfate
- Form of polymorphic
- People w/ prolonged QT
- QRS rotates around the baseline
- MC – drug that prolongs QT
- Why is important to differentiate this from a regular polymorphic VT?

-
V-fib
- completely chaotic
- no pattern
- cannot measure anything
- person is in arrest
- remember always check pt clinically please another lead if it was just a one lead pattern you got
- tx – defibrillation & use of adrenaline & amiodarone
Asystole
- try to look for reversible causes – kalemia, tamponades, pneumothorax
- epinephrine & amiodarone & shock

Monomorphic Ventricular Tachycardia

- Rate- regular
- Rhythm- r wave to r wave
- P wave often not seen or present
- QRS widened
- Causes:
o MI
o Ischemia
o Coronary artery disease
o Valvular heart disease
o Heart failure
o Cardiomyopathy
o Drug intoxication- digoxin
o Hypokalemia

Polymorphic:
- Varying shapes

Torsades de Pointe:
- Form of polymorphic VT
- In people with a prolonged QT
- QRS rotates around the baseline
- Most common- drugs that prolong QT
- Why is it important to differentiate this one from a regular
o Treatment: magnesium sulphate
Unstable V Tach:
- Synchronised DC cardioversion
- And if pulseless- treat like v. fib
Stable
- IV antiarrhythmic drugs
- Amiodarone, Procanimide

V-Fib:
- Desynchronized cardioverter
- Completely chaotic
- No pattern to it
- Cannot measure anything
- This person is in arrest
o Remember to say you would always check the patient ABCs
o Treat- defibrillation and use adrenaline and amiodarone

Asystole:
- Try to look for reversible causes
- Give epinephrine and amiodarone
RAD: “reaching”
- Generally seen with any pulmonary condition that places a strain on the heart
o Also right ventricular hypertrophy
- Extra muscle- extra strength
- Lead 1 becomes negative and 2 and 3 remain positive

LAD: “leaving”
- Generally a conduction defect if pathology present
- Again a specific pattern
- Positive in lead 1 and 2 and 3 become negatives

Axis deviation may be completely normal

- Often in people who are tall/small/fat/thin
- However, they may also point you in the direction of something else going on

Anterior STEMI: Left Anterior Descending

- Most severe
- “Widow Maker:
- LAD supplies area
o Also supplies branches to septum therefore V1 and V2 may be involved
- V3/V4 definitively
- Blockage in early LAD
o Can effect all leads from V1-V6 and perhaps all the lateral leads- this is an extensive anterior
MI (diagonal branch of the LAD supplies the lateral leads)
o If it occurs in the mid LAD- the septal branches may be excluded given rise to an ST
rise from V3 and V4
- “Tombstoning pattern” – ST becomes so raised
Inferior STEMI
o Inferior leads involved: 2/3/aVF
o ST elevation in all 3
o Reciprocal depression in leads 1 and aVL

Posterior Wall MI:

- This one can have varying signs
- Wall supplied by the Posterior Descending Artery
- 80% of people- branch of the Right Circumflex Artery
- Therefore we can get posterior and inferior
- Posterior is opposite to the anterior- ST depression from V1-V4
- 2, 3, avF are raised – inferior

Please remember that an MI should not be interpreted with LBBB present… treat as if new in
particular

MI triad- Need 2 of 3:
- Troponin
- ECG
- Chest pain
Complications of MI:
- Ischemia
o Reinfarction
o Infarct extension
o Angina
- Mechanic
o Cardiac failure
o Cardiogenic shock
o Mitral regurgitation
o Ventricular aneurysm
o Cardiac rupture- ventricular septum, papillary muscle or cardiac wall
- Arrhythmic
o Atrial or ventricular arrhythmia
o Sinus or AV node dysfunction
- Embolic
o Central nervous system embolus
o Peripheral
o Left ventricular mural thrombus
- Inflammatory
o Pericarditis

29 year old male:- 2 day history of feeling vaguely unwell

- Thinks he’s having temps at times
- No cough/wheeze
- Now complaining of a pain on the left side of his chest
- ECG:
o Pericarditis
- What other questions would you like to ask?
- How would you treat?
o NSAIDs
o Pericarditis:
§ Acute phase: concave ST elevation in most if not all leads
§ Clinically sick..
§ As it progresses… T wave inversion may stick

Right axis deviation

- Dominant R wave in V1- > 7 mm tail
- Dominant S wave in V5 or V6 (>7mm eep)
- +/-
- Right atrial enlargement- P pulmonale
- Right ventricular strain patter- ST depression/T wave inversion in the right precordial (V1-V4) and
inferior (2, 3, aVF) leads
Causes:
- Pulmonary hypertension
- Mitral stenosis
- Pulmonary embolism
- Chronic lung disease(cor pulmonale)
- Congenital heart disease
o E.g. tetralogy of gallot, pulmonary stenosis
- Arrhythmogenic right ventricular cardiomyopathy

Left Ventricular Hypertrophy:

- Left sided pressure overload
- Increased r wave amplitude in the left-sided ECG leads (I, aVL, V4-V6)
- Increased S wave depth in the right-sided leads (3, aVR, V1-V3)
- Other features

Another rhythm to note:

- WPW
o Preexcitation pathway,, where there is early activation of the ventricles because of a bypass
tract around the AV node
§ Short PR interval
 § Slurred upstroke on R wave due to delta wave
o There are multiple forms of accessory pathways and syndromes… this is the only one you
should really should recognize
o Can predispose you to Atrioventricular re-entry tachycardia

BIOCHEMISTRY

Sodium

Hyponatremia
- Description:
o Plasma Na+ concentration depends on the amount of both Na+ and water in the plasma
o Hyponatremia therefore does not necessarily imply Na+ depletion
§ Assesing fluid status is the key to diagnosis
- Signs & symptoms
o Confusion, lethargy, seizures, coma
o Think of the elderly patient – changes in mental status – don’t forget to check …
o Look for anorexia, nausea and malaise initially, followed by headache, irritability, confusion,
weakness, decreased GCS and seizures, depending on the severity and rate of change in
serum sodium
o Cardiac failure or odema may indicate the cause
o Hyponatremia also increased the risk of falls in the elderly*
- Subdivided into 3 sections
o Hypovolemic
§ Think about pt losing Na from body for a reason you can see/think
§ Lower fluid/blood volume = lower Na level
§ Usually the Na is low than the overall fluid level
§ GI – Vomiting, diarrhea, IBD patients
§ Renal/endo – nephropathy, diuretics, mineralocorticoid deficiency, dialysis
§ Others – pancreatitis, peritonitis, rhabdomyolysis, burn patients
o Hypervolemic – thinking high blood volume – concentration of Na is decreased
§ Causes? – CCF, renal failure, liver failure, hyperglycemia
o Euovolemic
§ Difficult one
§ Where fluid levels are okay – why is the pts Na on the lower side?
§ Causes – primary polydipsia (drinking in), poor Na intake, hormonal
insufficiency (Addison’s, low TFT, occasionally in pregnancy)
§ SIADH (dx of exclusion)
• Where ADH is continuously released even the pt is fluid balanced
• Gives rise to some fluid retention (mild)
• Na levels decrease
• Seen with
o Malignancies – small cell lung cancer, mesothelioma, GI, GU,
lymphoma, sarcoma
o Pulmonary – pneumonia, asthma, COPD, Tb
o Drugs – desmopressin, opioids, nicotine, SSRIs, TCA,
cyclophosphamide, ecstasy
o CNS – meningitis, tumors, subdural hematoma, head trauma
o Transient – nausea, pain stress
- What to do
- Stepwise
o Look @ clinical features – is person dehydrated?
o Want a urinary Na & urinary osmolality
§ If person is hypovolemic
• Urinary Na > 20mmol/L suggest renal cause
• Urinary Na < 20 mmol/L suggests non-renal cause
§ If person is normovolemic
• Urine osmolality is all important
• If this is high – indicates SIADH (>500mmol/kg- Oxford handbook
saying >100 mmol/Kg *)
• If its low – think of the other primary polydipsia/dietary
- Management
o Hypovolemia
§ Treatment – isotonic saline
§ Treat – cause?
 o Hypervolemia
§ Treatment– fluid restriction/diuretics – cause?
o Euvolemia –
§ Treatmet- fluid restrict – cause?
- Essential to be aware of the complications for rapid Na replacement
- Rapid correction leads to a fluid imbalance in the brain (brain has too much & then suddenly has
too little)
- Demyelination can occur
- Replace by <10mmol/24 hours

SIADH (Syndrome of inappropriate ADH secretion):

- An important, but over-diagnosed, cause of hyponatremia
o The diagnosis requires concentrated urine(Na+ >20 mmol/L and osmolality
>100mosmol/kg) in the presence of hyponatremia (plasma Na+ <125mmol/L) and low
plasma osmolality (<260mosmol/kg), in the absence of hypovolemia, odema or diuretics
- Causes:
o Malignancy: small cell lung Ca, pancreas, prostate, thymus, lymphoma
o CNS disorders: meningoencephalitis, abscess, stroke, subarachnoid or subdural hemorrhage,
head injury, neurosurgery, Guillain Barre, vasculitis or SLE
o Chest disease: TB, pneumonia, abscess, aspergillosis, small-cell lung cancer
o Endocrine disease: hypothyroidism (not ture ISADH, but perhaps due to excess ADH release
from carotid sinus baroreceptors triggered by low cardiac output)
o Drugs: opiates, psychotropics, SSRI, cytotoxics
o Other: acute intermittent porphyria, trauma, major abdominal or thoracic surgery,
symptomatic HIV
- Treatment:
o Treat the cause and restrict fluid
o Consider salt and loop diuretic if severe
o Demeclocycline is used rarely
o Vasopressin receptor anatagnoists (‘vaptans’) are emerging class of drug used in SIADH and
other types of hyponatremia

Hypernatremia
- S &S
o Extreme thirst
o Confusion – lethargy
o Coma, seizures, irritability
- Causes
o Usually due to water loss in excess of sodium loss
o Again divide into 3 sections
§ Hypovolemia – Fluid loss without replacement
• Sweating, GI loses, diuretics, renal failure, burns
 § Hypervolemia –
• Increased Na ingestion, increased aldosterone (Primary
hyperaldosteronism), IV drips
§ Euvolemia
• Those in ICU – mechanical ventilation
• Diabetes insipidus (suspect if arge urine colume, this may follow head
injury or CNS surgery, especially pituitary), fever
- Management
o Rehydrate – treat the cause
- Look @ Renin-AIdosterone system

BIOCHEMISTRY

Calcium
- Acts to contract skeletal/cardiac/smooth muscle
- Controls nerve impulses
- Involved in clotting
- Increased à depressed nervous system
- Decreased à excited nervous system

Calcium and phosphate homeostasis:

- Maintained through:
o Parathryoid hormone:
§ Overall effect is to increase Ca2+ and decrease PO43-
§ Secretion by 4 parathyroid glands is triggered by decreased serum ionized Ca2+,
controlled by negative feedback loop
§ Actions are:
• Increased osteoclast activity, releasing Ca2+ and Po43- from bones
• Increased calcium and decreased phosphate reabsorption form the kidney
• Increased renal production of 1,25-dihydroxy-vit D
o Vit D and Calcitriol:
§ Vit D is hydroxylated first in the liver to 25-hydroxy-vit D, and again in the kidney to
1, 25-dihydroxy-vit D (calcitriol), the biologically active form and 24,25-dihydroxy-
vit D
§ Calcitrol production is stimulated by decreased Ca2+, decreased phosphate and PTH
§ Actions are:
• Increased calcium and phosphate absorption form the gut, inhibition of PTH
release, enhanced bone turnover, increased calcium and phosphate
reabsorption from the kidney
o Note: Decreased magnesium prevent PTH release and may cause hypocalcemia
Calcium and Albumin:
- Calcium has ability to appear low- but actually be normal
- Due to albumin level
- 40% of calcium is bound to albumin* and the rest is free ionized Ca2+ which is the physiologically
important amount
o Therefore, low albumin levels can give false reading
- Corrected calcium (CaC)à calcium corrected fro albumin level
o Correct total Ca2+ for albumin as follow: add 0.1 mmol/L to Ca2+ level for every 4g/L that
albumin is below 40g/L

Hypocalcemia
- Apparent hypocalcemia may be an arterfact of hypoalbuminemia
- Signs and Symptoms:
o ‘SPASMODIC’
§ Spasms (carpopedal spasms: Trousseau’s Sign)
§ Perioral paraesthesia
§ Anxious, irritable, irrational
§ Seizures
§ Muscle tone increased in smooth muscle,
• Colic, wheeze and dysphagia
§ Orientation impaired (time, place and person) and confusion
§ Dermatitis (e.g. atoipic/exfoliative)
§ Impetigo herpetiformis (Decreased ca and pustules in pregnancy- rare and serious)
§ Chvostek’s sign, choroathteosis, cataract, cardiomyopathy (long QT on ECG)
o Tetany, lethargy, perioral tingling, hyperreflexia
- Signs
o Chovsteks – tap on the facial nerve – facial muscle to twitch
o Trousseau’s – BP cuff on and you get contraction of hand
- Seizures – increased excitability of neurons
- Cataracts – chronic hypocalcemia
- Carpo-pedal spasm – tetany of muscles
- Causes
 o Low calcium/low phosphate
§ Osteomalacia (increased alk phos)
§ Acute pancreatitis
§ Over-hydration
§ Respiratory alkalosis (total Ca2+ is normal, but decreased ionized Ca2+ due to
increase pH: symptomatic)
o Low calcium/high phosphate
§ Chronic kidney disease
§ Hypoparathyroidism (including thyroid and parathyroid surgery)
§ Pseudohypoparathyroidism
§ Acute rhabdomyolysis
§ Vitamin D deficiency
§ Hypomagnesemia
o Drug induced
§ Phenytoin
o Others
§ Cell lysis – rhabdomyolysis – Ca bind to damaged muscle cells
§ Acute pancreatitis
§ Hypercalciuric hypocalcemia
§ Low chronic Mg levels

-
- Secondary hyperparathryoidism à associated w /low Ca while primary & tertiary are associated
w/ high Ca
- Treatment:
o Mild symptoms:
§ Give calcium 5mmol/6h PO, and repeat daily plasma Ca2+
o In chronic kidney disease:
§ May require aldacalcidol, e.g. 0.5-1ug/24h PO
o Severe symptoms:
§ Give 10mL of 10% calcium gluconate 2.25mmol IV over 30 min
• Repeat as necessary
§ If due to respiratory alkalosis, correct the alkalosis

Hypercalcemia
- Bones/stones/abdominal groans/ psychic moans
o Bones- aches, ectopic calcifications- e.g. cornea
o Stones: RENAL STONES— renal failure
§ Formation of Ca Phosphate crystals at very high levels of Ca – renal stones
o Abdomina: pain, vomiting, constipation, polyuria, polydipsia, anorexia, weight loss
o Psychic moans: Depression, tiredness, weakness, confusion
o Depressed nervous system à slow reflexes
o Polyuria, polydipsia
o Decreased QT interval
o Decreased contractility & decreased neuron activity
- Causes
o Malignancy: Most common- suspect with decreased albumin/chloride
§ Bone metastases, myeloma, PTHrP
 o Primary & tertiary hyperparathryoidisms
§ In secondary à calcium is normal or low bc PTH is produced in response to a low Ca
level in an attempt to normalize (CFR)
o Others:
§ Sarcoidsosi
§ Vit D intoxication
§ Thyrotoxicosis
§ Lithium
§ Tertiary hyperparathyroidism
§ Milk-Alkali syndrome
§ HIV can cause both increased and decreased calcium
- Investivation:
o The main distinction is malignancy v primary hyperparathyroidism
§ Pointers to malignancy: decreased albumin, dcreased chloride, alkalosis,
hypokalemia, increase phosphate, increased alk phos
§ Increased PTH indicated hyperparathyroidism
§ Also FBC, protein electrophoresis, CXR, isotope bone scan, 24h urinary Calcium
excretion (for familial hypocalciuric hypercalcemia)
- Management:
o Diagnose and treat the underlying cause. If Ca2+ is over 3.5 mmol/L and symptomatic:
§ Correct dehydration:
• If dehydration is present, correct with IV 0.9% saline
§ Bisphosphonates:
• Prevent bone resorption by inhibniting osteoclast activity
• A single dose of pamidronate lower Ca2+ over 2-3d; maximum effect is one
week
• Infuse slowly, e.g. 30mg in 300mL 0.9% saline over 3h via a largish vein
• Max dose 90mg
• Side effects:
o Flu symptoms, decreased phosphate, bone pain, myalgia, nausea,
vomiting, headache, lymphocytopenia, decreased magnesium,
decreased calcium, seizures
Bloods you need to focus on
- calcium
- phosphate
- alk phos
- then consider PTH/Vit D
- then albumin

Need to know
- disease processes & how to recognize the table
- how to manage & further investigate
o osteoporosis
o DEXA
o Bisphosphonates/denosumab
Potassium:

Hyperkalemia: See below

- A plasma potassium of >6.5mmol/L is an emergency and needs urgent treatment
o The worry is of myocardial hyperexcitability leading to ventricular fibrillation and cardiac
arrest
- Concerning signs and symptoms:
o Include a fast irregular pulse, chest pain, weakness, palpitations and light headedness
o ECG:
§ Tall, tented T waves
§ Flattened P waves
§ Wide QRS complex
§ Ventricular fibrillation
- Note: Artefactual results:
o If the patient is well and ahs none of the above findings, repeat the test urgently as it may be
artefactual- caused by:
§ Hemolysis (difficult venipuncture, patient clenched fist)
§ Contamination with potassium EDTA anticoagulant in FBC bottles (Do FBC after
U&Es)
§ Delayed analysis (K+ leaks out of RBCs)
- Causes:
o Oliguric renal failure
o K+ sparing diuretics
o Rhabdomyolysis
o Metabolic acidosis
o Excess K+ therapy
o Addison’s Disease
o Massive blood transfusion
o Burns
o Drugs
§ E.g. ACE-inhibitors, suxamethonium
o Artefactual result
- Treatment of non-urgent causes:
o Treat the underlying cause; review medications
o Polystyrene sulfonate resin (Calcium Resonium 15 g/8h PO) bings K+ in the gut preventing
absorption and bringing k+ levels down over a few days
§ If vomiting prevents the PO administration, give 30 g enema, followed at 9h by
colonic irrigation
U&Es

Hyperkalemia
- ECG
o Tall, tented T waves
o Wide QRS
o Prolonged PR interval
o Depressed ST segment
o Flattened P wave
- What to do
o IV Calcium Gluconate 10% 10ml – myocardial stabilizer
§ Give undiluted over 5 mins, if patient is on digoxin give more slowly in 100ml
Glucose 5% over 20mins. Repeat at 5min intervals if needed until ECG normal (max.
3 doses in total)
o Insulin (Actrapid 10 units) + Glucose (50% 50mL)
§ Give into a large vein over 30 minutes
o Salbutamol 10 mg Neb
§ Caution in patients with a history of arrhythmias or ischemic heart disease
o If pH <7.2 consider Sodium Bicarbonate if advised by the Renal Registrar
o Stop all potassium containing/sparing drugs, promote urinary potassium loss (use of
appropriate fluids or diuretics), if the patient does not response to above measures call Renal
Registrar on call urgently to discuss dialysis
o CORRECT THE CAUSE!
V-fib (common after the widening QRS and ventricular tachycardia)
- Shock the patient!

Potassium
 - Expect it on the exam
- Mostly intracellular in nature 97-98%
- Should be between 3.5-5mmol/L
- Causes problems whether low or high

Shifting of K+
- Inwards
o Hypokalemia: Alkalosis, aldosterone
- Outwards: Hyperkalemia

Hyperkalemia
- Emergency
- Level >6.5 or increases in K+ w/ ECG changes must be treated
- Dialysis patients typically always have slight hyperkalemia- refer to dialysis team
- Causes
o Renal failure
o Rhabdomyolysis
o DKA
o Addisions
o Drugs? –
§ aldosterone antagonists
§ ACEi,
§ Beta Blockers
§ Sprionolactone
§ NSAIDs
o Don’t forget hemolysed sample
- ECG
o Wide, flat p wave
o Prolonged PR interval (normal is 3 small boxes)
o Decreased R wave amplitude
o Widened QRS
o Depressed ST segment
o Tall tented T waves
o Features you have to mention – tall tented T wave, prolonged PR interval, widened QRS!
- If he has MI – need to interpret it as that!
- Treatment
o 10mls of 10% calcium gluconate IV – myocardial stabilizer
o Insulin dextrose – push K back into cells
o Beta agonists nebulizer - salbutamol
o Correct cause!

Hypokalemia
- Number of different ways to divide classifications:
o GI loss
§ Excessive vomiting or diarrhea
§ High stoma or fistula output
o Renal tubular disease
o Endocrine syndromes
§ Conns or Cushings
o Metabolic alkalosis
o Drugs
- Renal
o Anything that causes increased Na+/K+ exchange
§ Conns
§ Inherited – Gittlemans/Barters/Liddles
§ Secondary hyperaldosteronism
o Decreased Na/Hydrogen Ion exchange
§ Renal Tubular Acidosis Types 1 & 2
o Impaired proximal tubular reabsorption
§ Decreased Mg/Fanconi syndrome
o Excessive Na+ for exchange
- Non renal
o GI losses
§ V&D
§ Don’t forget anorexic teenager
o Redistribution syndromes – glucose/insulin, catecholamines
 - Patient complains of:
o Muscle twitching, fasciculation’s
o Weakness
o Cramps in limbs
o Tetany
o *Appears like hypocalcemia
- ECG
o Slightly peaked p wave
o Prolonged PR interval
o ST depression
o Shallow T wave
o Prominent U wave
o Need to mention – prolonged PR interval, ST depression, presence of U wave
- Treatment
o Always cautious
o If mild à always oral
o If severe & symptomatic
§ IV but carefully
§ <20mmol/hr & <40mmol/L- SLOW
- Remember in management to say what you want to do to overall manage the person- if they come in
with atrial flutter, for instance, send of routine bloods and white cells to look for a precipitant like
infection

TUTORIAL 4: ECG
ECG Axes
- Normal axis bw 11-5
o Leads I/II/IIIàbipolar leads
§ Normal axis has + wave deflection in all of these leads
§ Lead II normally has biggest QRS complex because it is
the most in line
- V1-V4 = anterior
- II, III, aVF = inferior
- V5, V6, aVL = lateral
Right Axis Deviation
- Generally pulmonary conditions
- Also RVH
- Extra muscle = extra signal strength on R side
- Lead I goes negative, II/III positive
Left Axis Deviation
- Generally a conduction condition
- Lead I stays positive, lead II/III go negative
Axis deviation may be normal
- People who are tall/small/fat/thin
- However, may also point you in direction of something else going on
- For your exam – its just about recognizing when they are present!
- If left axis deviation - Look @ p waves, is PR interval increased
ECG patterns
- Need to know different arteries
 -
Anterior STEMi
- most severe
- widowmaker
- remember anterior leads are definitely V3/V4
- its LAD that supplies the area
- however, LAD supplies branches to septum – commonly involved V1/V2 & often lateral branches
- blockage in early LAD
o can affect all leads from V1 – V6 & perhaps all lateral leads – this is extensive anterior MI
o if occurs in mid LAD – the septal branches may be excluded – given rise to an ST rise from
V3/V4 +/- lateral branches

-
o This is tombstone look – not good
Inferior STEMI
- Inferior leads involved – II/III/aVF
- Often get reciprocal depression in leads I & aVL

-
- because the inferior MI is going on you get reciprocal depression in those other leads I & aVL
Posterior wall MI
- this one can have varying signs
- wall supplied by posterior descending artery
- 80% - right sided dominant – RCA
- therefore we can get posterior & inferior signs if there is a blockage here!
- If its just posterior
o Getting ST depression in leads V1-V4 à posterior to anterior leads
- Can get posterior-inferior MI

-
MI
- Please remember that n MI should not be interpreted w/ LBBB present – tx as if new in particular
- Need to have 2 of 3
o chest pain, troponin, ECG
Complications of MI
- Ischemic - reinfection, infarct extension, angina
- Mechanic - cardiac failure, cardiogenic shock, mitral regurg, ventricular aneurysm, cardiac rupture
(ventricular septum, papillary muscle, or cardiac wall)
- Arrhythmic – atrial/ventricular, sinus or AV node dysfxn
- Embolic – CNS embolus (stroke), peripheral embolus, LV mural thrombus
- Inflammatory – pericarditis, Dressler’s
Case
- 29 y/o male
 - 2 days hx of feeling unwell
- Thinks having temps at time
- No cough/wheeze
- Now complaining of a pain on the left side of his chest
- ECG shows
o ST elevation in every lead
§ Either every artery is blocked – really bad
§ Or something else going on
o Pericarditis
§ Saddle shape STEMI in every lead
§ Treatment
• NSAIDS, colchicine
Another ECG
- Right axis deviation (due to pulmonary problems that can give RV hypertrophy)
- Dominant R wave in V1 (>7mm tall)
- Dominant S wave in V5 or V6 (>7mm deep)
- +/-
- right atrial enlargement (P pulmonale)
- RV strain pattern à ST depression/T wave inversion in the right precordial (V1-4) & inferior (II, III,
aVF)
- Causes
o Mitral stenosis
o Pulmonary embolism
o Chronic lung disease
o Congenital heart disease (teratology of fallot, pulmonary stenosis
o Arrhythmogenic RV cardiomyopathy
LV hypertrophy
- Left sided pressure overload
- Increased R wave amplitude in the left sided ECG elads (I,aVL, & V4-6)
- Increased S wave depth in right sided leads (III, aVR, V1-3
- Generally recognized by following rule
- S wave depth in V1 + tallest R wave height in V5-V6>35mm
- Usually w/ ST segment depression & T wave inversion in left sided leads
- Other features
o L axis deviation?
Wolf-parkinson white syndrome
- Upstroke before the QRS
- Pre-excitation pathway – where there is early activation of ventricles b/c of bypass tract around the
AV node
- There are mult forms of accessory pathways & syndromes
- Reason to important to recognize à can predispose to AVRT (atrio-ventricular re-entry tachycardia)
- Features
o Shortened PR interval w/ slightly prolonged or widened QRS
o ST & T waves opposite direction to QRS
o Presence of delta wave à up-sloping pattern initial QRS complex
o Possible to have normal ECG & still have WPW
- Treatment
o Maneuvers- bearing down, massage
o Radiofrequency ablation
What to know
- Supraventricula
- A-fib/a-fluter
- Sinus tachy
- Atrial tachy
- V-tachy- mono/polymorphic
- Vfib
- Management
o Synchronous shocking vs desynchronizing
o Know medications

TUTORIAL 5: ABG/ANION GAP

Overview
- ABG is divided into 6 things you actually need to pay attention to currently
o pH
 o PaO2
o PaCO2
o HCO3
o Base excess
o Anion gap
PaO2
- Really mean the partial pressure of O2 in a persons blood
- Normal values (11-13) = where the person with normal lungs is breathing room air with 21% oxygen
- Logically if a person has an O2 mask on – can’t judge O2 properly
o If fraction of O2 the person is taking in increases – the PaO2 will also increase
- Where PaO2 comes into it own is in respiratory failure
o Value of <8kpa = failure
o The type of failure then depends on the PaCO2
o However, any abnormal decrease in PaO2 may indicate an underlying process such as
edema
- Type I respiratory failure – just hypoxia
- Type II respiratory failure – hypoxia & hypercapnia

Type I Respiratory Failure:

- PaO2 <8 & normal PaCO2
- Causes:
o LRTI
o Fibrosis
o PE
o Asthma
- Need to give them oxygen

Type 2 Respiratory Failure:

- PaO2 <8 & a raised PaCO2
- Causes:
o COPD
o Asthma
o Obesity
o Motor Neuron Disease
- Try to increase respiratory drive, decrease PaCO2 & bring back up paO2

Acidosis vs alkalosis:
- Respiratory acidosis/alkalosis vs metabolic acidosis/alkalosis
- Note if there is a venous sample
o Taken for ABGs sometimes
o Can’t determine the PaO2 – can’t determine oxygen level itself
o Where your venous is you can determine lactate!
- So if you see venous sample - most likely not a respiratory issue, maybe a metabolic or a DKA –
they want you to look @ the lactate

Normal values
- pH 7.35-7.45
- PaCO2 4.7 – 6.0kPa
- PaO2 >10kPA
- HCO3 22-26 mmol/L
- Base excess +/-2mmol/L
Step 1:
- Assess pH – normal 7.35-7.45
- Low <7.35 à acidotic
- High >7.45 à alkalotic
Step 2
- What is their PaCO2? – Likely due to respiratory cause or a metabolic cause
- High à acidotic
- Low à alkalotic
- If this is predominant feature à respiratory
Step 3
- Bicarb?
- High à alkalotic
- Low à acidotic
- If this is predominant feature à metabolic cause
Compensation
 - Body reacts to any sudden change – attempts maneuvers to reverse
For example
- Pt comes in with respiratory failure – developing respiratory acidosis
- ABG showing pH 7.30 & PaCO2 of 9.5
- Persons underlying system should be attempting to reverse trend
o How is does it do this.. it works on the opposing alkaline substance- the bicarb
What if HCO3 doesn’t shift? à no compensation
- If HC03 doesn’t shift – means underlying condition going on – elderly, comorbid

Respiratory Acidosis:
- Any cause of Resp failure

Respiratory Alkalosis:
- Hyperventilation
- Causes of this?
o Anxiety
o Altitude
o Pregnancy
o Subarachnoid Hemorrhage

Now to apply similar principles to metabolic processes:

- Firstly, think back to the 3 jobs of analysis
o pH analysis
o PaC02 analysis
o HC03 analysis
The basic principle
- Low pH
o High pPaCo2- resp acidosis
o Low HCO3- met acidosis
- High pH
o Low paCo2- resp alkalosis
o High hco3- metabolic alkalosis
Patient comes in with:
- pH 7.2 (low)
- HCO3 17 (low) 22-26
- paCo2 5
o Metabolic acidosis
- Repeat: Resp compensation
o 7.25
o hco3- 18
o paCo2- 3.2
- Now you havea metabolic acidosis with a respirtatory compensation
o i.e the body acts to reduce the CO2 levels in order to try to return the body to a normal pH

met acidosis with resp compensation:

- pH – low
- HCO3- low
- PCO2- low to normal
Met alkalosis with resp compensation
- Ph- high
- HC03- high
- Pco2- normal to high

Mixed picture- typ 1 diabetic with a DKA who is now in resp failure
- 2 acidotic process going on- therefore whats called is a mixed acidsosis
- pH low 7.2
- Pco2 high 11.3
- HCO3 – 17
o Show be high to compensate for the high PCO2
o Or normal if the person just isn’t compensating
- Just think whenever something should be normal or compensating- but instead has shifted
completely wrong way
o Mixed picture – look at the history

Anion Gap
 - (Na +K) – (Cl + HCO3) – always calculate gap especially in metabolic acidosis
o K may be excluded
o Normal AG = 8-12 (without K)
o 12-16 if K is included
- Typically used in metabolic cause for acidosis!
o Basically a means to allow us to see if a person is acidotic or alkalotic
o It is primarily used to allow us to see if you have a metabolic cause for an acidosis and then
to narrow down the cause and finally to monitor how the patient is responding to treatment
- Blood consists of cations & anions
o K, Na, HCO3, Cl makes up mostly 100%
o Other things in gap - Albumin, phosphate, organic acids
- We therefore have a formula to calculate how much of these excess ions are present in the blood
- A normal gap should be somewhere between 12-16 mmol/L
o A metabolic acidosis with this is therefore a normal anion gap metabolic acidosis
- Anything >16 (with K) or >12 (w/out K) à gives rise to raised anion gap, metabolic acidosis

Raised Anion Cap Causes:

- Cyanide, Carbon monoxide
- Alcoholic ketoacidosis
- Toluene- Methylbenzene
- Methanol, metformin
- Uremia
- DKA
- Paracetamol
- Iron, isonazid
- Lactate
- Ethanol, ethylene glycol
- Salicylate
- Pneumonic is CAT MUDPILES

Normal Anion Gap Causes:

- Generally, due to loss of HCO3 – which in turn is replaced by Cl
- Hyperchloremic acidosis
- Addison’s, bicarb loss (GI or renal – RTA tubular acidosis), chloride, drugs (acetazolamide, acids)

Metabolic alkalaosis
- Hypercalcemia
- Diuretics
- Primary or secondary hyperaldosteronism (Conns/renal artery stenosis)
- GI losses
- Bicarb ingestion

Base excess
- If it is negative & the pH is negative à points towards a metabolic acidosis
- If the base excess is opposite to pH – (e.g. its positive while pH is negative) à primary problem is
resp acidosis & the base has increased to compensate

TUTORIAL HEME 23/2/18

Myeloma
Description:
- Hematological malignancy
- Malignancy of plasma cells – which then interfere with production of normal blood cells
- Plasma cells produce abnormal antibodies and immunoglobulins in the body
- Associated with increased age
o Radiation exposure
o MGUS à Myeloma
o Genetic element
Pathogenesis:
- Arises due to monoclonal (same repeated plasma cell) à large amount of Ig production
- These are referred to as a paraprotein band or an M band – on serum electrophoresis
- May be IgG/IgA/IgM
- Most common is IgG – usually other 2 will actually decrease production in response
- Proteins produced by plasma cells à urine = bence jones proteins
 - Huge amount of plasma cells exist w/in the bone marrow - disturbing bone formation
o Patients begin to develop fractures easily as osteoclasts work but no osteoblasts
(hormone stimulated by the myeloma cells)
- Calcium levels start to soar

Patients present with: ‘ CRAB’: HyperCalcemia, Renal failure, Anemia (and thrombocytopenia) and Bone
fractures
- Bone problems – easy fractures/lytic lesions on scans/bone pain +/- vertebral collapse
- Decreased RCC/WCC/Platelets – due to abnormal bone marrow à anemia/increased
infections/bleeding
- Renal failure – due to deposition of light chains Ig in kidney
- Symptoms of increased calcium
- Lack of normal Ig à increased risk of infection
Complications
- Recurrent infections
- Recurrent fractures
- Spinal cord compression
- Hyperviscosity symptoms (headaches/bleeding/heart failure etc)
- Amyloidosis – can cause problems anywhere in the body

Diagnosis
- Two of the following factors should be present
o Paraproteinemia or Bence jones proteins
o Radiological evidence of lytic lesions – Pepperpot skull
o Increased bone marrow plasma cells >30%
o >1g of light chains excreted/day
o Monoclonal band of Ig in serum or monoclonal light chains in urine on electrophoresis
o Major criteria
§ Plasmacytoma (as demonstrated on evaluation of biopsy specimen)
§ 30% plasma cells in a bone marrow sample
§ Elevated levels of M protein in the blood or urine
o Minor criteria
§ 10% to 30% plasma cells in a bone marrow sample.
§ Minor elevations in the level of M protein in the blood or urine.
§ Osteolytic lesions (as demonstrated on imaging studies).
 § Low levels of antibodies (not produced by the cancer cells) in the blood.
o Hypercalcaemia in myeloma
§ Primary factor: due primarily to increased osteoclastic bone resorption caused by
local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
§ Much less common contributing factors: impaired renal function, increased renal
tubular calcium reabsorption and elevated PTH-rP levels
Investigations
- Monoclonal proteins (usually IgG or IgA) in the serum and urine (Bence Jones Proteins), Increased
plasma cells in the bone marrow, historically a skeletal survery has been done to look for bone
lesions, However, a whole body MRI is increasingly used and recommended in the 2016 NICE
guidelines
- Bloods
o FBC –
§ Hb, WCC, & platelet – may be normal or low
o ESR –
§ Almost always high, CRP always raised
o Blood film –
§ Rouleaux formation due to increased paraproteins
o U&E–
§ Renal failure- light chain immunoglobulin deposition
o Calcium –
§ Normal or high
o Alk phos –
§ High
- Specialized test
o Skeletal survey –
§ Show lytic lesions – common in skull
o Serum protein electrophoresis –
§ Determines type of protein
o Urine protein electrophoresis –
§ Bence Jones
o Bone marrow aspirate –
§ Plasma cell infiltration of bone marrow
Treatment
- Largely supportive
o Idea is to prevent complications that are most likely to kill you – infection/heme/renal
failure
o Vaccines
o Correction of anemia
o Treatment of bone pain
- Bisphosphonates
o Not used to help reduce progression
- Chemo
- Thalidomide – now druge in vogue
Follow on or part C questions – lead to complications of myeloma

Thrombocytopenia
- Normal platelet count 150-300 x 10^9/L
- Thrombocytopenia <150 x 10^9/L
- A platelet’s half life is 9-10 days
- 1/3 of platelets stored in spleen
4 reasons for decreased platelet count
- Dilutional
o Transfusion situations
o Someone post-Renal Tubular Acidosis
o Received large amount of packed Red Blood Cell (no platelets)
§ Need to monitor pt – may need platelets
- Sequestration
o May be seen w/ myelofibrosis or portal HTN secondary to liver disease
o Splenic feedback & enlargement (platelets can get trapped, as in malignancy)
§ Gets increased sequestration of platelets in the spleen
§ Get decreased circulation platelet count
§ Often no actual signs – but bloods
o Anything that causes an enlarged spleen
§ Liver disease, myelofibrosis
 - Decreased production
o Divide causes into 3 sections
§ Marrow damage
• Aplastic
• Drugs (chemo)
• Toxins
• Malignancy
• Hepatitis
§ Congenital
• Fanconis/Rubella
• Wiskott Aldrich
• TAR syndrome
• May Hegglin
§ Ineffective production
• B12/folate deficiency – megaloblastic
- Increased destruction
o Immune vs Non-Immune
o Immune
§ Drug induced
§ ITP
• Idiopathic thrombocytopenic purpura (ITP) is a bleeding disorder in
which the immune system destroys platelets, which are necessary for
normal blood clotting. People with the disease have too few platelets in the
blood. ITP is sometimes called immune thrombocytopenic purpura or
simply, immune thrombocytopenia.
§ Secondary to SLE/AIDS etc
o Non-Immune
§ DIC- Disseminated Intravascular Coagulation
• Severe, rapidly evolving DIC, in contrast, causes thrombocytopenia and
depletion of plasma coagulation factors and fibrinogen, which cause
bleeding. Bleeding into organs, along with microvascular thromboses, may
cause dysfunction and failure in multiple organs.
§ TTP
• Thrombotic thrombocytopenic purpura (TTP) is a rare blood disorder. In
TTP, blood clots form in small blood vessels throughout the body. The clots
can limit or block the flow of oxygen-rich blood to the body's organs, such as
the brain, kidneys, and heart. As a result, serious health problems can
develop.
§ HUS
• Hemolytic-uremic syndrome (HUS) is a disease characterized by a triad of
hemolytic anemia (anemia caused by destruction of red blood cells), acute
kidney failure (uremia), and a low platelet count (thrombocytopenia). It
predominantly, but not exclusively, affects children.
§ HELLP syndrome (hemolysis, elevated liver enzymes, low platelets)
Coagulation
- 3 things
o Vessel walls
o Coag factors
o Platelet factors
- Prothrombin time
o Depends on clotting factors 1,2,5,7,10 (all made w/in the liver)
o Synthetic function of the liver
o The prothrombin time (PT)—along with its derived measures of prothrombin ratio (PR)
and international normalized ratio (INR)—are assays evaluating the extrinsic pathway
of coagulation.
o PT measures factors I (Fibrinogen), II (Prothrombin), V (Proaccelerin), VII
(Proconvertin), and X (Stuart–Prower Factor)
- INR
o Converted PT into a lab format
o Warfarin monitoring
o Normal is 2-3 for warfarin & a-fib
o 2.5-3.5 for metallic heart valve
- Activated PTT
o all clotting factors besides 7
o Used for heparin infusion
 o Not really a concern where LMWH is now used
o Partial thromboplastin time (PTT) measures the overall speed at which blood clots by means
of two consecutive series of biochemical reactions known as the "intrinsic" (now referred to
as the contact activation pathway) and common coagulation pathways.
§ The partial thromboplastin time (PTT) is used in conjunction with another measure
of how quickly blood clotting takes place called the prothrombin time (PT). The
prothrombin time measures the speed of clotting by means of the extrinsic pathway
(also known as the tissue factor pathway).
- Bleeding time
o Old test
o Time taken for bleeding to stop
o Elevated where low or defective platelets

DIC- Disseminated Intravascular Coagulation

- 2 processes involved clashing with each other
- Fibrin deposition leads to infarction
o Infarction = use of all clotting factors à bleeding
o Thrombo-hemorrhagic disorder
- Occurs secondary to something else – in the case of exam often sepsis/trauma
- Anything that can cause extensive endothelial damage or release of tissue thromboplastin &
activation of factors
- Suspect on exam when
o Raised PT & APTT
§ Reduced clotting factors
o Reduced fibrinogen
§ Increased clotting due to deposition
o Raised D-dimer
§ Attempts to break down clots
o Almost always see Thrombocytopenia – not always there to start in every case – in your
exam it will probably be – but the platelets gradually drop so at the beginning they maybe
normal
o Schistocytes may be seen on smear/film – not specific
- For DIC you have to consider whats going on
o Thrombosis – likely to need heparin
o If bleeding/loss of platelets – need Fresh Frozen Plasma
o Most important answer is that you treat underlying precipitant
- Causes
o Sepsis or severe infection
o Trauma (poly trauma/fat embolism)
o Organ dysfunction: Fulminant hepaitits, severe pancreatitis
§ Obstetric – amniotic embolism/placental abruption
o Malignancy: Solid tumours, myeloproliferative, lymphoproliferative
o Transfusion reaction or transplant rejection
o Toxins
- P/C:
o Those with an underlying inciting condition ± symptoms of thrombosis, embolism, organ
dysfunction, or bleeding (petechiae, ecchymosis, blood loss from IV lines & catheters)
- Lab Pattern:
o Platelet count: Moderate/severe thrombocytopenia (<50x10^9), repeat counts
o aPTT and PT: Prolonged (clotting factors reduced/used up elsewhere)
o Reduced fibrinogen: widespread fibrin formation
o Raised D-Dimer: body’s attempt to break down fibrin deposits
- Blood filmd:
o Microangiopathic pathologic (schistocytes) on peripheral smears are suggestive – ISTH
scoring system of over DIC (>5)
- Treatment:
o ABCDE
o TREAT THE CAUSE! Monitor vitals, assess extent of hemorrhage, correct hypovolemia and
administer basic hemostatic procedure
o Administration of blood components and coagulation factors based on clinical and
laboratory results combined
o Fibrinogen concentrate in conjunction with fresh frozen plasma
§ Anticoagulation: LMWH

TTP –thrombotic thrombocytopenia purpura

- Generally 5 features (FAT RN) – Fever, Anemia, Thrombocytopenia, Renal, Neuro
 o Low platelets
o Fever
o Neuro deficits
o Kidney failure
o Red cell fragments on smear
- TTP & DIC can be distinguished based on occurrence in different settings – trauma or sepsis for DIC;
fever & microangiopathic hemolytic anemia for TTP
- Patients with TTP –HUS do not demonstrate lab abnormalities frequently encountered in DIC
- Results of blood coagulation assays in TTP are normal but blood results indicative of hemolytic
anemia are present – LDH, etc
- Treatment
o Plasma exchange/plasmaparesis
o Steroids
o RBC transfusions
o Occasionally immunosuppressants
o DO NOT do platelet transfusion à makes it worse

Hemolytic uremic syndrome

- More common in children
- Lot of same features as TTP
- Associated with EHEC 0:0157

HITS – Heparin Induced Thrombocytopenia

- Usually 4-10 days after exposure (Type 2)- Platelets release microparticles that activate thrombin,
thereby leading to thrombosis
- P/C
o Thrombosis and abnormal clotting- need to be anticoagulated
o Thrombocytopenia
o Thrombosis
o Acute systemic reaction following use of unfractionated heparin given IV
- Often skin lesions @ site of heparin injection
- On occasion – acute anaphylaxis
- Diagnosis of exclusion- when other causes can be ruled out
o Thrombocytopenia
o Timing of thrombocytopenia relative to heparin exposure
o Thrombosis or other sequaliae of HIT
o Exclude other causes of thrombocytopenia
- Usually platelet drop can be between 5-10 days
o With prior exposure, it may be within 24-48 hours
- Tx:
o Discontinue heparin products immediately (caution- heparin in flush)
o Patients at high risk of thrombotic events
§ Tx with direct thrombin inhibitor ( argatroban) or indirect factor Xa inhibitor
(fondaparinux in pregnancy)
§ NOACs? Awaiting FDA approcal

ITP – Immune Thrombocytopenic Purpura

- May be idiopathatic or secondary
- Idiopathic
o Platelets <100
o No other cause of thrombocytopenia
o No other evidence of secondary cause
o Think of it in females when patient is <60
- Symptoms
o Excessing bleeding w/ minor injuries
o Spontaneous bleeding from mouth or nose
o Unexplainable or spontaneous bruising (purpura)
o Extravasation of blood form capillaries in the skin (petechiae)
o Excessive internal bleeding
§ Intracranial hemorrhage: headache, blurred vision, loss of consciousness, HTN and
bradycardia
o Disturbed sleep cycle/insomnia
o Irregular appetite
o Depression
o Chronic:
§ Females with menorrhage and epistaxis
 o Acute:
§ Child post infection
o What is NEVER present? Splenomegaly
- Immune based
- Antibodies directed against platelet membrane antigens
- Lack of compensatory effect combines w/ destruction
- Secondary
o Post-infection – HIV/Hep C
o Lymphoproliferative disorders
o Vasculitis
o Drugs ex: sulfa based antibiotics
- Seen in investigations:
o Low platelets
o Platelets may be described as large on blood film
§ Raised megakarycocytes in marrow
o WCC & RCC generally normal (not seeing schistocytes) & not seeing increased WCC like WCC
abnormalities/sepsis)
- Treatment
o No treatment usually needed if platelet >50 and asymptomatic
o Often even if >20 – no need to treat if asymptomatic
o Symptomatic or platelets <20-
§ Treat with 1mg/kg/d prednisiolone PO, reduce after remission and taper dose
§ Aim to keep platelets >30
o If severe---
§ Platelet transfusion: splenectomy or life threatening hemorrhage
§ IV Immunoglobulin (temporarily raise platelet count for pregnancy or surgery)
§ Relapse: splenectomy or B cell depletion w/ rituximab
o Eltrombopag (oral thrombopoietin-receptor agonist) & romiplostim (injectable
thrombopoietin analogoue) for refractory dz
Neutropenic sepsis

Neutropenic sepsis is a relatively common complication of cancer therapy, usually as a consequence of

chemotherapy. It may be defined as a neutrophil count of < 0.5 * 109 in a patient who is having anticancer
treatment and has one of the following:
• A temperature higher than 38ºC or
• Other signs or symptoms consistent with clinically significant sepsis

Prophylaxis
If it is anticipated that patients are likely to have a neutrophil count of < 0.5 * 109 as a consequence of
their treatment they should be offered a fluoroquinolone

Management
• Antibiotics must be started immediately, do not wait for the WBC
• NICE recommend starting empirical antibiotic therapy with piperacillin with tazobactam (Tazocin)
immediately
• Many units add vancomycin if the patient has central venous access but NICE do not support this
approach
• Following this initial treatment patients are usually assessed by a specialist and risk-stratified to see
if they may be able to have outpatient treatment
• If patients are still febrile and unwell after 48 hours an alternative antibiotic such as meropenem is
often prescribed +/- vancomycin
• If patients are not responding after 4-6 days the Christie guidelines suggest ordering investigations
for fungal infections (e.g. HRCT), rather than just starting therapy antifungal therapy blindly there
may be a role for G-CSF in selected patients

LIVER FUNCTION TESTS

Jaundice
- Bilirubin
o Bilirubin not confied to the liver
o Comes from heme molecules in body
o Heme à bilverdin à bilirubin
o All within the reticuloendothelial system
§ System is made up of the spleen, liver, parts of kidney
- Why does it affect the liver?
o Taken up in liver
o Conjugated by glucoronyl transferase to a product that can be excreted
o It is joined to glucoronic acid
o May then be excreted as bile – passed into intestine
o Then passed out –
§ Stool = stercobilogen and urine = urobilinogen
o Bilirubin is not normal in urine
- Jaundice arises if there is an issue w/ this process (above)
- Best way to do this is divide process into 3
o Pre-hepatic
o Hepatic
 o Post-hepatic

Pre-Hepatic Jaundice
- Excessive RBC or any RBC precursor breakdown (reticulocytes etc)
- Needs to be in large amounts to actually show up
- Most common signs we will get is
o Initially normal urine – turns black if left to stand (but for exam its normal)
o Stool normal to darker
- Causes
o Sickle cell
o Thalassemia
o Any kind of hemolytic anemia
o Neonatal jaundice
o Drugs – sulphasalazine (GI- Crohns)/Methyl dopa most commonly
- Tests
o Need to do an FBC
o LFTS – what would you expect
§ Indirect bilirubin (unconjugated)
o Urine
o What sings & symptoms?
§ Normal
- Conditions
o Gilberts - Crigler najarr
o Some people classify them as pre-haptic or hepatic
o Whichever – remember its unconjugated bilirubin
o But the issue is with conjugating system (UDP-glucuronyl transferase) – Crigler Najar is
worse and is seen in infancy

Hepatic jaundice
- Inability of liver to excrete +/- conjugate bilirubin
- Damage to liver cells- hepatocytes
- May have both increased conjugated & unconjugated bilirubin as a results
- However often but not always predominantly conjugated – therefore the tendency is towards
darker urine but often normal stools
- Causes
o Viral hepatitis
o Drug induced hepatitis – paracetamol
o Autoimmune hepatitis – think of young woman (anti-smooth muscle antibodies)
o Alcohol
o Infections – leptospirosis
o Decompensated cirrhosis

Post-hepatic
- Confusing term – because its not all outside the liver
- Rather what it means is – its outside the conjugation process
- So here the bilirubin will be conjugated fine but there will be an issue with biliary drainage
- This can be from within the liver or outside the liver
- Another classification subdivision:
o Intrahepatic cholestasis
§ PBC
§ PSC
§ Dubin Johnson Syndrome
§ Rotor syndrome
§ Drugs (phenothiazines in particular)
• Phenothiazine antipsychotics are medications used to treat schizophrenia
and manifestations of psychotic disorders
o Extrahepatic cholestasis
§ Gallstones
§ Carcinoma of the head of the pancreas
§ Bile duct stricture
§ Cholangiocarcinoma
§ Gallbladder cancer
§ Pancreatitis
- Stool – pale; Urine – dark
x
- As rule of thumb for serum bilirubin w/ high total bilirubin
o <20% conjugated – unconjugated hyperbilirubinemia
o >50% conjugated – conjugated hyperbilirubinemia
- Investigations
o LFTs is obvious one
o Blood film/smear – hemolytic?
- Specifics:
o ESR - Inflammatory signs – what could it be raised in?
o LDH – hemolytic anemias
o Coagulation screen
o ANA/ASMA (autoimmune hepatitis)
o Serum electrophoresis (thalassemia)
- Imaging
o Ultrasound 1st; then CT
o Procedures – Endoscopy, MRCP à ERCP

Remaining LFTS
- Divided into – AST, ALT, GGT, Alk phos, INR
- AST & ALT
o Indicated intracellular damage to the liver, AST can also raise with skeletal or cardiac
muscle damage
o ALT can go as high as 50 x normal limit:
§ Most commonly raised this high if a viral or drug induced hepatitis
§ More specific than AST for liver
§ Very high levels suggest acute parenchymal liver damage
o AST levels x20 normal limit = viral hepatitis/Skeletal muscle trauma
§ Levels x 10 – alcoholic cirrhosis
§ Mildly raised – fatty liver or liver mets
• Rule of thumbs
o AST is higher than ALT in cirrhosis, Intrahepatic neoplasia,
hemolytic jaundice, & alcoholic hepatitis
o ALT is raised more than AST in acute hepatitis & in extrahepatic
obstruction
- Alk phos
o Not as specific for liver issues
o Definitely not of major use in pregnancy
o Raised in liver injury/bone pathology/pregnancy
 o High levels à bile duct blockage (small rise in hepatocyte issues)
- GGT
o Used to look @ Alk Phos firstly, if GGT is also raised then likely to be liver
o Alcoholics will almost always have raised GGT
o Seen with obstruction of bile ducts
o GGT + high MCV à alcohol
o GGT + high ALP à think obstruction (gallstone)
o GGT + high ALT à think liver cell issues
- If all 4 are raised (AST, ALT, Alk phos, GGT)
o GGT & ALP way higher & out of proportion to AST/ALT à Obtructive
o AST & ALT may rise due to increase pressure
o If AST/ALT way higher à internal liver
§ Viral hepatitis, autoimmune hepatitis, drugs (paracetamol), ETOH, metabolic
(Wilson), CCF, malignancy, fatty liver
- INR – synthetic function
o Clotting profile
o How well is this liver functioning
o Intrahepatic issues
o Albumin likely to be low was well
Auto-antibodies
- Primary Biliary Cholangitis/Cirrhosis – anti-mitochondrial
- Auto-immune hepatitis
o Anti-nuclear
o Anti- smooth muscle
o Anti liver/kidney microsomal – 1
- Anti-dsDNA – SLE
- Anti-mitochondrial – PBS
- P-Anca – Ulcerative Colitis, Primary Sclerosing Cholangitis
- C-Anca – Wegners Granulomatosis
- Anti-endomysial/gliadin/transglutaminase celiac
- Anti-centromere – crest/scleroderma
- Anti-Ro -, anti la – sjogrens
- Anti- Jo – polymositis
- RF – RA, Sjorgrens, SLE
More tests
- Wilsons – copper studies – low ceruloplasm
- Hemochromatosis – iron studies
- IgG – high autoimmune disease/chronic infection/PBC
- IgM – acute hepatitis

Rush – Anemia:

Basic Principles:
- Reduction in circulating RBC mass
- Presents with signs and symptoms of HYPOXIA: weakness, fatigue, dyspnea
o Pale conjunctiva and skin
o Headache and lightheadedness
o Angina, esp. with preexisting CAD
- Hb, HCT and RBC count are used to measure RBC mass
- Definition:
o Hb <13.5 g/dL in males, <11.5 g/dL in females
- MCV <80 = microcytic, >100 = macrocytic

FBC:
 - Myeloid v lymphoid progenitors
o Lymphoid-
§ Natural Killer Cell
§ Small Lymphocyte
• B Lymphocyte
o Plasma Cell
• T Lymphocyte
o Myeloid –
§ Megakaryocyte
• Thrombocytes
§ Erythrocyte
§ Mast Cell
§ Myeloblast
• Basophil
• Neutrophil
• Eosinophil
• Monocyte
o Macrophage

Components:
- White cell count
o Broken down into a differential of 5
o Linked to its WCC differential
o Overall white cell count:- raised: infection/inflammation/cancer/leukemia
§ Neutrophils
• Raised:
o Bacterial infections
o Steroids
o Inflammation
o Post MI necrosis
o Malignancy
• Decreased:
o Viral infection
o Chemotherapy
 o Radiotherapy
o Widespread severe bacterial infection
o Aplastic anemia
§ Lymphocytes
• Raised:
o Viral
o Leukemia:
§ Chronic Lyphocytic Leukemia
o Lymphomas
o Chronic infections
• Deceased:
o Chemotherapy
o HIV
o Leukemia
o Radiation
o Steroids
o Sepsis
§ Eosinophils
• Allergies
• Parasites
• Hypersensitivity
§ Basophils
• Post splenectomy
• CML
• Infections
§ Monocytes
• Chronic infections
- Hemoglobin
o Link to the MCV
o Link to the MCHC
- Red cell count
o No. of red cells per unit volume blood
- Platelets
o No. of platelets per unit volume blood
o Link to all the others
o Plus don’t forget your LFTs
- Hematocrit
o Amount of space your red cells take up in your blood
- Mean Corpuscular Volume
o Measurement of the average size of your red cells
- Mean corpuscular Hb concentration
o Calculation of the average Hb in the red cells
- Red Cell Distribution Width

Connections to disease processes and bloods:

Anemia:
- Symptoms:
o Eyes: yellowing
o Central: fatigue, dizziness, fainting
o Skin: paleness, coldness, yellowing
o Respiratory: shortness of breath
o Muscle: weakness
o Heart: rapid heart rate, palpitations

Blood Component: Increases

- Red cell count
o Increased:
§ Either increased production or
§ Fluid/volume loss
- Hemoglobin:
o Increased production of Red Cells
- MCV:
o Liver disease
o Underactive thyroid
 o Pregnancy
o Alcohol excess,
o Some bone marrow disorders
o B12/Folate deficiency
o Decreased:
§ Iron deficiency
§ Longstanding disorders
§ Thalassemia
- MCHC:
o Generally follows MCV
- Red distribution width:
o Abnormal in B12/Folate and iron disorders

Reticulocytes:
- Have to request them, do not appear in the normal FBC profile
- Early Red Blood Cell
- Increased if there is rapid loss/destruction

Anemia workup- MCV:

- Microcytic <80:
o Iron deficiency anemia
o Chronic infections
o Thalassemias
o Hemoglobinopathies
o Sideroblastic anemia
- Normocytic 80-100:
o Anemia of chronic disease
o Early IDA
o Hemoglobinopathies
o Primary marrow disorders
o Renal failure
o Aplastic anemias
- Macrocyte >100:
o Megaloblastic anemias
§ B12/Folate Deficiencies
o Liver disease/alcohol
o Hemoglobinopathies
o Metabolic disorders
o Increased destruction
o Reticulocytosis
§ Reticulocytosis is a condition where there is an increase in reticulocytes, immature
red blood cells. It is commonly seen in anemia. They are seen on blood films when
the bone marrow is highly active in an attempt to replace red blood cell loss such as
in haemolytic anaemia, haemorrhage.
o Myleodysplastic syndromes

Microcytic Anemias:
- ANEMIA WITH MCV <80
o What you need to be thinking is iron deficiency anemia or chronic disease
o Know the hemogloinopathy causes and thalassemia
- Due to decreased production of Hb à
o RBC progenitor cells in the bone marrow are large and normally divide multiple times to
produce smaller mature cells (with MCV 80-100) à microcytosis is due to an extra
division which occurs to maintain Hb conc.
- Hemoglobin = Heme + Globin
o (Heme = Protoporphoryn + Iron)
- Causes:
o Iron deficiency anemia (most common type – most common nutritional deficiency in the
world)
o Anemia of chronic disease
o Sideroblastic anemia
o Thalassemia
- FBC:
o Low MCV and MCH and Low Hb
Iron Deficiency Anemia:
- Microcytic, hypochromic RBCs with increased RDW
- Iron Studies:
o Low ferritin
o Low serum iron
o High TIBC (Total Iron Binding Capacity), low % sat
o High free erythrocyte protoporphyrin
- Treatment: supplemental iron (ferrous sulfate)

Note – Iron:
- Consumed in heme (meat derived) and non heme (veg) forms
- Absorbed in duodenum, heme form more readily absorbed
- Transferrin transports iron in blood, delivers it to liver and bone marrow macrophages for storage
- Stored intracellular iron bound to ferritin, preventing iron from forming free radicals (Fenton
reaction)
- Lab measurements:
o Serum iron – measurement of iron in the blood
o TIBC – measure of transferrin molecules in the blood
o TIBC % saturation – percentage of transferrin molecules that are bound by iron (normal is
33%)
o Serum ferritin – reflects iron stores in macrophages and the liver

Anemia of Chronic Disease:

- Associated with chronic inflammation (examples: endocarditis, autoimmune conditions)
o Most common type of anemia in hospitalized patients
- Chronic disease results in production of acute phase reactants from the liver, including
HEPCIDIN
o Hepcidin sequesters iron in storage sites by:
1. Limiting iron transfer from macrophages to erythroid precursors
2. Suppression EPO production
- Iron Studies:
o Low serum iron
o High ferritin
o Low TIBC , low % sat
o High free erythrocyte protoporphyrin
- Treatment: address underlying cause, give exogenous EPO (esp for cancer patients)

Sideroblastic Anemia:
- Due to defective protoporphoryn synthesis (part of heme)
- Iron is transferred to erythroid precursors and enters the mitochondria to form heme
- If proto is deficient, iron remains trapped in mitochondria
- Iron-laden mitochondria form a ring around the nucleus à “ringed sideroblast”
- Congenital or acquired:
o Congenital – defect in enzyme involved in heme synthesis: ALAS (rate limiting)
o Acquired: alcoholism (mito poison), lead poison (inhibits ALAD and ferrochelatast), Vit B6
def (cofactor for ALAS – side effect of isoniazid treatment for tb)
- Lab findings:
o High ferritin
o Low TIBC
o High serum iron
o High % sat (iron overloaded state)
Thalassemia:
- Issue with the globin chains
- Normal types of Hb = HbF (alpha, gamma – fetal), HbA (alpha, beta), and HbA2 (alpha, delta)
- Alpha thalassemia – gene deletion (chr 16) – 4 genes – symptoms depend on how many genes
are deleted
o 3 genes deleted à severe anemia; beta chains form tetramers (HbH) that damage RBCs,
can be seen on electrophoresis
o 4 genes deleted – hydrops fetalis – gamma chains form tetramers (hb Barts)
- Beta thalassemia – point mutations, more common in Africa and Mediterranean descent - 2 genes,
chr 11
o Target cells on blood smear
o Increased HbA2 on electrophoresis
o Major and minor à major presents in first few months of life, high HbF at birth is temporary
protective
o Massive erythroid hyperplasia à expansion of hematopoiesis into skull (crewcut
appearance on XR) and facial bones (chipmunk facies) – extramedullary hematopoiesis
with hepatosplenomegaly, risk of aplastic crisis with parvo virus b19 infection
- Treatment for major = transfusions – risk of secondary hemochromatosis
- Smear: microcytic, hypochromic RBCs with target cells and nucleated RBCs
- Electrophoresis: little/no HbA with increased HbA1 and HbF
- Hemachromatosis:
o Serum iron raised
o Serum ferritin raised
o TIBC decreased
o Blood work looks the same as his Dads
o Feels well however- looks well

Causes of Iron Deficiency:

- Increased needs
o Adolescence
o Menstruation
o Pregnancy
o Lactation
o Cancer
- Insufficient intake
o Vegan
o Limited diet
o Malnutrition
- Decreased absorption

Malabsorption syndromes:
- Coliaec/Whipples
- Whats the work up?
o Antibodies.. biopsies
§ Antitissue transglutaminase, anti endomysial, anti gliadin, anti reticulin
§ IgA
§ OCGD- d2 biopsy, villous atrophy, crypt hyperplasia with inflammatory cells
§ Biochemistry- Ca, B12, Folate
o What are the complications
o What are the treatments?

Tests for Thalassemia versus IDA:

- reticulocytes increased in thalassesmia
- normal in others
- can also do Hb electrophoresis for the abnormal blood conditions

Treatment:
- Iron deficiency
o Treat the cause- if there a malignancy?
o Iron replacement
- Anemia of chronic disease
o Treat the cause
o May think EPO if secondary to renal failure
- Sideroblastic – body unable to get the iron into RBC
o Inherited or acquired e.g. medication/lead
 o Treat cause

Normocytic:-
- Sadlier tends to like asking RA or renal disease
- Generally a normal MCV and MCH
- But obviously Hb is decreased à
o Due to increased peripheral destruction or underproduction – reticulocyte helps
distinguish
- The important test here is
o Reticulocyte count
§ Reticulocyte: young RBC – larger cells with bluish cytoplasm
§ Normally count is 1-2%
§ Properly functioning marrow responds to anemia by increasing the reticulocyte
count to >3%
o Often a smear as well

Low reticulocyte count:

- Chronic disease
o Renal/endocrine
- Acute inflammation
o Rheumatoid arthritis
- Leukemia
- Myelofibrosis
Increased reticulocytes:
- Hemolysis
- RC enzyme defects like G6PD
- Sickle cell
- DIC/HUS
- Hypersplenism
- Blood loss

Work-ups:
- Aplastic anemia:
o Deficiency of all elements
o Treatment:
§ Transfusion/supportive treatment/immunosuppression/bone marrow transplant
(allogenic marrow transplant from a HLA matched sibling is curative), otherwise,
immunosuppression with ciclosporin and antimymocyte globulin
- Thalassemia
o Deficiency of globin chains
o Transfuse >9/iron chelators/folate/occasionally splenectomy
- Sickle Cell Disease:
o Issue with inheriting of beta gene for Hb
o Varies from trait to full blown
o Proper diagnosis via electrophoresis/film

Macrocytic:
- MCV >100, most commonly due to folate or B12 def à necessary for DNA precursor synthesis
o Impaired division and enlargement of granulocytic precursors
o Hypersegmented neutrophils
o Megaloblastic change also seen in rapidly dividing epithelial cells ex. Intestinal –
macroglossia (englarged tongue)
o Other causes: alcoholism, liver disease, drugs
- Reticulocytes
o Low:
§ Folate def
§ B12 def
§ Drugs: anticonvulsants
• E.g. valproate
§ Hypothyroid
§ Complete BM failure e.g. aplastic anemia
o High
§ Active hemolysis

Megaloblastic:
- RBC in delayed development in the bone marrow
 - B12-folate deficiency the usual causes
- Often asymptomatic until late on
- Key words can be:
o Hypersegmented polymorphs
o Target cells
- Folate def/vit b12
o Insufficient uptake or intake/excessive use
§ Folate – green veg, absorbed in jejunum, develops within months as body stores
are minimal ** drugs such as methotrexate!! (inhibit dihydrofolate reductase)
§ B12 – animal derived proteins, def. less common because large hepatic stores, takes
years to develop. Absorbed in ileum
• Causes: pernicious anemia, pancreatic insufficiency, damage to terminal
ileium (crohn’s, diphyllobothrium latum/fish tapeworm), dietary def rare
unless vegan
§ Lab findings: macrocytic RBCs and hypersegmented neutrophils (>5 lobes),
glossitis, high serum homocysteine (increases risk for thrombosis) – found in both
• Folate only: decreased serum folate, normal methylmalonic acid
• B12 only: subacute combined degen of spinal cord (B12 conversion of
methylmalonic acid to succinyl coA, important in fatty acid metabolism à
increased levels of methylmalonic acid impairs spinal cord myeliniation à
poor proprioception and vibratory sensation (posterior column) and spastic
paresis (lateral corticospinal tract), low serum B12, high methlmalonic acid
o Treatment orally

Pernicious anemia:
- Most common cause of b12 def
- Autoimmune destruction of parietal cells (body of stomach) à intrinsic factor deficiency
- Lack of production of intrinsic factor and thus decreased B12 uptake
- Remember the associated autoimmune condition
- Easy to throw in alongside a RA or thyroid question
- Megaloblastic anemia on BM
- Treat with IM Hydroxycobalmin

*Hemolytic anemias common on the exam

Hemolytic anemia:
- Hemoglobin è bilirubin èconjugated in the liver and passed into the bowel as urobilinogen
- With hemolysis è increase in unconjugated plasma bilirubin
- Increased urobilinigen in urine
- And increased LDH in the blood
- Haptoglobin normally binds free Hb in the blood vessels
- Too much in that case however è low haptoglobin level, hemoglobinuria may occur

*** Peripheral RBC destruction (hemolysis) – divided into extravascular and intravascular hemolysis à both
cause anemia with GOOD MARROW RESPONSE (ie. an elevated RC count >3%)
- Extravascular: destruction by reticuloendotheial system (macrophages of spleen, liver, and LNs)
o Globin à amino acids, heme à iron and protoporphyrin (iron is recycled), proto à
unconjugated bili, bound to serum albumin and delivered to liver for conjugation and
excretion
o Lab findings: anemia, splenomegaly, jaundice (unconjugated bili), increased risk for
bilirubin gallstones, marrow hyperplasia with corrected RC >3%
- Intravascular: destruction within vessels
o Lab findings: hemoglobinema, hemoglobinuria, HEMOSIDERINURIA (renal tubular cells
pick up some of the Hb that is filtered into the urine and break it down into iron,
accumulates as hemosiderin à tubular cells are shed resulting in hemosiderinuria),
decreased serum HAPTOGLOBIN

So far we now know:

- Decreased Hb
- Decreased haptoglobin
- Increased reticulocytes
- Increased urobilinogen
- Increased LDH

Therefor: hemolytic anemia can be further subdivided

 - Varying ways:
o Intravascular v extravascular
o Hereditary v acquired
§ Hereditary:
• Abnormalities of RBC interior:
o Enzyme defects
o Hemoglobinopathies
• RBC membrane abnormalities
o Hereditary spherocytosis
o Paroxysmal nocturnal hemoglobinuria
o Spur cell anemia
• Extrinsic factor
o Hypersplenism
o Antibody: immune hemolysis
o Microangiopathic hemolysis
o Infections, toxins, etc

Hints that might indicate whats going on:

- Presence of spherocytosis on blood film
o Plus positive Coombs test = autoimmune cause
o Plus negative Coombs test = hereditary spherocytosis
- Occurs with infection/post commencement of a particular medication = G6D deficiency
- Sickle cells- sickle cell disease
Presence of schistocytes:
- Hemolytic uremic syndrome or DIC (adults)
Presence of fever infection:
- Septic process

Coombs test:
- Sample of the patients red blood cells are mixed with antihuman antibiodies- coombs reagent
- If they are coated with antibodies- as in hemolytic anemia- the antihuman antibodies will stick to the
affected red blood cells
- The sample with agglutinate- positive

Everybody should have:

- FBC
- Retics
- Blood film
- LDH
- Bilirubin
- Urobilinogen
- Haptoglobin

Then consider:
- Coombs
- Hb electrophoresis
o Abnormal red cells
- Osmotic fragility
- Enzyme assays
- Bone marrow aspirates
Treating the cause in many cases-
- Autoimmune
o Infection
o Lymphoproliferative disease
o Cancer

Hereditary Spherocytosis:
- Inherited defect of RBC cytoskeleton-membrane tethering proteins (spectrin, ankyrin)
- Membrane BLEBS* - formed and lost over time à loss of membrane renders cells round
(spherocytes) instead of disc shaped
o Spherocytes are less able to maneuver through splenic sinusoids à consumed by splenic
macrophages à anemia
- Lab findings:
o Spherocytes with loss of central pallor
o Increased RDW and MCHC
o Splenomegaly, jaundice (unconjugated), risk of bili gallstones
 o Risk for aplastic crisis with parvovirus B19
- Diagnosis:
o Osmotic fragility test (rupture in hypotonic solution)
- Tx: splenectomy (anemia resolves but spherocytes persist and howell jolly bodies (fragments of
nuclear material in RBCs) emerge on blood smear

Sickle Cell:
- AR mutation of beta chain (glutamic acid replaced with valine)
- African descent, protective against malaria
- Disease = 2 abnormal beta genes - >90% HbS
- HbS polymerizes when deoxy, aggregate into needle like structures
o Increased risk of sickling: hypoxemia, dehydration, acidosis
o HbF protects against sickling, first few months of life
o Hydroxyurea increases levels of HbF
- RBC membrane damage, vaso occlusion
o Anemia (extra vascular and intra vascular hemolysis)
o Dactylitis, autosplenectomy, acute chest syndrome, pain crisis, renal papillary necrosis
- Sickle trait – one normal beta chain à <50% HbS,
- Labs:
o Sickle cells and target cells on smear (not seen in trait)
o Metabisulfite screen causes cells to sickle (both disease and trait)
o Hb electrophoresis confirms the presence and amount of HbS

Hb C:
- AR mutation in beta chain à glutamic acid replaced by lysine
- Mild anemia due to extravascular hemolysis
- HbC crystals on smear

Paroxysmal Nocturnal Hemoglobinuria

- Acquired defect in myeloid stem cells resulting in absent glycosylphosphatidylinositol (GPI) à cells
susceptible to destruction by COMPLEMENT
o DAF on surface of blood cells inhibit C3 convertase
o DAF secured to cell membrane by GPI
- Intravascular hemolysis occurs episodically, often at night when mild resp acidosis develops (shallow
breating during sleep) and activates complement
- RVCs, WBCs, and platelets lysed
- Intravascular hemolysis à Hb in blood and urine especially in morning
- Sucrose test to screen, confirm with acidified serum test or flow cytometry to detect lack of
CD55(DAF)
- Thrombosis of hepatic, portal, or cerebral veins (can cause death)
- Complications: iron def anemia (chronic loss of Hb in urine) and AML

G6PD:
- X linked recessive à reduced half life of G6PD renders cells susceptible to oxidative stress
o Glutathione neutralizes H2O2 and becomes oxidized in the process, NADPH is needed to
regenerate reduced glutathione, need G6PD to make NADPH
- Intravascular hemolysis
- Oxidative stress precipitates Hb as Heinz bodies à removed from RBCs by splenic macrophages à
BITE CELLS
- Causes of oxidative stress: infections, drugs (** primaquine, sulfa drugs, dapsone), fava beans
- Presentation: hemoglobinuria and back pain for hours after exposure
- Heinz prep used to screen (precipitated Hb can only be seen with special Heinz stain), enzyme
studies to confirm

Immune Hemolytic Anemia:

- Antibody (IgG or IgM) destruction
- IgG – extra vascular, IgM – intravascular
o IgG – warm agglutinin, membrane of antibody coated RBC is consumed by splenic
macrophages à spherocytes *** associated with SLE, CLL, and certain drugs (***penicillin!!)
o IgM – binds RBCs and fixes complement in cold temp of extremitites (cold agglutinin) ***
associated with mycoplasma pneumonia
- Coombs test to diagnose
o Direct coombs test: confirms presence of antibody coated RBCs, anti IgG is added to pts RBC
à agglutination is RBCs are already coated with antibody
o Indirect coombs test: presence of Abs in serum à anti IgG and test RBCs are mixed with the
patients serum à agglutination if serum Abs present
Underproduction:
- Decreased production of RBCs by BM à LOW RC COUNT IN THE SETTING OF ANEMIA!
- Causes: causes of micro/macrocytic anemia, renal failure (decreased EPO!), damage to BM precursors
cells (pancytopenia)

Parvovirus B19:
- Infects progenitor RBCs, temporarily halts erythropoiesis à anemia in the setting of
preexisting marrow stress
- Tx is supportive, infection is self limited

Aplastic Anemia:
- Damage to hematopoietic stem cells à pancytopenia with low RC
- Drugs, chemicals, viral, AI
- Biopsy: empty, fatty BM
- Tx: stop causative drugs and supportive care (transfusions, BM stimulating factors ex. EPO, GM-CSF
etc)
o Last resort: BM transplant

Myeolophthisic process:
- Pathologic process (ex. Cancer mets) that replaces BM
- Hematopoiesis is impaired à pancytopenia

ADRENAL

Overall:
- Cortex- corticosteroids
- Medulla- adrenaline and noradrenaline
- Function: ‘GFR’
o Glomerulosa: Mineralocorticoids – ex: aldosterone
§ Acts primarily on the electrolytes
§ Mainly K+/Na+ affected
o Fasciculata: Glucocorticoids – ex. Cortisol
§ Metabolic hormone
§ Affects glucose/fat/protein metabolism
o Reticulata: Androgens
§ Sex hormones

Specific Functions:
Aldosterone:
- Increased Na absorption, K secretion in kidneys
- Hyperaldosteronism:
 o Increase aldosterone: Increased Na+, decreased K+
- Hypoaldosteronism:
o Decreased aldosterone: High Extracellular K+, low Na+
Cortisol:
- Glucocorticoid
- Stress hormone
- Works on Cardiovascular system/muscular skeletal system/pituitary
- Major impact on inflammation and immunity
- Adverse Effects:
o Immunologic:
§ Immunosuppression
§ Lymphocytopenia,
§ False negative skin test
o Opthomalogy:
§ Cataract
§ Narrow angle glaucoma
Cushings:
- Due to high cortisol
- Cushing’s Syndrome – 50% mortality at 5 years if untreated
- Generally 20-40
- Higher risk in women than men
- Whats the difference?
- Cushing’s disease results from pituitary
o Due to excess level of ACTH
o High levels of ACTH increase cortisol release
o MC endogenous cause of Cushings syndrome
- Adrenal Cushing’s
o Cortisol directly from adrenal cortex
o Adenoma/hyperplasia
- Ectopic Cushing’s
o Increased ACTH from outside of the adrenal axis
o Most commonly small cell lung Ca
o X-ray will show mass:
§ Work up:
• FBC, High Resolution CT Thorax, Bronchoscopy, PET Scan
- Iatrogenic
o Steroid treatment
- Pseudo-cushings

Cushing’s Work up:

Work- Up:
- 1st test: 24 hour free cortisol level or 11pm salivary cortisol level or low dose dexamethasone
suppression test
o 24 hour urine cortisol= >100mg, do 2nd test
- 2 test: ACTH
nd

o If low= Cushing’s Syndrome

§ CT/MRI adrenals
o If high= Cushing’s Disease or Ectopic source so do 3rd test
- 3rd test: High Dexamethasone
o If suppressed: Cushing’s Disease (Pituitary)
§ MRI showing mass
§ If no mass on MRN then do an inferior petrosal sinus sampling
o If not suppressed:
§ CT chest to rule out ectopic ACTH secretion (can also come from the pancreas)

Dexamethasone Suppression Test:

- 1 mg given at midnight
- Cortisol measured at 8 am
- Normally decreased
- In Cushing’s – fails to decrease
- Need to move to high dose to localize
- May also CT adrenals/chest
- MRI pituitary
- Ectopic? à Small cell lung cancer (or any neuroendocrine tumor)

Treatment:
- Goal is to restore hormone balance and reverse Cushing’s Syndrome
o Surgery:
§ Removal pituitary adenoma
§ Removal of adrenal glands in refractory disease
o Medication:
§ Cortisol synthesis inhibitors (ketoconazole)
 § Glucocorticoid type II receptor antagonist (mifepristone)
o Radiation:
§ Gamma knife
o Lifestyle:
§ High protein diet for those with muscle wasting
§ Regular exercise
§ Clean and inspect all wounds
- Pituitary:
o Removed by transphenoidal surgery
- Need to replace the corticosteroids
o Failure = adrenal crisis
- Same will occur with removal of adrenal adenoma
- Otherwise remove the source for ectopic
- Occasionally Nelson syndrome may arise (When both glands are removed)
o Nothing to stop the pituitary and a tumour in the pituitary then arises as a result:
Secretes ACTH
§ ACTH stimulate melanocytes (hyperpigmentation), skin tone changes,
headaches, visual disturbances etc.
Signs:
- Hands/Arms:
o Bruising
o HTN
o Shoulder power is reduced
- Face:
o Rounded
o Thin, greasy skin,
o Acne
- Visual fields!
o Bitemporal hemianopia with pituitary adenoma

Primary Hypoadrenalism/Addison’s:
- Definitely must know for exam
- Loss of adrenal cortex
o Therefore, decrease in all its products
o Also therefore a loss of feedback on the pituitary
- Vague symptoms, vague presentation – Typically, FEMALES! ** Most common cause is
autoimmune adrenalitis
o Autoimmune à RA, SLE, Graves, pernicious anemia all associated
- Need to recognize it – adrenal crisis!
- Causes:
o Primary:
§ Autoimmune adrenalitis
o Secondary:
§ Infection (TB, HIV), fungal,
§ Bleed into adrenal (anticoags)
- Signs and Symptoms:
o Weight loss,
o Dizziness,
o Altered skin pigmentation (bronze),
o Anorexia,
o Myalgia,
o Fainting,
 o Depression

- Remember you are expecting to see:

o Low Na+,
o Low glucose,
o Low BP/fluid balance,
o High K+
o HIGH K+ AND LOW NA+ = HYPOALDOSTERONE
Adrenal Crisis:
- Severe vomiting and diarrhea
- Seizures
- Hypoglycemia,
- Severe hyponatremia!!
Investigations:
- Random serum cortisol will often be low, but it can be normal
- However, if random cortisol is very high, it is unlikely to be Addison’s
- SYNACTHEN TEST
o Synthetic ACTH given to the patient
o ACTH should cause sharp rise in cortisol levels
o Cortisol checked at 0 and 30 minutes
o Levels depend on the lab
o Usually says it’s not Addison’s if cortisol >550 nmol
Workup:
- FBC – anemia
- U&E – K+ high, Na+ low
- Glucose - low
- Calcium – hyperkalemia may be seen (stones, bones, abdo groans, psychic moans)
- CXR
- Serum aldosterone may be low
- Check for TB – quantiferon, CXR (bilateral hilar LAD), Mantoux
Treatment:
- Before any diagnosis, if the patient is in crisis
 o IV fluids
o Steroids
o Glucose
o Underlying cause
- If there’s a chronic element:
o Don’t forget education
o Steroid bracelet
o Patients should know to increase steroid therapy during times of illness (dose
should be doubled)
o Patients also need to know they should increase their dose of hydrocortisone by 5-
10mg a day before strenuous exercise
Addison’s associations: Think Autoimmune
- Chronic thyroiditis
- Grave’s Disease
- Hypoparathyroidism
- Hypopituitarism
- Myasthenia gravis
- Pernicious anemia
- Testicular dysfunction
- Type 1 DM
- Vitiligo

Secondary hypoadrenalism:
- 2 Causes:
o Hypothalamic-pituitary disease = ACTH malproduction
o Long term steroid usage = suppression of the hypothalamic-pituitary pathway
§ Diseases using long term steroids: IBD, asthma, polymyalgia, Giant Cell Arteritis
(high ESR, >65 years old, women)
o ** Think of this if told patient has a long term illness, come in with nausea, vomiting, low
glucose, low Na, high K… etc
- Synacthen test – results are the same
o But you should also check the ACTH….
§ With Addison’s- the ACTH is high because issue is in adrenals and you have
feedback but here you have ACTH that is low

Conn Syndrome:
- Primary hyperaldosteronism
- Often asymptomatic
- Expecting:
o HTN,
o High Na,
o Low K+
o (Opposite of Addison’s)
- What you need to look out for is an ECG with signs of low K and associated U&E
o U wave, inversion

Secondary Hyperaldosteronism
- Telling the difference between Conn’s and Secondary Hyperaldosteronism
o Renin is low in Conn’s
§ Aldosterone to Renin ratio in Conn’s is >20
o Renin is high in secondary
§ Renin Secreting Tumours etc
• Low K, High Na, High Renin, High aldosterone

Thyroid
- Know graves, hyper, hypo and how to recognize

RADIOLOGY:

Chest X-Ray:
- Idea is that you inspect:
o Mediastinum
o Heart and great vessels
o Bronchi
o Lungs
 o Diaphragm
o Bone surrounding
- First:
o Use the identifiers and what information is given to you
§ “This is a PA/AP CXR of…. Taken on ….”
o PA = way you want generally (AP usually with a portable)
- Other things you can tell straight off:
o Adult vs paed,
o Male vs female (generally)
o Shape and symmetry of the CXR
o Presence of foreign bodies/objects
§ Chest drain
§ ECG leads
§ Pacemaker,
§ Glass, etc

Bone wise:
- Shoulder girdles
- Ribs
- Cervical and thoracic vertebrae
- Clavicles
- Scapulae
- Unlikely to get fractures, but do look
- Intercostal spaces should also be looked at

Soft Tissues:
- Extra shadow on XR
- Breast tissue most common, occasionally nipple
- Can get soft tissue masses overlying that lungs that can appear (lipomas, for instance)
o These need CT scanning with or without biopsy

From the top:

- Trachea:
o Midline radiolucency
o Deviates slightly to the right at the level of the aortic arch = normal
o Divides at about T5 into the bronchi
- Right main bronchi:
o 2 major branches off same, but into 3 lobes
- Left main bronchi:
o 2 major branches – more lateral division, 2 lobes
- LNs:
o Anterior (mediastinal)
o Paratracheo-broncial
o Hilar lymphadenopathy?
o Normal = can’t be seen in general
- The Hilum then brings things together:
o LNs
o Bronchi
o Bronchial blood vessels
o Pulmonary artery/veins
o Left hilar is normally slightly higher than the right
o If the left is lower = looks for signs of lung collapse in the left lower or right upper lobes
- Hilar Lymphadenopathy:
o Unilateral:
§ Infection:
• TB, viral infection in children
§ Vascular:
• Pulmonary artery stenosis, pulmonary artery aneurysm
§ Tumor:
• LNs (mets, lymphoma, bronchial carcinoma)
o Bilateral:
§ Sarcoidosis
§ Tumor:
• Mets, lymphoma
§ Vascular:
• Pulmonary arterial hypertension (COPD, L-R Shunt)
 § Infection: TB
- Diaphragm:
o Should all around the posterior arc of 10th rib
o Higher on right side (liver)
o Gastric bubble on left
- Heart:
o Aortic notch
o Borders
§ Right atrium and right ventricle and left ventricle
- Lungs:
o Know where the lobes are
o 3 lobes on the right side
§ Right lower lobe lies behind! – If given PA and lateral, will be able to see
o 2 lobes on the left side

Conditions to be weary of:

Unilateral mastectomy:

- Right Lower Lobe Collapse:

Above: left lower lobe collapse, sail sign
- Triangular opacity in the posteromedial aspect of the left lung
- Edge of collapse lung may create a “double cardiac contour”

Causes of lobe collapse:

- Luminal
o Aspirated foreign material
o Mucous plugging
- Mural
o Bronchogenic ca
- Extrinsic
o Anything that compresses

Consolidation:
- Fluffy, not a solid ball

Fluid line:
- Ex. right upper lobe consolidation

Pleural Effusion
 - Know causes
o Transudate vs exudate and lights criteria
- Effusions are easy to recognize
- Need to know criteria
- Treatment options
- Recognize clinical picture
o Spike in temp
o Sats dropping

Pneumothorax:
- Vertical line
- Treatment:
o if less then 2 cm and asymptomatic – do nothing
o If less than 2 cm and symptoms or >2cm– treat

Tension Pneumo:
- Needle decompression 2 ICS MCL
- Chest drain
Above: chest drain on CXR

- Need to also consider clinical history

- Above: lung cancer
- Well circumscribed opacity
- Differentials: neoplastic, inflammatory consolidation
- Send for CT
Cannon ball mets
Hyperinflation

Need to know:
- Pulmonary edema
- ARDS
- Cancer
- COPD
- Management , work up
- Tb, Hilar LAD, Sarcoid
- Will be a question on infectious diseases somewhere - HIV, malaria, TB
- Basic CXR, CT scans (esp brain!), pulmonary fibrosis

TOXICOLOGY:

Toxicology/Overdose:
- Simple to move onto something else after it:
o Cardiac: ECG
o Acidosis/Alkalosis
o Kidney/Liver injury
Sometimes the history is obvious:
- Pills found
- Alcohol intake

Sometimes there are subtle hints:

- History of depression
- Previous suicide attempt
- Concert attendance

Exam may direct you:

- Pupils most common
 - Sats- resp: depression
- Or really out there- drooling etc
What you need to start thinking?
- Some drugs excite/ increase the body’s physiology
o anticholinergics
o SNS simulants
o Withdrawal effects
- Alternatively those that depress
o Parasympathetic nervous system stimulants
o Cholinergic
o Alcohol
- Then the tricky ones..:
o TCA
o Salicylates
o Hypoglycemic
o Cyanide
o NERVE AGENTS
Absorption v elimination:
- If someone had ingested a toxin
o Prevent its absorption
o Stimulate its elimination
o Use an antidote

Absorption:
- Gastric lavage
o Never used if your unconscious unless the patient is intubated due to aspiration
o Suctioning of stomach contents- saline injection and wash out
o Can be used 2 hours after TCA and up to 4 hours after aspirin
- Induced vomiting
o Risk of aspiration
o May be seen in pediatrics on occasion
o Ipecac is the substance given
- Activated charcoal
o Absorbs the toxins and thus inhibits the GI absorption
o Often repeated doses given-
§ Works well for aspirin, theophylline, phenobarbital
o Dose not work with lithium, organic solvents, alcohol

Elimination:
- Renal/fecal elimination
o Medication to stimulate urination or defecation
o Laxative effect
- Forced diuresis
o Infusion of sodium bicarb
o Used to eliminate acidic drugs such as aspirin
o May get electrolyte disturbances so watch this (acid base balance off with sodium
bicarb)
- Hemodialysis
o Needs to be a dialyzable drug
o Only something that is protein bound usually
o Temporary vs permanent
§ Trying to wash the drug out

What ones to concentrate on?

- Paracetemol/Aspirin
- Opiates
- Benzodiazipines
- TCA
- Digoxin
o Remember: ECG patterns
- Lithium
- Antibiotics
o E.g. gentamicin- hearing loss
- Illegal drugs –
o cocaine, amphetamines
Paracetemol:
- No excuse for not knowing this
- Can run through a question on metabolic alkalosis or acidosis, LFTs etc
- Paracetemol- 95% become paracetomol conjugates and 5% is NAPQI which is
hepatotoxic—
- Toxicity is influenced by:
o Dose taken
o Depletion of glutathione stores due to malnutrition or chronic alcohol ingestion
o Excessive CYT p450 activity due to induction by chronic alcohol or other drugs-
§ E.g. TB patients: rifampicin/isoniazid or epileptics on phenytoin
§ The CYT p450 is being used elsewhere
- Features:
o Stage 1: up to 24 hours
§ Asymptomatic
§ Nausea and vomiting
o Stage 2- up to 72 hours
§ Elevations of AST/ALT
§ Right upper abdominal pain (RUQ)
§ PT (prothrombin) now starts to go off –
• Synthetic factors in terms of the liver are albumin, PT, INR
o Stage 3- up to 96 hours
§ Jaundice
§ Confusion= encephalopathy
§ Sharp rise in LFTs
§ Lactic acidosis appears
• Metabolic acidosis
o Stage 4- around day 4/5
§ If recovery is starting- starts here
- Normograms:
o Need to plot concentration against time
o Do not take what the patient tells you
o Peak serum concentration is 4 hours after the ingestion
o Can be delayed if ingested alongside anything that delays gastric emptying e.g. opiates
(anti-cholinergic)
- Treatment
o Activated charcoal- within 4 hours of ingestion
§ 1g/kg
§ Can reduce the absorption by 90%
o NAC: N-Acetylcysteine
§ NAC- glutathione precursor
§ Limits the formation of the toxin (NAPQI)
§ Beyond 8 hours the efficacy fades
§ S/E=
• Nausea
• Urticaria(Hives)
• Hypotension
• Chills
§ Usually runs up to 36 hours
§ Bloods at the end
• Enzymes
• INR
• Creatinine
• If normal- discharge – if you know that this patient has had a suicide
attempt- discharge from the medical consult and seek psychiatric
consult
- Transplant:
o Where there is fulminant hepatic necrosis
§ pH<7.3
§ PT>100
§ Creatinine >300 mcg/l
§ Grade 3 encephalopathy
§ A grossly abnormal PT of 20 seconds at 24 hours/40 secs at 48 hours = early
referral
TCA:
- Need to know now and obviously for psych in the future
- Don’t get into the pharmacology
- Symptoms:
o Arrhythmias:
§ Wide QRS/PR
§ Prolonged QT interval
§ Heart block
§ VF
o Hypotension
o Anticholinergic toxicity
§ Flushed
§ Dilated pupils
§ Sinus tachy
§ Urinary retention
o Confusion/seizures/delirium
- Management:
o ABC- intubate?
o Gastric lavage if <2 hours
o Activated Charcoal
o Use of Na HCO3:
§ This is what you need to know in terms of antidote
§ Used to stabilize the cardiac system
§ Increase pH- narrows the QRS/increases BP/controls arrhythmias
§ Aim for a higher pH than normal 7/5-7/55
§ Danger of going to met alkalosis but worth it
- Things to be wary of-
o 1a and 1c antiarrhythmic agents- not used
o Can occasional use magnesium to stabilize
o Flumazenil may worse

Aspirin/Salicylate:
- Levels usually peak at an hour after ingestion-
o But in overdose may run to 6 hours
- Measured at 4 hours and every 2 hours after that until falling
- For exam:
o Need to recognize that because of the anion gap it is metabolic acidosis that results
o Due to accumulation of organic acids- e.g. lactic and ketoacids
o Get a mixed respiratory alkalosis and met acidosis with a raised anion gap
generally
- Treatment
o Need to increase the pH= NaHCO3
o Fluids
o Glucose generally needed as is often low
o Hemodialysis*
§ Altered mental status
§ Pulmonary or cerebral odema-
• Cushings triad or signs of raised intracranial pressure
§ Fluid overload- preventing NaHC3
§ Clinical deterioration
- Although you have respiratory alkalosis you still want to increase the pH
-
Opiates:
- Know the signs
- Your respiratory depression- the drug addicts
- What’s your antidote? Naloxone

Digoxin:
- Presentation:
o Cardiac disturbances
o GI symptoms
§ Anorexia, N/V/D, abdominal pain
o CNS effects
§ Weakness, blurred vision, halos around light
o In severe cases can cause hyperkalemia- treatment with 10ml 10% calcium gluconate,
insulin dextrose, salbutamol neb
- Slows nodal conduction while increading automaticity
o More likely in patient with CAD, particularly active ischema and are potentiated by low
magnesium or potassium
- ECG pattern
o T wave inversion
o Downward slurring ST depression
o VF/VT
o Heart block
- Levels increased in
o Verapamil, amiodarone, arthyromycin, tetracycline
o NB- be wary in patients with new or chronic renal impairment
§ Levels can accumulate quickly in this subset
 - Treatment
o If early after intentional overdose, can give activated charcoal
o Bradycardia
§ If asymptomatic- keep serum K at least 4.0 or higher
• Potassium will affect affinity for Na/K pump
§ Symptomatic – atropine, pacing
o Digibind
§ Nb malignant hyperthermia
§ Digibind is the trade name for a digoxin antidote containing Digoxin-specific
antibody Fab fragments
§ There is often a reluctance to give digibind due to cost and underestimating the
mortality associated with digoxin toxicity
o Dialysis will not decrease the serum concentration!

Lithium:
- Bipolar patients
- Very narrow therapeutic window
- Normal range: 0.4-1.5
o If levels between 1.5-2- discontinue and give fluids
o If >2: DIALYSIS

Amphetamines:
- No side effect- signs/symptoms and treatment of illegal drugs

PLEURAL EFFUSIONS:
Definitions:
- A pleural effusion is fluid in the pleural space
- Effusions can be divided by their protein concentration into transudates (<25g/L) and
exudates (>25g/L)
- Blood in the pleural space is a hemothorax, pus in the pleural space is an empyema and chyle
(lymph with fat) is a chylothorax, both air and blood in the pleural space is a called a
hemopneumothorax
Symptoms:
- Asymptomatic
- Dyspnea
- Pleuritic chest pain
Signs:
- Decreased expansion
- Stony dull percussion note
- Diminished breath sounds on the affected side
Divide into:
- Pleural fluid comes back:
o Divide into pleural fluid appearance
o Biochemical tests-
§ Protein/LDH
o Cytological-
§ Malignant cells/differential cell count
o Microbiological tests-
§ Gram stain/AFB/Culture
o pH analysis and glucose
o Amylase and RF-
§ Rheumatoid or pancreatitis causing
Appearance:
- Bloody /Hemorrhagic
o Trauma/malignancy/PE
- Turbid/milky:
o Chylothorax/empyema
o Parapneumonic effusion (inflammation of the pleura casued by pneumonia may lead to
infected pleural fluid (empyema), if it is not infected, the term parapneumonic effusion is
used)
- Putrid
o Empyema
- Straw-
o Normal **
Cytology/Micro:
- Cell count differential*
 - Neutrophils:
o Bacterial/Parapneumonic effusion/PE
- Lymphocytes:
o Malignancy/RA/sarcoidosis
§ Think TB if >80%
- Mesothelial cells
o Pulmonary infarction
- Abnormal merothelial cells
o Mesothelioma
- Eosinophils
o Fungal/parasite/PE
- Multineucleated giant cells
o RA
- Lupus erythematous cells
o SLE
- Mononuclear:
o TB/Malignancy
pH and Glucose:
- Normal pleural fluid: pH 7.6
o Low (Under7.2):
§ Empyema
§ Rheumatoid Arthritis
§ Malignant Effusion
§ TB
§ RA
§ SLE
- Glucose <3.3mmol/L
o Empyema, malignancy, TB, RA, SLE
Clinical Chemistry:
- Protein
o <25 g/L: Transudate
o >35g/L: Exudate
o 25-35g/L: if pleural fluid protein/serum protein >0.5 effusion is an exudate
- LDH (pleura:serum >0.6)
o Empyema
o Malignancy
o TB
o RA
o SLE
Amylase:
- High with:
o Pancreatitis
o Malignancy
o Bacterial pneumonia
o Esophageal rupture
Immunology:
- Rheumatoid factor:
o RA
- Antinuclear antibody
o SLE
- Low complement levels
o RA, SLE, malignancy, infection
Lights Criteria:
- Know if its transudative or exudative
o Transudative: associated with ‘failures’
o Exudative: anything that pumps out protein!
- Transudative:
o Transudates may be due to increased venous pressure (cardiac failure, constrictive
pericarditis, fluid overload) or hypoproteinema (cirrhosis, nephrotic syndrome,
malabsorption)
o Cardiac/liver/renal failure
o Hypothyroidism
o Meigs syndrome (right pleural eddusion and ovarian fibroma)
o Poor nutritional status
- Exudative:
 o Due to increased leakiness in the pleural capillaries secondary to infection, inflammation
or malignancy
o Malignancy: Bronchial carcinoma, mesothelioma, malignant mets, lymphoma
o Infectious Pneumonia, TB, Sarcoid
o Inflammatory: PE, pancreatitis, pulmonary infarction, SLE, RA
o Pleural fluid is considered an exudate if one or more of the following hold true:
§ Pleural fluid protein/serum protein >0.5
§ Pleural fluid LDH/serum LDH >0.6
§ Pleural fluid LDH >2/3 upper limit of normal LDH
Investigations:
- CXR:
oSmall effusions blunt the costophrenic angles, larger ones are seen as water-dense
shadows with concave upper borders
o A completely flat horizontal upper border iplies that there is also a pneumothorax
- Pleural tap (U/S based)/ draining and analysis
o Infiltrate down to the pleura with 5-10mL of 1% lidocaine
o Attach a 21G needle to a syringe and insert it just above the upper border of an
appropriate rib 1 or 2 intercostal spaced below the upper border of the pleural effusion
(avoids the neurovascular bundle)
- Occasional VATs
o Video-assisted thoracoscopic surgery (VATS) is a type of thoracic surgery performed
using a small video camera that is introduced into the patient's chest via small incisions
- Occasional pleural biopsy if suspicious for TB or malignancy
- Bronchoscopy rarely
Management:
- Treat the underlying cause
- Drainage:
o Aspiration for symptomatic improvement
o If the effusion is symptomatic, drain it, repeatedly if necessary
o Fluid is best removed slowly (0.5-1.5L/h)
o May be aspirated the same was as a diagnostic tap or using an intercostal drain
- Pleurodesis in recurrences
o Teracycline, bleomycin or talc
o Thorascopic talc pleurodesis is most effect for malignant effusions
- Surgery
o Persistent collections and increasing pleural thickness (on U/S) requires surgery

EMPYEMA:
- Also secondary to infections in the lungs
o Pneumonia (CURB Criteria), TB, Rupture of subphrenic abscess
- Management:
o Non-TB:
§ Chest drain: U/S guided
§ May need suction and regular flushing
§ Combination antibiotics
o TB:
§ Tuberculosis medications-RIPE

Peritoneal Fluid:
- Think the same as with pleural fluid
- Exudative v transudative
- Primarily tapped for trying to associate disease process
- Also to detect infection: SBP!
o Exact same requests as with pleural fluid generally
- Transudative:
o <25 g/L of protein
o Causes:
§ CCF
§ Cirrhosis
§ Nephrotic syndrome
§ Hypoalbuminemia
- Exudative:
o Here- >25 g/L pf protein
o Causes:
 § Infection
§ Malignancy
§ Pancreatitis
§ Hypothyroid

Spontanous Bacterial Periontinitis:

- Cirrhotic ascitic patients, classically
- Looking at WCC here
o Neutrophils >250
o Urgent antibiotics and draginage
o Will often have systemic features
o Look for possible source: e.g. strep bovis? Perforation?

Side Effects:
- Diuretics:
o Thiazides (hydrochlorothiazide)
§ Low K+
§ Low Na+
§ Hypotension,
§ Hyperglycemia,
§ Hyperuricemia,
§ Metabolic alkalosis
o Loop (furosemide)
§ Low K+,
§ Low Mg,
§ Hypotension,
§ Ototoxicity,
§ May cause metabolic alkalosis
o K Sparing (Spironolactone)
§ Increased K+, gyenocomastic, metabolic alkalosis
o Carbonic anhydrase (dorzolamide)
§ Low K+,
§ Metabolic alkalosis
o Osmotic (Mannitol)
§ Dehydration,
§ Hypernatremia!
o Ace-Inhibitors
§ Side effects:
• Cough,
• Angioedema,
• Proteinuria,
• Taste changes,
• Orthostatic hypotension
§ Contraindications:
• Pregnancy
• Renal artery stenosis
o ARBS:
§ Side effects:
• Hypotension,
• Acute renal failure,
• Increased K+,
• Headache
§ Contraindications:
• Pregnancy
- Beta Blockers:
o Bronchoconstriction
o Bradycardia
o Hypothermia
o Hypoglycemia
o Adverse increase in lipids (Increased triglycerides/decreased HDL)
- CCB:
o Dizziness
o Peripheral edema
 o Gingival hypertrophy
o Constipation
o Palpations
- Alpha blockers:
o Postural hypotension
o Tachycardia
o Headaches
o Impotence
o Nasal Congestion
- NSAIDs
o Peptic ulcer disease
o Itching/Pruiritis
o Contraindicated:
§ In kidney damage
§ Previous ischemic heart disease

Don’t Forget about simple calculations:

- Serum osmolality
o Plasma osmolality measures the body's electrolyte-water balance
o Osmolality and osmolarity are measures that are technically different, but functionally
the same for normal use. Whereas osmolality (with an “ℓ”) is a measure of the osmoles
(Osm) of solute per kilogram of solvent (osmol/kg or Osm/kg), osmolarity (with an “r”)
is defined as the number of osmoles of solute per liter (L) of solution (osmol/L or
Osm/L). As such, larger numbers indicate a greater concentration of solutes in the
plasma.
§ Osmolarity is affected by changes in water content, as well as temperature and
pressure. In contrast, osmolality is independent of temperature and pressure
o Among other applications, serum osmolality is indicated to evaluate the etiology of
hyponatremia and may be used to screen for alcohol intoxication by means of the
osmolal gap.
o The reference range of serum osmolality is 275–295 mosm/kg (mmol/kg)
o Conditions associated with increased serum osmolality include the following:
§ Marked hyperglycemia, including diabetic ketoacidosis and nonketotic
hyperosmolar hyperglycemic coma
§ Diabetes insipidus (central and nephrogenic)
§ Hypernatremia due to dehydration
§ Hypernatremia due to iatrogenic or accidental excessive sodium chloride (NaCl)
or sodium bicarbonate (NaHCO 3) intake
§ Alcohol ingestion (eg, ethanol, methanol, ethylene glycol, polyethylene glycol)
o Conditions associated with decreased serum osmolality include the following;
§ Hyponatremia with euvolema
• Psychogenic polydipsia, SIADH (Syndrome of inappropriate antidiuretic
hormone), Hypothyroidism, adrenal insufficiency
§ Hyponatremia with hypervolemia
• Cirrhosis, Congestive heart failure, nephrotic syndrome
o Serum osmolality calculation:
§ Calculated serum osmolality: (2xSerum[Na]) + (glucose mmol/L) +(Urea
mmol/L)
§ With ethanol:
• Calculated serum osmolality = (2xserum[Na]) + (glucose mg/dL)/18
+(BUN mg/dL)/2.8 + (ethanol mg/dL)/3.7
o The disparity between measured serum osmolality and calculated serum osmolality is
termed osmolal gap. An osmolal gap of greater than 10 is considered abnormal and may
suggest the presence of toxic alcohols such as methanol, isopropyl alcohol, ethylene
glycol, or polyethylene glycol in the appropriate clinical context
- GCS
Blood Films
- Elliptocytes
o Hereditary elliptocytosis
o Myeloproliferative disorder
o Myelodysplastic syndrome
- Spherocytes
o Nearly spherical, diameter is smaller than normal
o Lack central pale area, smaller eccentric pale
o Seen in
§ Hereditary spherocytosis
§ Some causes of autoimmune hemolytic anemia
§ Direct physical or chemical injury
- Target cells
o Seen in thalassemia
o Chronic liver disease
o Hereditary hypo-betalipoproteinmia
o Fe deficiency anemia
o Hemoglobinopathies (HbC, Hb H, sickle cell anemia),
o Post- splenectomy
- Schistocytes
o Fragmented erythrocytes, smaller than normal
o Genetic
§ Thalassemia
§ Congential dyserythropoietic
o Acquired
§ Megaloblastic,
§ Mechanical
- Rouloux formation
o Stacked coin pattern
o Multiple myeloma
Radiology Revision Tutorial:

Head to Toe:
- Neuro
- Chest
- Abdominal
- MSK

Basic Descriptor Terms:

- What study is it? MRI, CT, Radiograph etc
o Plane:
§ Sagittal,
- What’s white on radiograph is an opacity
o Anything dark is a lucency
- Well confined confluent opacity, consistent with consolidation
- Hyper- echoic
o Cholelithiasis
- Low attenuation- dark on CT
o High attenuation- bright on CT
- Bright on MRI- high signal projectios
o MS- Dawnson’s finger on MRI – high signal projections in the corpus collusom
- Area of low attenuation involving grey and white matter- effacement of sulci (always compare)

Acute Stroke:
- Non contrast CT brain:- within 6 hours the CT may be normal
o Mainstay of imagining in acute stroke
o Purpose: exclude acute intracranial hemorrhage
§ Thrombolysis
o May see evidence of acute ischemic infact,
§ Loss of grey-white matter diffentiation
§ Area of low attenuation/cerebral odema
• Aspects score
o ‘High attenuation’
- CT angiogram:
o Identify large vessel thrombus: thrombectomy
o Could have a large occlusion on angio
- Diffuse weighted imaging:
o Diffusion restriction- infarct
- MRI brain:
o

Subdural hemorrhage:
- Crescent shaped
- Acute or chronic
o High or low attenuation
o Acute on chronic
o Low attnetuaion is chornic
- Crescentic shape
- Can extend beyond sutures lines

Extradural hemorrhage:
- Associated with trauma and skull fractures (95%)
- Blood in potential space between cranium and dura
- Classic lucid interval in 20-50%
- Don’t extend beyond the sutures lines

Intracranial hemorrhages:
- Mass effect
o Sulcal effacement
o Ventricular effacement
o Midline shift

Trifurcation/Bifurcation of the MCA* often see aneurysm

Saccular Cerebral aneurysms:
- AKA beerry aneurysm
- Most common cause of non-traumatic SAH
- Most common site- ACOM
- Familial tendency
- Usually consider treatment when aneurysm is 7cm
- Associated with PCKD

Vasogenic Odema:
- Only involves the white matter
- Usually associated with tumours/infections

Cytotoxic odema:
- Affect both grey and white matter
- Involves cell death
- Associated with infarction

Post Contrast MRI Brain:

- Ring enhancing cerebral lesion
o Probably vasogenic odema around it
o Low signal intensity around it
o T1 MRI
- Associated with:
o Malignancy
§ Primary
§ Mets- more common
• Lung
• Breast
• Renal Cell
o Abscess
o Toxoplasmosis/TB
o Acute MS- Acute dyemyelination – open ring enhancement

Carotid Duplex (Doppler with colour)

- Based on the velocity
- Any very fast moving blood implies a stenosis
- Next scan
o CT angiogram:
§ Can see tight stenotic plaque
• 70% stenosis – for carotic endarct
- Carotid stenosis:
o Atherosclerotic disease: 15% of TIAs and Strokes

Chest X-Ray:
- Continuous diaphragm side
- Rigger’s sign
- Pneumoperitoneum
o Erect chest radiograph:
§ Air under the diagphragm

Cardio:
- Interstitial pulmonary odema (cardiac) or alveolar pulmonary odema
o Peribronchial cuffing
o Kerley B lines
- Stage of Congestive Heart Failure:
o Stage 1:
§ Redistribution
§ PCWP- 13-18mmHg
o Classified on radiograph pattern – two phases
§ Interstial
§ Alveolar
 o Intersittial
§ Precurostor of alceolar odema
• 2 key features:
o fluid in fissures
o kerley B lines
§ Alveolar-

Bilateral hilar opacities:

- Hilar lymphadenopathy
o Sarcoidosis – often have parenchymal changes and may have pulmonary fibrosis
o Lymphoma
o TB
o Metastases

White out of left hemithorax:

- Endotracheal tube should be 5 cm above the carina
- Have complete left lung collapse

Sail Sign:
- Left lower lobe collapse
o Left bronchus plled down
o Can’t see the left hemidiaphragm- Silhoutte sign
§ Diaphragm elevated

Mild hyperinflation associated with emphysema:

- Right pancoast tumour
o Eroded back into the rib
- Present with horners syndrome and brachial plexus involvment
o Tumour is pressing on the sympathetic chain

Pancoast tumours:
- Bronchogenic carcinoma in the lung apex
- 5% of smokers

Mammogram of a breast:- MLO—medial lateral oblique or CC

- Ill defined opacity in the right breast
- Has spiculations – highly suggestive of malignancy
- Axillary lymphadenopathy
- Skin thickening
- Inflammatory breast cancer- associated
o 1-4% of breast ca
§ Usually invasive ductal
o Erythematous, thickened and odematous skin
§ Clinically mimics mastitis
§ 50% present wih axillary LB
§ T4 in terms of TNM staging
§ Treated with neoadjuvant chemotherapy
§ All breasr cancer
• Triple assmessemtn
• Tissue sampling
• MDT review

Abdominal: PFA-
- Obstruction
o Location of the bowel
o Pattern
§ Transverse bands- haustra – Large bowel
 o Comment on perforation
o See if there is small bowel-
§ Ileocecal valve is competent if there is no small bowel obstruction
o If they have a competent ileocecal valve the most likely place of perforation is cecum
§ It is better in these cases to have an incompetent ileocecal valve
- Applecore lesion on CT
o Specific for tumour

MRI Liver:
- Can be done with gallivan or preemavist
o Liver takes up preemavist well
o Mets do not take up premavist
o Bilobar hepatic mets
o Hepatic resection in unilobar disease

Bowel Obstruction:
- PFA-initial investigation
- Large bowel
o Peripherally located
o LBO appearance will depend on the state of the ileocaecal valve
§ Competent- risk of carcal perforation
• Once cecum gets to 9cm the perforation is immitent
§ Incompetent- large and small bowel dilation look like ileus

Sigmoid Volvulus:
- Coffee bean sign
o Cleft of the two bowel walls pushed together
- Volvulus
o Twisting of a segment of bowel about its axis with subsequent obstruction

PFA- Thumbprinting:
- Radiographic sign for colonic thickening
- Cannot by definition get it in the small bowel- they are thickened haustra
- CT-
- Differential:
o Colitis:
§ Inflammatory
• IBD
§ Ichemic colitis
§ Infectious colitis
• C. diff
- Relevant negatives:
o Toxic megacolon- 6 cm- Dilatation
o No evidence of perforation

Acute cholecysttis:
- GB distension
- Thickened wall of GB
- Pericholecystic free fluid
- Sonographic murphy’s sign positive
- 95% calculus
o Acalculous:
§ Trauma
§ Burns

MRCP:
- Really dilated intrahepatic ducts
- Obstruction of the common bile duct: Biliary obstruction
o Primary sclerosing cholangitis
o Cholangiocarcinoma
o Pancratic Cancer
 o Choledocolithiasis
o Mirizzi’s Syndrome
§ Squashing the common bile duct
§ Ascending cholangitis

Testicular mass:
- malignant
o Seminoma
o Metatastic
o nsgct
- Non malignant
o Orichitis
o Testicular infarction – secondary to torsion
o Hematoma
o Sarcoidosis

PET-CT:
- PET-
o Radiolabelled glucose analogue
o Tumours have high metabolic rate- radiotracer accumulates in tumour cells
- PET CT
o Combined antomic information with anatomic information

Diffuse sclerotic osseouslesions mets-

- Mets
o PSA – men
o Breast- women
- Metabolic:
o Hyperparathyoidism
o Renal osteodystrophy
- Pagets disease
- Sickle cell

Visible pleural line—should not see it, unless there is a pneumothorax

3 signs of hemidiaphragm:
- Tracheal shift
- Mediastinal shift – right or left heart border is displaced
- Flattened hemidiaphragm-
o Right should be higher than the left
Radiography:

Chest Radiograph:
- Basic Views
o Posterior Anterior (PA) View:
§ The closer an object is to the film, the sharper the borders
§ Most of the important structures in the chest, such as the heart and great vessels are
located anteriorly. Therefore, it is not surprising that the best way to take a chest
radiograph is with the patient’s front against the film
§ X-ray is shot from the patient’s back and is therefore shot from a posteroanterior
view and the heart size is thus minimally magnified and the heart borders are sharp
§ This is the standard position for obtaining a routine adult chest radiograph
§ Patient stands upright with the anterior wall of the chest places against the front of
the film
§ The shoulders are rotated forward enough to touch the film, ensuring that the
scapular do not obscure a portion of the lung fields
§ Usually taken with the patient in full inspiration
§ The PA film is viewed as if the patient is standing in front of you
o Anterior Posterior (AP) view:
§ Sometimes the patient is too sick to stand or sit for a PA view- in this case, a lower
quality AP view is taken
§ A film is placed under the patient’s back and an X-ray is shot through the patient
from the front
§ In this view, the heart is further from the film- therefore, it appears larger than it
really is and its borders are fuzzier
 § Used when the patient is debilitated, immobilized or unable to cooperate with the
PA procedure
§ Film is placed behind the patient’s back with the patient in a supine position
§ Heart is at a greater distance form the film hence appear more magnified than in a
PA
§ The scapulae are usually visible in the lung fields becaue they are not rotated out of
the view as they are in a PA
o Lateral:
§ Patient stands upright with the left side of the chest against the film and the arms
raised over the head
§ Allows the viewer to see behind the heart and diaphragmatic dome
§ Typically used in conjunction with a PA view of the same side of the chest to help
determine the three-dimensional position of organs or abnormal densities
o Lateral Decubitus
§ The patient lies on either the right or left side rather than in the standing position as
with a regular lateral radiograph
§ The radiograph is labeled according to the side that is placed down (a left lateral
decubitus radiograph would have the patient’s left side down against the film)
§ Often useful in revealing a pleural effusion that cannot be easily observed in an
upright view, since the effusion will collect in the dependent position

Relative Densities:
- The images seen on a chest radiograph result form the differences in densities of the materials in the
body
- Least dense (Black) to most dense (white) below:
o Gas (air in the lungs)
o Fat (fat layer in soft tissue)
o Water/fluid (same density as heart and blood vessels)
o Bone (the most dense of the tissues)
o Metal (foreign bodies)

Before Interpreting the Radiograph:

- Patient identification details
- X-Ray view: PA, AP, Lateral
- Breath: Inspiration or Expiration
o The chest radiograph should be obtained with the patient in full inspiration to help assess
the intrapulmonary abnormalities
o At full inspiration, the diaphragm should be observed at about the level of the 8th or 10th rib
posteriorly, or the 5th to 6th rib anteriorly
- Rotation
o Patient rotation can be assessed by observing the clavicular heads and determining
whether they are equal distance from the spinous processes of the thoracic vertebral bodies
 - Penetration
o On a properly exposed chest radiograph:
§ The lower thoracic vertebrae should be visible through the heart
§ The bronchovascular structures behind the heart (trachea, aortic arch, pulmonary
arteries etc) should be seen

ABCDEFGHI approach:
- A- Airway
o Trachea
o Carina- Left and Right Main Bronchus
- B- Bones and soft tissue
o Bones:
§ Look at each rib in turn
§ Clavicles
§ Scapulae and humeri if visible
§ Lower cervical and thoracic spine
o Soft Tissue:
§ Thick soft tissue due to obesity may obscure some underlying structures such as
lung markings
 § Breast tissue may obscure the costophrenic angles
§ Abnormal examples:
• Lateral chest wall- surgical emphysema
• Supraclavicular fossae: enlarged nodes
• Under the diaphragm: pneumoperitoneum
- C- Cardia
o 2/3rds of the heart should lie on the left side of the chest, with one-third on the right
o The heart should take up less than half of the thoracic cavity (Cardiac/Thoracic ratio <50%)
o The left atrium and the left ventricle create the left heart border
o The right heart border is created entirely by the right atrium (the right ventricle lies
anteriorly and therefore does not have a border on the PA view)
- D- Diaphragm
o Both diaphragms should form a sharp margin with the lateral chest wall
o Both diaphragm contours should be clearly visible medially to the spine
o The right side is often slightly higher than the left due to the liver
o Causes of raised hemidiaphragm: trouble above the diaphragm- lung volume loss, trouble at
the diaphragm- stroke; phrenic nerve palsy, any mediastinal mass cause?, trouble below the
diaphragm- hepatomegaly, subphrenic abscess
- E- Effusions
o The pleura and pleural spaces will only be visible when there is an abnormality present
o Common abnormalities seen with the pleura include pleural thickening, or fluid or air in the
pleural space
§ Meniscus sign can be seen
- F- Fields (Lung Fields)
o Normally, there are visible markings throughout the lungs due to the pulmonary arteries and
veins, continuing all the way to the chest wall
o Both lungs should be scanned, starting at the apices and working downward, comparing the
left and right lung fields at the same level
- G- Gastric bubble
- H- Hila and mediastinum
o The hila consist primarily of the major bronchi and the pulmonary veins and arteries
o The hila are not symmetrical, but contain the same basic structures on each side
o The hilar may be at the same level, but the left hilum is commonly higher than the right
o Both hila should be of similar size and density
o Mediastinum:
§ The trachea should be centrally located or slightly to the right
§ The aortic arch is the first convexity on the left side of the mediastinum
§ The pulmonary artery is the next convexity on the left and the branches should be
traceable as it fans out through the lungs
§ The lateral margin of the superior vena cava lies above the right heart border
- I- Impression/ ICU- Tubes and lines

Silhouette Sign:
- An intrathoracic lesion touching a border of the heart, aorta or diaphragm will obliterate part of that
border on the radiograph
Opacification:
- Nodules (if over >3cm then called a mass instead)
o Neoplasia: metastases (often missed if small)lung cancer, hamartoma, adenoma
o Infections: varicella pneumonia, septic emboli, abscess, hydatid
o Granulomas: military TB, sarcoidsosis, granulomatosis with polyangiitis, histoplasmosis
o Pneumoconioses (except asbestosis)
- Reticular opacification:
o Lung parenchymal changes, can be acute (interstitial odema, e.g. cardiac, atypical
pneumonia, e.g. viral) or subacute/chronic
§ Acute interstitial odema
§ Infection: acute- viral, bacterial, chronic – TB, histoplasmosis
§ Fibrosis- usual interstitial pneumonia, non-specific interstitial pneumonia, drug-
methotrexate, bleomycin, crack cocaine, connective tissue disorders- RA, SLE, PAN,
systemic sclerosis- sarcoidosis, industrial lung diseases (silicosis, asbestosis)
§ Malignancy – lymphangitis carcinomatosa
- Alveolar opacification:
o Airspace opacifaction, an be due to any material filling the alveoli, usually divided into one or
a combination of the following:
§ Pus- pneumonia
§ Blood- hemorrhage
§ Water- renal or liver failure, ARDS, smoke inhalation, drug (heroin), O2 toxicity, near
drowning
§ Cells-lymphoma, bronchioalveolar carcinoma
§ Protein- alveolar proteinosis, ARDS, fat emboli (around 7 days post fracture)

Air bronchogram sign:

- When the internal tubular outline of a bronchus is visible within a thoracic opacity… that is an air
bronchogram
- It is most commonly associated with a simple pneumonia
o Sometimes it occurs with pulmonary odema

The Cardiac Density:

- The density (opacity) of the cardiac shadow should be equal on both sides of the spine
- If there is any difference in density then look for evidence of pneumonia, or lower lobe collapse or a
lower lobe mass on the denser side
- There should be no abrupt change in density across the cardiac shadow

Lung Apices:
- Thickening of the apical pleura- sometimes referred to as an apical cap- occurs normally in 10% of
middle-aged and elderly people
- Unfortunately, a superior sulcus carcinoma (e.g. a Pancoast Tumour) can mimic an apical cap

Peripheral Opacities:
- An intrapulmonary opacity abutting the pleura forms an acute angle at the interface
- A pleural or extrapleural lesion forms an obtuse angle
PLEURAL EFFUSION/HEMOTHORAX/EMPYEMA:
- A pleural effusion is just a collection of fluid between the visceral pleura and the parietal pleura
(i.e. – in the pleural space)
- This fluid could be a serous fluid (effusion), blood (hemothorax), pus (empyema)
- On an upright PA- fluid collects in the lateral costophrenic angle due to gracity--- giving it the
‘blunted’ appearance
o The posterior costophrenic angle is the deepest and fluid collects there first
o This angle is hidden by the dome of the diaphragm on a PA view – however, it is well seen on
the lateral view—for this reason, the upright lateral view is superior to the PA for
demonstrating small amounts of pleural fluid
- Immobile pleural fluid is called loculated effusion – if the parietal and visceral pleura are stuck to
each other (adhesion), fluid may not be able to move when patient changes position

CONGESTIVE HEART FAILURE:

- CHF occurs when the heart becomes unable to pump out the same amount of blood that it is receiving
- The heart becomes enlarged (cardiomegaly)
- When there is left ventricular failure, fluid backs up in the pulmonary veins and lung
- Fluid seeps out into the interstitium first and then eventually into the alveoli and pleural space
o 1. Vascular redistribution: blood vessels in the upper zone become larger than the ones in
the lower lung zones (the normal)
o 2. Interstitial pattern and Kerly B lines
o 3. Peribronchial cuffing: bronchi seen head on are surrounded by fluid
o 4. Pleural effusions
o 5. Batwing pattern (symmetrical air space disease in the lung adjacent to the hila)

Chronic interstitial lung disease:

- An abnormal white area that has not changed compared to a previous exam and a honey comb
pattern that is suggestive of scarring

Nodule/Mass:
- Nodules and masses in the lung appear as round white fluid densities
- If the lesion measures less than 3 cm, it is called a nodules, whilst if its larger than 3 cm it is called a
mass
- Caused by either a malignant (lung cancer, mets) or benign process (granuloma)
- Primary lung cancers tend to have ill-defined, speculated borders and grow overtime
- Mets tends to produce multiple smooth round lung nodules- often of variable size
- Benign lesions tend to be small, well defined, smooth, roung and maybe calcified- they are stable in
size when compared to the prior films

ABDO:

CT BRAIN:

Radiographic anatomy:
- The brain is divided into four pairs of lobes- including the frontal, temporal, parietal and occipital
- At the centre of the brain, there are paired thalamus and basal ganglia (caudate nucleus, putamen and
globus pallidus)
 - Around these structures swirlds the ventricular system, which includes the two lateral ventricles, the
third ventricle and the fourth ventricle
- The brain is covered by several layers of protective tissue
- The mnemonic PAD may be used to remember them
- The pia mater is closest to the brain, followed by the arachnoid mater and the dura mater

Vascular Territories:
- The cerebral arteries originate from the circle of Willis, which is located in the “Star”
o The anterior, middle and posterior cerebral arteries grossly supply anterior, middle, and
posterior part of the brain from the "X" to "Mr. Sad" lever. However, from the "Worm" to the
"Coffee Bean" level, the anterior cerebral artery supplies most of the midline from anterior to
posterior
o

Bottom- X part of the brain:

Supply:
1. The X
Look at the "X" level. Specifically look at the lower leg of the "X" itself, which represents the mastoid air cells,
to see if they are of the same thickness on both sides. This is to de- termine if the slices were taken at the same
level on each side.
If the patient's head had been tilted in the CT scanner, these structures will appear asymmetrical. This may
account for apparent asymmetry between the cerebral hemispheres or
other structures on several or all images.
2. Black Strokes
Look for any abnormally black (dark) area, which could represent an infarcted portion of brain (discussed in
Stroke section).
3. White Hemorrhage
Look for any abnormally white (bright) area, which could represent acute hemorrhage in the ventricular
system, in the brain, or around it (discussed in Hemorrhage section).
4. Ventriloquist Ventricular and sulcal size
Look at the ventricles to see if they are abnormally en- larged. Look at the sulci to see if they are too big or too
small (discussed in Hydrocephalus section)
5. Break Fractures
Look for abnormal dark lines in the white bone (fractures)
and for black air inside the skull (discussed in Trauma section).
6. Mass and/or Mass effect
Look for any big mass (tumor or abscess) in the brain. En- sure that the brain is not pushed to one side
because of a mass
or intracranial hemorrhage.

Hemorrhage:
- The CT appearance of fresh blood (also known as acute hemorrhage) is that of a white (hyperdense)
area in comparison to the gray colored brain.
- After a week, blood starts to appear gray like the brain or slightly darker than the brain.
- At this point, it is called a subacute hemorrhage (isodense or slightly hypodense).
- After several weeks, blood appears much darker than the gray brain, and it is then called a chronic
hemorrhage (hypodense).
- Bleeds may occur in four areas within the skull, as intraparenchymal, subarachnoid, subdural or
epidural hemorrhages.

Intraparenchymal Hemorrhage:
- Acute intraparenchymal hemorrhage is easily recognized on CT scans as an abnormal white area in
the brain tissue.
- As the blood becomes older, it degrades and eventually becomes darker than brain tissue (chronic).
- Intraparenchymal hemorrhage is bleeding within the brain tissue itself. It is most commonly caused
by hypertension, but is also seen with trauma, brain malignancy or infarct (see section on
hemorrhagic stroke).

Subarachnoid:
- On CT scan, some of the CSF appears white rather than its usual dark appearance, because it is mixed
with bright blood. Hemorrhage is seen in the Sylvian fissure, the suprasellar cistern, the basal cistern
and the quadrigeminal cistern
- There may also be bright blood in the ventricles.
- The best location to examine for intraventricular hemorrhage is the occipital horns of the lateral
ventricles, where the blood collects due to gravity (Fig.9-14).
- In subarachnoid hemorrhage, blood appears in the subarachnoid space, which is located between the
pia mater and the arachnoid mater. Blood may also appear in the ventricular system (intraventricular
hemorrhage), as this is connected to the subarachnoid space.
- Subarachnoid hemorrhage is most commonly caused by leakage of blood from an aneurysm, but may
also be caused by trauma.

Subdural:
- On CT scan, this appears as a bright "moon crescent" between the brain and the skull
- It crosses suture lines but never crosses dural reflections (i.e. falx cerebri and the tentorium). In this
entity there is blood in the subdural space, which is located between the dura mater and the
arachnoid mater.
- It is most often caused by a venous tear, and occurs often in elderly patients. It frequently occurs
secondary to minor trauma (half of the patients cannot even recall the injury that caused the bleed).
It is relatively rare to find a skull fracture when a subdural hematoma is present.

Epidural:
- On CT scan, this has the appearance of a biconvex white lens, located between the brain and the skull.
Un-like the subdural hematoma, the epidural hematoma may cross dural reflections, but does not
cross suture lines
- In this entity, there is blood in the epidural space, which is located between the dura mater and the
skull.
- It often caused by an arterial tear (especially the middle meningeal artery).
- It is usually caused by significant trauma and is often associated with skull fractures.

Stroke:
- On CT scans, this entity may have a normal appearance for the first 12 hours.
 - The first manifestations of an infarct are subtle and include a white clot in one of the vessels, loss of
normal gray-white differentiation, and sulcal flattening (effacement).
- Thereafter, the appearance often progresses to a wedge-shaped dark area, extending to the edge of
the brain, involving both the gray and white matter
- Infarction occurs when an area of brain gets insufficient blood perfusion and dies. Causes of stroke
include atherosclerosis, emboli, low cardiac output and vasospasm.
- Infarcts may be very small and round. These are lacunar infarcts and are often located in the deep
brain (basal ganglia, thalamus, internal capsule and the brain stem)

Mass Effect:
- Several space occupying lesions may appear within the brain, including abscesses, tumors and
hematomas.
- When these occur, the brain may be pushed away, causing loss of normal symmetry between the two
cerebral hemispheres.
- If severe enough, parts of the brain may slide (herniate) under either the dural reflections (falx,
tentorium) or down the foramen magnum of the skull. There are three types of herniation: subfalcine,
transtentorial, and tonsillar herniation.

HYDROCEPHALUS:
- Hydrocephalus occurs when either all (communicating hydrocephalus) or part (non-communicating
hydrocephalus) of the ventricular system is dilated

Non-Communicating (normal 4th ventricle)

- This type is secondary to an obstruction of the ventricular system (foramen of Monro, 3rd ventricle,
aqueduct of Sylvius or 4th ventricle)
- It results in dilation of the sytem proximal to the obstruction
- The choroid plexi in the lateral ventricles continue making CSF oblivious to the obstruction
- Pressure within the lateral ventricle pushes the brain tissue against the skull and causes sulcal
effacement or flattening
- Pressure within the lateral ventricle pushes the brain tissue against the skull and causes sulcal
effacement or flattening (similar to an old man squishing his face in a window, resulting in wrinkle
effacement). Often, the pressure is great enough within the ventri- cles so that some CSF spreads into
the brain tissue around the ventricles, through the ventricular wall (the ependyma).
- Therefore the CT scan findings may include sulci ef- facement, transependymal spread of CSF, and
dilation of all the ventricles proximal to the level of blockage (Fig.9-20). Therefore, if the blockage is
between the third and the fourth ventricle, the 4m ventricle will be of normal size. If the blockage is
located between the lateral ventricles and the third ventricle, both the third and the fourth ventricle
will be normal. Common causes of non- communicating hydrocephalus include tumors and con-
genital defects.

Communicating Hydrocephalus (dialted 4th ventricle)

- In this type, the obstruction occurs distal to the fourth ventricle (i.e. in the subarachnoid space or in
arachnoid granulation tissue where CSF is resorbed).
- The CT findings are similar to the avoid, except that the entire ventricular system, including the 4th
ventricle, is filated
- This entity is often caused by meningitis, subarachnoid hemorrhage and trauma

Ex vacuo hydrocephalus (cerebral atrophy)

- Cerebral atrophy occurs when there is less brain tissue than normal
- This is more commonly seen with old age
- Because there is less brian, te ventricles fill the increased space and appear enlarge
- In contrast with other types of hydrocephalus, the cerebral sulci are bigger instead of being squished
against the skull
- There is no blockage and no increased pressure in the ventricular system
- Ex vacuo hydrocephalus is of no clinical significance and is not to be confused with other types of
hydrocephalus

STROKE:
- Content of lecture:
o Stroke/TIA definitation
o Types of stroke
o Imaging
o Case based destruction
Stroke:
- Focal neurological deficit lasting greater than 24 hours
 - TIA- focal neurological deficit lasting less than 24 hours

Types of stroke:
- Ischemic v hemorrhagic
- anterior v posterior
o Anterior- loss of power of the arm or leg or loss of speech
o Posterior- cerebellar symptoms and hemianopias
- Aetiology

Normal CT Brain:
- Want to be able to see the basal ganglia
- Clearly defined and equal on both sides

Case 1:
- 76 year old male
- 2 hour hisotry of left sided weakness
- no known past medical history
- smoker 30 pack year history
- o.e BO 190/80, HR 105, RR 16, Temp 37.5
- Upper and lower lumb weakness, right facial drool
- Blood sugars are normal
Differential:
- Ischemic stroke
- Hemorhagic stroke
- Hypoglycemia
- Space occupying lesion (tend to develop more gradually)
Risk factors
- Older
- Male
- Smoker
- Hypertensive
- Blood sugar on the high side
Risk factors for stroke are broken into modifiable and non modifiable

Management:
- CT brain

Need to decide from thrombolysis, thrombectomy, both or neither

- If the CT scan shows a lot of ischemia you can not give thrombolysis
- Thrombolysis needs to be within 4 and half hours
o Relatively normal CT brain with no hemorrhage on the CT brain
- Exclusion criteria:
o Absolute-
§ INR greater than 1.7,
§ Hemorrhage on the CT,
§ A known bleeding problem (hemophiliac or thrombocytopenic),
§ Someone with a BP of greater than 200/105
o One in 100 will die from thrombolysis that you give them
o Only about 10% of people will get better from thrombolysis

Thrombectomy:
- Anterior circulation timing is 6 hours
- Is an argument for doing it up to 12 hours but for exam purposes 6 hours is the correct answer
- Do not want to see hemorrhage on the CT
- Proximal vessel occlusion in the internal carotid or MCA
- Exclusion criteria-
o Sufficent ichemic changes
o Greater than 6 hours
o Hemorrhage

Scan at 24 hours:
- Dark grey area is established ischemic change
- Post thrombolysis bleed- white where it shouldn’t be is always blood

Carotid stenosis greater than 70% on the ipsilateral side is a big risk factor*
Case 2:
- 56 year old man with a 30 minute hisotry of loss of power in his left hand
- event occurred yesterday, GP referred him to the fast clinic for review
- PMH: MI at 49, hypertension, hyperlipidemia
- Recovered from event in less thant24 hours

TIA
- Stratifying risk
- ABCD2
o Age
o Blood pressure
o Clinical Features
o Duration of Symptoms
o Diabters

Work up:
- Bloods
- Imaging
o Carotid dopler- anterior symptoms with a 70% occlusion on the ipsilateral side
o MR angiogram or CT angiogram
- Cardiac
o A fib with Holter Monitor- need at least 72 hours
- Secondary prevention:
o Antiplatelet versus anticoagulation
§ Antiplatet for anyone in sinus rhythm
• High dose aspirin
• Or dual antiplatelet for 90 days- and then either aspirin or clopidogrel
§ Anticoagulant for afib (CHAD VAS score is automatically over 2)
o Statin
§ High potency statin-
§ LDL less than 2.6
o BP
§ ACE inhibitor
§ 2 agents at the lowest dose that gets their blood pressure controlled
§ CCB
§ Less than 140/90 or if DM 130/80
o DM
 § HbA1c less than 5
o Lifestyle
§ Healthy diet and exercise
- Should be able to discuss the long term dicuss long term anticoagulation options and pros and cons of
both

Case 3:
- 76 year old female, found on floor by daughter this am
- Drowsy, not moving right side
- History of mechanical valve replacement- on warfarin, DM and hypertension
- Scan on admission
o Bright white area in the middle- hemorrhage
o Not equal on both sides
- 2 types of hemorrhage
o Deep- basal ganglia
§ hypertension
o Lobar hemorrhage- more peripheral
§ Cerebral amyloid angiopathy
- Risk factors
o Hypertension
o Anticoagulation > antiplatelets
o Cerebral amyloid angiopathy
§ Beta amyloid deposited in the arteries and small vessels in the brain – we pick this
up with an MRI with blood sequences
§ Only way to make this diagnosis definitively is autopsy
§ Linked somewhat to alzheimers
o Trauma
- General emergent treatment:
o BP control
o Start treatment if sBP is over 150 mmHg
o Aim for sBp under 140
o IV labetalol (first line except with bradycardia or ashtma)
o IV GTN (not for PDE5 inhibitors)
o IV nicardipine (contraindicated in advanced aoritc stenosis)
- If caused by warfarin- Vit k and Prothrombin complex

Case 4:
- 84 year old man with a history of recurrent falls
- Wife reports more unsteady on his feet in recent days, increasingly confused. She has also noted he is
unable to hold anything in his left hand
- On aspirin for previous MI- 15 years ago
- Scan:
o Convex area of hemorrhage on the outside of the brain
o Mass effect ventricle has been moved
o Acute on chronic subdural hematoma
- Risk factors:
o Brain atrophy
§ Venous bleed rather than arterial bleed
o Anticoagulation>antiplatelet
o Trauma
§ Common in chronic alcoholics
§ Frequent falls
o Increasing age
§ Related to brain atrophy
- Treatment:
o Stop antithrombotics and reverse
o Regular neuro obs
o Discuss with neurosurgery re burr hole evacuation
- Criteria for evacuation
o Acute SDH thicker than 5mm and have any neurological signs
§ Focal neurological deficit- speech or limb weakness
o Mass effect

Case 5:
 - 28 male present with sudden onset of occipital headache- like he was hit on the back of head
- Non smoker
- Non drinker
- family history of PCKD (link between this and Berry aneurysms)*
- Subarachnoid hemorrhage
- CT brian: blood in the sulci (pathopneumonic for subarachnoid)
- Risk factors
o Smoking
o Alcohol misuse- coagulopathies
o Hypertension
o Bleeding disorders
o Mycotic aneurysm (SBE)
o Family history
§ Close relative have 3-5 fold increased risk of SAH
- Investigation
o CT brain- detects > 90% of SAH within the 1st 48 hours
o LP (>12 h after heachache onset)
§ Bloody tap
§ Xanthachromia
o CTAngiography
o Formal angiography
- Treatment:
o Refer to neurosurgery
o Supportive care: keep well hydrated and aim for SBP >160 mmHg
§ Make sure they are getting enough blood to the more peripheral areas
o Nimodipine (CCB) reduces vasospasm
§ Worry about this because they are more likely to get an ischemic insult to the brain
if they get vasopasm after the aneurysm
o Coiling
§ Done by the neuroradiologist
§ Only not done if they neck of the aneurysm is particular wide and cannot be coiled
o Clipping of aneurysm

NEURO EMERGENCIES:

STATUS EPILEPTICUS:
- This means seizures lasting for >30 min, or repeated seizures without intervening consciousness
- Mortality and the risk of permanent brain damage increase with the length of the attack
- Aim to terminate seizures lasting more than a few minutes as soon as possible (<20 min)
- Status usually occurs in patients with known epilepsy
- If it is the 1st presentation, the chance of a structural brain lesion is high (>50%)
- Diagnosis of tonic-clonic status is usually clear
- Non-convulsive status (e.g. absence status or continuous partial seizures with preservation of
consciousness) may be more difficult; look for subtle eye or lid movement

Could the patient be pregnant? If so, eclampsia is the likely diagnosis, check the urine and BP

Investigations:
- Bedside glucose, the following tests can be done once treatment has started: lab glucose, ABG, U&E,
Ca2+, FBC, ECG
- Consider anticonvulsant levels, toxicology screen, LP, culture blood and urine, EEG, CT, carbon
monoxide level
- Pulse oximetry, cardiac monitor

Treatment:
- Lorazepam:
o 0.1mg/kg (usually 4mg) as a slow bolus into a large vein
o if no response within 10 mins give a second dose
o beward respiratory arrest during the last part of the injection
o have full resuscitation favilities to hang for all IV benzodiazepine use
o The rectal route is an alternative for diazepam if IV access is difficult
- Buccal midazolam: is an easier to use oral alternative; dose for those 10 years old and odler 10mg; if
1-5 years 5mg, if 5-10 years; 7.5mg, squirt half the volume between the lower gum and the cheek on
each side
o While waiting for this to work, prepare other drugs and if fits continue…
 - Phenytoin infusion: 15-20mg/kg IVI (roughly 1g if 60kg and 1.5g if 80 kg, max 2g) at a rate of
<50mg/min (don’t put diazepam in same line; they don’t mix)
o Beware if BP dropping and do not use if bradycardic or heart block
o Requires BP and ECG monitoring
o 100mg/6-8h is a maintenance dose (check levels)
o if fits continue…
- Diazepam infusion:
o E.g. 100mg in 500mL of 5% dextrose; infuse about 40mL/h (max 3mg/kg/24h) until seizures
respond
o Close monitoring, especially respiratory function is vital
o It is most unusual for seizures to remain unresponsive after this
o If they do, allow the idea to pass through your mind that they could be pseudoseizures-
particularly if there are odd features (pelvic thrusts, resisting attempts to open lids and your
attempts to do passive movements; arms and legs flailing around)
- Dexamethasone:
o 10mg IV if vasculitis/cerebral odema (tumour) possible
- General anesthesia
o For refractory status- get anesthetist/ICU involved early – never spend longer than 20 min
on someone with status epilepticus without having help at the bedside from and anesthetist

MENINGITIS:
- When to act now:
o Headache, pyrexia, neck stiffness, altered mental state
§ If any 2 co-exist and not yet in hospital, give benzylpenicillin 1.2g IM/IV before
admitting
- Organisms:
o Meningococcus or pneumococcus
o Less commonly Haemophilus influenza, listeria monocytogenes, CMV, Cryptococcus or TB if
immunocompromised, e.g. HIV positive, organ transplant, malignancy
- Differential:
o Malaria, encephalitis, septicemia, subarachnoid, dengue, tetanus
- Features:
o Early:
§ Headache, leg pains, cold hands and feet, abnormal skin colour
o Later:
§ Meningism: neck stiffness, photophobia, Kernig’s sign (pain and resistance on
passive knee extension with hip fully flexed)
§ Conscious level declining, coma
§ Seizures (around 20%) ± focal CNS signs (around 20% ± opisthotonus (spasm of the
muscles causing backward arching of the head, neck, and spine, as in severe tetanus,
some kinds of meningitis, and strychnine poisoning)
§ Petechial rash (non-blanching; may be only 1 or 2 spots or none)
o Signs of galloping sepsis: slow capillary refill time; DIC, BP declining, temperature and pulse:
increased or normal
- Management:
o Start antibiotics immediately
o Signs of disease causing meningitis:
§ Zoster; cold sore/genital vesicles (HSV)
§ HIV signs (lymphadenopathy, dermatitis, candidiasis, uveitis)
§ Leptosporosis (bleeding and red eye)
§ Mumps (parotid swelling)
§ Glandular fever (sore throat ± jaundice ± nodes
§ Splenectomy scar will indicate the patient is immunodeficient
o If ICP is raised: summon help immediately and inform neurosurgeons
o Prophylaxis: Discuss with public health/ID
§ Household contacts in droplet range
§ Those who have kissed the patient’s mouth
§ Give rifampicin (600mg/12h PO for 2d; children >1y 10mg/kg/12h; <1y
5mg/kg/12h) or ciprofloxacin (500mg PO, 1 dose child 5-12years: 250mg stat)
neither is guaranteed in pregnancy but are recommended
o Antibiotic therapy for meningitis:
§ Local policies vary. If in doubt, ask. Where the organism is unknown:
• <55 years: cefotaxime 2g/6h slow IV
• >55 year: cefotaxime as above + ampicillin 2g IV/4h (for Listeria)
• Aciclovir if viral encephalitis suspected
• Once organism isolated, seek urgent microbiological advice
 - Investigations:
o U&E, FBC (WBC decreased in immunocompromised: get help), LFT, glucose, coagulation
screen
o Blood culture, throat swabs (1 for bacteria, 1 for virology), rectal swab for viruses. Serology
e.g. EBV, HIV
o Lumbar puncture: is usually done after CT but if GCS is 15, no symptoms of raised ICP and no
focal neurology- can be done without
§ Contraindications: suspected intracranial mass lesion, focal signs, papillodema,
trauma, middle ear pathology, major coagulopathy
§ Measure opening pressure:
• 7-18cm CSF is normal
• In meningitis may be >40- typically 14-30
o Send CSF for MC&S, gram stain, protein, glucose, virology/PCR and lactate
o In aseptic meningitis (usually self-limiting) do CSF PCR: 46% are from enteroviruses (e.g.
Coxsackie A and B, echoviruses) 31% herpes simplex type 2; 4% HSV1, HSV meningitis is
self-limitng if immunocompetent, unlike HSV encephalitis (a different entity
o CXR: signs of TB? If so, consider TB meningitis

Lumbar Puncture in Meningitis: CSF

 - Pyogenic:
o Appearance: often turbid
o Predominant cell: polymorphs
o Cell count/mm3: e.g. 90-1000 ro more
o Glucose: <1/2 plasma
o Protein (g/L): >1.5
o Bacteria: in smear and culture
- Tuberculosis:
o Appearance: often fibrin web
o Predominant cell: mononuclear
o Cell count/mm3: e.g. 10-1000
o Glucose: <1/2 plasma
o Protein (g/L): 1-5
o Bacteria: often none in smear
- Viral (‘aseptic’)
o Appearance: usually clear
o Predominant cell: mononuclear – also may be lymphocytes in TB, listerial and cryptococcal
meningitis
o Cell count/mm3: 50-1000
o Glucose: >1/2 plasam
o Protein g/L: <1
o Bacteria: none seen or cultured
- Normal values:
o <5 lymphocytes. Mm3 may be normal, so long are there are no neutrophils
o Protein: 0.15-0.45g/L
o CSF glucose: 2.8-4.2mmol/L
§ Causes of decreased CSF glucose: sepsis, parasitic, meningitis, e.g. form eating snails
(do CSF eosinophil count) also herpes encephalitis, hypoglycemia, sarcoid, CNS
vascultiis
§ A CSF lactate level of >3.5 mmol (31.5 mg/dL) predicts bacterial meningitis quite
well

ENCEPHALITIS:
- Suspect encephalitis whenever off behavior, decreased consciousness, focal neurology or seizure is
preceded by an infectious prodrome (increased temperature, rash, lymphadenopathy, cold sores,
conjunctivitis, meningeal signs)
- It is often wise to treat before the exact cause is known- usually viral, and often never identified
- Without the infectious prodrome consider encephalopathy: hypoglycemia, hepatic encephalopathy,
diabetic ketoacidosis, drugs, hypoxic brain injury, uremia, SLE, beri-beri (give vit B1 if in doubt)
Signs and Symptoms:
- Bizarre encephalpathic behavior or confusion
- Decreased GCS or coma
- Fever
- Headache
- Focal neurological signs
- Seizures
- History of travel or animal bite
Causes:
- Viral: HSV1 and 2, arboviruses, CMV, EBV, VZV (varicella-zoster virus), HIV (seroconversion),
measles, mumps, rabies, Japanese B encephalitis, West Nile virus, tick-borne encephalitis
- Non-viral: any bacterial meningitis, TB, malaria, listeria, Lyme disease, legionella, leptospirosis,
aspergillosis, crytococcus, schistosomiasis, typhus
Investigations:
- Bloods: blood cultures, serum for viral PCR (also throat swab and MSU), toxoplasma, IgM titre,
malaria film
- Contast-enhaved CT: focal bilateral temporal lobe involvement is suggestive of HSV encephalitis
o Meningeal enhavement suggests meningoencephalitis
o Do before LP
o MRI is alternative if allergic to contrast
- LP: typically moderately raised CSF protein and lymphocytes and decreased glucose
o Send CSF for viral PCR including HSV (CSF PCR is 95% specific for HSV-1)
- EEG: urgent EEG showing diffuse abnormalities may help confirm a diagnosis of encephalitis, but
does not indicate a cause
Management:
- Mortality in untreated viral encephalitis is around 70%
 - Aim to start acyclovir within 30 mins of the patient arriving (10mg/kg/8h IV over 1h) for 14 days as
empirical treatment for HSV (21 days if immunosuppressed)
- Adjust acyclovir dose according to eGFR: use every 12 hours if eGFR 25-50; every 24h if eGFR 10-25
- Consult product literature if eGFR <10
- Specfici therapies also exist for CMV and toxoplasmosis
- Supportive therapy- in a high dependency unit or ICU environment if necessary
- Symptomatic treatment: e.g. phenytoin for seizures

CEREBRAL ABSCESS:
- Suspect this in any patient with increased ICP, especially if there is fever or increased WC
- It may follow ear, sinus, dental or periodontal infection, skull fracture, congenital heart disease,
endocarditis, bronchiectasis
- It may also occur in the absence of systemic signs of inflammation
- Signs:
o Seizures, fever, localizing signs, or sings of increased ICP
o Coma, signs of sepsis elsewhere (e.g. teeth, ears, lungs, endocarditis)
- Investigations:
o CT/MRI (e.g. ‘ring enhancing lesion’)
o Increased WCC
o Increased ESR
o Biopsy
- Treatment:
o Urgent neurosurgical referral; treat increased ICP
o If frontal sinuses or teeth are the source, the likely organism will be Strep. Milleri
(microaeopholicc) or oropharyngeal anaerobes
o In ear abscesses, B. fragilis or other anaerobes are most common
o Bacterial abscesses are often peripherall toxoplasma lesions are deeper (e.g. basal ganglia)
o NB: ask yourself – is the patient immunocompromised?
RAISED INTRACRANIAL PRESSURE:
- The volume inside the cranium is fixed, so any increase in the contents can lead to raised icp
- This can be mass effect,odema or obstruction to fluid outflow
- Normal ICP in adults is <15mmHg
- Causes:
o Primary or metastatic tumours
o Head injury
o Hemorrhage (subdural, extradural, subarachnoid, intracerebral, intraventricular)
o Infection: meningitis, encephalitis, brain abscess
o Status epilepticus
o Cerebral odema
- Signs and symptoms:
o Headahce (worse on coughing, leaning forwards), vomiting
o Altered GCS: drowsiness, listlessness, irritability, coma
o History of trauma
o Falling pulse and rising BP (Cushing’s response), Cheyne-Stokes respiratory
o Pupil changes (constriction at first, later dilatation- do not mask these signs by using agents
such a tropicamide to dilate the pupil to aid fundoscopy)
o Decreased visual acuity; peripheral visual field loss
o Papilloedema is an unreliable sign, but venous pulsation at the disc may be absent (absent in
around 50% of normal people, but loss of it is a useful sign)
- Investigations:
o U&E, FBC, LFT, glucose, serum osmolality, clotting, blood culture
o Consider toxicology screen
o CXR- any source of infecton that might indicate abscess
o CT head
o Then consider lumbar puncture if safe. measure the opening pressure
- Treatment:
o The goal is to reduce ICP and avert secondary injury
o Urgent neurosurgery is required for the definitive treatment of increased ICP from focal
causes (e.g. hematomas)
o This is achieved via a craniotomy or burr hole
o Also, an ICP monitor (or bolt) may be placed to monitor pressure
o Surgery is generally not helpful following ischemic or anoxic injury
- Herniation syndromes:
o Uncal herniation: is caused by a lateral supratentorial mass, which pushes the ipsilateral
inferomedial temiral lobe (uncus) through the temporal incisura and against the midbrain
 § The 3rd nerve, travelling in this space, gets compressed, causing a dilated ipsilateral
pupil, then ophthalmoplegia ( a fixed pupil localizes a lesion poorly but is ipsi-
lateralizing)
§ This may be followings (quickly) by contralateral hemiparesis (pressure on the
cerebral peduncle) and coma from the pressure on the ascending reticular activating
system (ARAS) in the midbrain
o Cerebral tonsil herniations:
§ Is caused by increased pressure in the posterior fossa forcing the cerebellar tonsils
through the foramen magnum
§ Ataxia, 6th nerve palsies, and upgoing plantar reflexes occur first then loss of
consciousness, irregular breathing and apnea
§ This syndrome may proceed very rapidly given the small size of and poor
compliance in the posterior fossa
o Subfalcian (cingulate) herniation:
§ Is caused by a frontal mass
§ The cingulate gyrus (medical frontal lobe) is forced under the rigid falx cerebri
§ It may be silent unless the anterior cerebral artery is compressed and causes a
stroke- e.g. contralateral leg weakness ± abulia (lack of decision making)
GI EMERGENCIES
:
UPPER GI BLEED

Haematemesis:
- The vomiting of blood. It may be bright red or look like coffee grounds
Melaena:
- Means black motions, often like tar and has a characteristic smell of altered blood
- Both indicate upper GI bleeding

Is the patient shocked?

- Peripherally shut down/cool and clammy; capillary refilling time >2s- urine output <1/2 mL/kg/h
- Decreased GCS (tricky to assess in decompensated liver disease) or signs of encephalopathy
- Poor urine output, e.g. <25mL/h or <1/2 mL/kg/hr
- Tachycardic (pulse >100 bpm, and JVP not raised)
- Systolic BP <100 mmHg, postural drop >20mmHg
- Do the Rockall score or the Glasgow Blatchford score
 o If GBS=0, admission can be avoided ie Hb >130g/L (or >120g/L); systolic BP >110mmHg,
pulse <100/min, urea <6/5 mmol/L, no melaena or syncope + no past/present liver disease
or heart failure

Common causes:
- Peptic ulcers
- Mallory-Weiss tear
- Oesophageal varices
- Gastritits/gastric erosions
- Drugs (NSAIDs, aspirin, steroids, thrombolytics, anticoagulants)
- Oesophagitis
- Duodenitis
- Malignancy
- No obvious cause
Rare Causes:
- Bleeding disorders
- Portal hypertensive gastropathy
- Aorto-enteric fistula
- Angiodysplasia
- Haemobilia
- Dieulagfoy lesion
- Meckel’s Diverticulum
- Peutz-Jegher’s syndrome
- Osler-Weber-Rendu syndrome

Acute Management:
- Start by protecting the airway and giving high-flow O2, then:
o Insert 2 large-bore (14-16g) IV cannulae and take blood for FBC (an early Hb may be normal
because haemodilution has not yet taken place) U&E (increased urea out of proportion to
creatinine is indicative of massive blood loss), LFT, clotting and crossmatch 4-6 units (give 1
unit for each 10g/L that the Hb is less than 140g/L)
o Give IV fluids to restore intravascular volume while waiting for blood to be crossmatched
§ In dire emergency- ie hemodynamically deteriorating despite fluid resuscitation
measure- give group 0 Rh-ve blood
o Insert a urinary catheter and monitor hourly urine output
o Organize CXR, ECG and check ABG
o Consider a CVP line to monitor and guide fluid replacement
o Transfuse (with crossmatched blood if needed) until hemodynamically stable
o Monitor pulse, BP, and CVP (keep >5cmH20) at least hourly until stable
o Correct clotting abnormalities (vit K, FFP, platelets)
o Omeprazole, e.g. 80mg as a bolus dose IV then continuous IVI at 8mg/h for 3d
o Arrange an urgent endoscopy, preferably at a dedicated endoscopy unit
o Inform surgeons of severe bleeds on admission- if endoscopic control fails, surgery may be
needed- or emergency mesenteric angiography/embolization
- Note: Risk of rebleeding: posterior duodenal ulcers are highest risk as they are nearest to the
gastroduodenal artery

Further Management:
- Re-examine after 4 h and ask about the need for Fresh frozen plasma if >4units transfused
- Hourly pulse, BP, CVP, urine output (4hrly in hemodynamically stable may be ok)
- Transfuse to keep Hb>100g/L; always keep 2 units of blood in reserve
- Check FBC, U&E, LFT and clotting daily
- Keep nil by mouth for 24h
o Allow clear fluids after 24h and light diet after 48 hours, as long as there is no evidence of
rebleeding
Endoscopy:
- Should be arranged after resuscitation, within 4h of the suspected variceal hemorrhage, or when
bleeding is ongoing within 24h of admission
- It can:
o Identify bleeding sites
o Help estimate risk of rebleeding
 o Aid treatment- sclerotherapy, variceal banding or argon plasma coagulation (for superficial
lesions)
- Endoscopic signs associated with risk of rebleeding:
o Active arterial bleeding (80% risk), visible vessel (50% risk), adherent clot/black dots (30%
risk)

Rebleeding:
- 40% of rebleeders die of complications
- Identify high-risk patients and monitor closely for signs of rebleeding
- IVI of omeprazole has a preventive role
- Get help; inform a surgeon at once if:
o Hematemesis with melena
o Increased pulse rate
o Decreased central venous pressure (assess via JVP or CVP line)
o Decreased BP
o Decreased urine output

Indications for surgery:

- Severe bleeding or bleeding despite transfusing 6u if >60 years (8u if <60)
- Active or uncontrollable bleeding at endoscopy- or rebleeding
- Initial Rockall score >3 or final Rockall score >6

Acute variceal bleeding:

- Resuscitate until hemodynamiccaly stable (avoid saline)
o If very anemic, transfuse to Hb of 80g/L
o NB: over-resuscitating may augment bleeding
- Correct clotting abnormalities with vitamin K, FFP, and platelet transfusions
o Studies on Factor VIIa failed to show benefit in terms of mortality
- Start IVI of terlpressin, e.g. 1-2 mg/6h for <3d, relative risk of death reduced by 34%
o Somatostatin analogues are alternatives
- Endoscopic banding or sclerotherapy should be tried (banding may be impossible because of limited
visualization)
- If bleeding uncontrolled, a Minnesota tube or Sengtaken-Blakemore tube should be placed by
someone with experience- get an anesthetists help
Balloon tamponade with a Sengstaken-Blakemore tube:
- In life-threatening variceal bleeding, this can buy time for transfer to a specialist liver centre or for
surgical decompression
- It uses balloons with a measured volume (120-300mL) of air giving pressure of 60mmHg
- Leave in situ until bleeding stops
o Remove after <24 h

TIPS:
- Shunts blood away from the portal circulation through an artificial side-to-side porto-systemic
anastomosis in the liver
- Also used in uncontrolled variceal hemorrhage
- Patients with associated renal failure, decreased cardiac preload and decreased cardiac performance
benefit mort form TIPS
Management
• Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and Clotting (as a
minimum)
• Patients with on-going bleeding and haemodynamic instability are likely to require O negative blood
pending cross matched blood
• Early control of airway is vital (e.g. Drowsy patient with liver failure)
• Patients with suspected varices should receive terlipressin prior to endoscopy
• Ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper GI
endoscopy within 24 hours of admission. In those who are unstable this should occur immediately
after resuscitation or in tandem with it. The endoscopy department is a potentially dangerous place
for unstable patients and it may be safer to perform the endoscopy in theatre with an anaesthetist
present.
• Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active
bleeding then a Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be
done with care; gastric balloon should be inflated first and oesophageal balloon second. Remember
the balloon with need deflating after 12 hours (ideally sooner) to prevent necrosis. Portal pressure
should be lowered by combination of medical therapy +/- TIPSS.
• Patients with erosive oesophagitis / gastritis should receive a proton pump inhibitor.
• Mallory Weiss tears will typically resolve spontaneously
 • Identifiable bleeding points should receive combination therapy of injection of adrenaline and either
a thermal or mechanical treatment. All who have received intervention should receive a continuous
infusion of a proton pump inhibitor (IV omeprazole for 72 hours) to reduce the re-bleeding rate.
• Patients with diffuse erosive gastritis who cannot be managed endoscopically and continue to bleed
may require gastrectomy
• Bleeding ulcers that cannot be controlled endoscopically may require laparotomy and ulcer
underruning

LIVER:

Liver Function Tests:

Approach to abnormal liver functions tests

- Abnormal LFTs can be found in around 17% of the asymptomatic general population
- Also remember that a normal LFT does not exclude liver disease

Tests of hepatocellular injury or cholestasis:

- Aminotransferases (AST, ALT) are released into the bloodstream after hepatocellular injury
o ALT is more specific for hepatocellular injury (but also expressed in kidney and muscle)
o AST is also expressed in the heart, skeletal muscle and RBCs
- Alkaline phosphatase may originate from liver, bone (so raised in growing children) placenta,
kidney, intestine and WCC
- Gamma-glutamyltransferase (GGT, gammaGT) is present in liver, pancreas, renal tubular and
intestine- but not bone, so it helps to tell if a raised alk phos is from bone (GGT normal) or liver (GGT
raised)
o NB: not specific to alcohol damage to the liver

Tests of hepatic function:

- Serum albumin, serum bilirubin, PT (INR)

Hepatocellular predominant liver injury:

- Raised AST and ALT
- Evaluate promptly, e.g. history from the family (increased consumption of alcohol?)
- Ultrasound for fatty liver, metastases etc, viral serology (hep A, B, C and Monospot)

Alcoholic liver disease:

- AST/ALT ratio is typically 2:1 or more
o When the history is not reliable, normal alk phos, GGT raised, and macrocytosis suggest this
condition

Acute viral hepatitis:

- AST and ALT raised, bilirubin may be normal
o NB: AST may be very raised

Chronic viral hepatitis:

- AST and ALT are raised, HBV and C are a leading cause worldwide

Autoimmune hepatitis (AIH):

- Occurs mainly in young and middle-aged females with concomitant autoimmune disorders (e.g.
rheumatological or thyroiditis)

Fatty infilitration of the liver

- Is probably the chief cause of mildly raised LFTs in the general population
- Risk factors for non-alcoholic fatty liver disease (steatohepatits):
o Obesity
o DM
o Increased lipids
- It’s a diagnosis of exclusion
- One study found that in 83% of patients with an elevated AST and ALT whose serum evaluation was
otherwise negative, biopsy revealed steatosis of no prognostic significance
- In 10% biopsy was normal- a reminder that mildly raised LFTs need not mean pathology
- Although US, CT or MRI may be helpful, biopsy is the gold standard

Ischemic hepatitis:
- Can be seen in conditions when effective circulatory volume is low (e.g. MI, hypotension,
hemorrhage)
 - AST and ALT are increased, as well as LDH

Drug-induced hepatitis:
- As no specific serology identifies most culprits a good history is vital
o Paracetamol overdose causes most acute liver failure in the UK

Cholestasis predominant liver injury:

- Alk phos and high GGT
o AST and ALT are mildly elevated

Management:
- For each specific diagnosis, manage accordingly
- If asymptomatic and other tests are negative, try lifestyle modification
- Help reduce weight and alcohol use, control DM and dyslipidemia, stop hepatotoxic drugs

Follow-up:
- Repeat tests after a few months, if still increased, do US (± abdominal CT)
- If diagnosis is unclear, get help: is biopsy needed?
- Consider alpha1-antitrypsin levels, serum caeruloplasmin (Wilson’s Disease), celiac serology, ANA
and ASMA (AIH)

JAUNDICE:
- Jaundice (icterus) refers to yellowing of skin, sclerae and mucosae from increased plasma bilirubin
(visible at over 60 umol/L)
- Jaundice is classified by the site of the problem (pre-hepatic, hepatocellular or
cholestatic/obstructive) or by the type of circulating bilirubin (conjugated or unconjugated)

Kernicterus = unbound bilirunin deposited in infant basal ganglia

Unconjugated hyperbilirubinemia:
- As unconjugated bilirubin is water insoluble, it does not enter the urine, resulting in unconjugated
(alcholuric) hyperbilirubinemia
- Over production: hemolysis (e.g. malaria/DIC), ineffective erythropoiesis
- Impaired hepatic uptake: drugs (contrast agents, rifampicin), right heart failure
- Impaired conjugation: eponymous syndromes: Gilbert’s, Crigler-Najjar
- Physiological neonatal jaundice: is caused by a combination of the above

Conjugated hyperbilirubinemia:
- Hepatocellular dysfunction:
o There is a hepatocyte damage, usually with some cholestasis
o Causes:
§ Viruses: hepatitis (A, B, C), CMV, EBV
§ Drugs
§ Alcohol: cirrhosis
§ Liver metastases/abscess
§ Hemochromatosis
§ Autoimmune hepatitis
§ Septicemia
§ Leptospirosis
§ Syphilis
§ Alpha-antitrypsin deficiency
§ Budd-Chiari
§ Wilson’s disease
§ Failure to excrete conjudated bilirubin (Dubin-Johnson and Rotor syndromes)
§ Right heart failure
§ Toxins- e.g. carbon tetrachloride, fungi
- Impaired hepatic excretion (cholestasis)
o Primarily biliary cirrhosis, primary sclerosing cholangitis, drugs, common bile duct
gallstones, pancreatic cancer, compression of the bile duct, e.g. lymph nodes at the porta
hepatis, cholangiocarcinoma, choledochol cyst, Caroli’s disease, biliary atresia, Mirrizzi’s
syndrome (obstructive jaundice from common bile duct compression by a gallstone
impacted in the cystic duct, often associated with cholangitis)
o As conjugated bilirubin is water soluble, it is excreted in the urine, making it dark
o Less conjugated bilirubin enters the gut and the faeces become pale
o When severe, it can be associated with an intractable pruritis with is best treated by relief of
the obstruction
Tests:
- Urine:
o Bilirubin is absent in pre-hepatic causes (=acholuris jaundice)
o In obstructive jaundice, urobilinogen is absent
- Hematology:
o FBC, clotting, film, reticulocyte count, Coombs test and haptoglobins for hemolysis
o Malaria parasites (e.g. if unconjugated bilirubin and fever)
o Paul Bunnell (EBV)
- Chemistry:
o U&E, LFT (bilirubin – unconjugated and conjugated), ALT, AST, alk phos, gamma GT, total
protein, albumin
§ If AST >1000, its probably viral hepatitis
o Paracetamol levels
- Microbiology:
o Blood and other cultures; leptospira and hepatitis A, B, C and serology
- Ultrasound:
o Are the bile ducts dilated >6mm (obstruction?)
o Are there gallstones, hepatitis metas or pancreatic mass
- ERCP
o If bile ducts are dilated and LFT not improving
- MRCP
o Or endoscopic ultrasound if conventional ultrasound shows gallstones but no definite
common bile duct stones
- Liver biopsy:
o If bile ducts are normal
- CT/MRI:
o If abdominal malignancy is suspected

Examples of drug induced jaundice:

- Hemolysis:
o Antimalarials (e.g. dapsone)
- Hepatitis:
o Paracetamol overdose
o Isoniazid, rifampicin, pyrazinamide
o Monoamine oxidase inhibitors
o Sodium valproate
o Halothane
o Statins
- Cholestasis:
o Flucloxacillin (may be weeks after treatment)
o Fusidic acid, co-amoxiclav, nitrofurantoin
o Steroids (anabolic, the Pill)
o Sulfonylureas
o Prochlorperazine
o Chlorpromazine
- Look for an eosinophilia ± DRESS ‘drug rash with eosinophilia and systemic symptoms (fever,
dyspnea)

Causes of jaundice in previously stable patients with cirrhosis:

- Sepsis (UTI, pneumonia, peritonitis)
- Malignancy (e.g. hepatocellular carcinoma)
- Alcohol, drugs
- GI bleeding
Signs of decompensation: ascites, dilated abdominal veins, encephalopathy, odema

PRIMARY BILIARY CIRRHOSIS:

- Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation
causing cholestasis which may lead to fibrosis, cirrhosis and portal hypertension
- Cause: unknown environmental triggers (>pollutants, non-pathogenic bacteria) + genetic
predisposition (e.g. IL12A locus) leadng to loss of immune tolterance to self-mitochondiral proteins
- Antimitochondrial antibodies (AMA) are hallmarks of PBC
- Prevalance: <4/100,000 female to male 9:1
- Risk increases if positive family history (seen in 1-6%); many UTIs, smoking, past pregnancy and
other autoimmune disease, increased use of nail polish/hair dye
- Typical age of presentation: around 50
The Patient:
- Often asymptomatic and diagnosed after finding increased alk phos on routine LFT
- Lethargy, sleepiness and pruritus may precede jaundice by years
- Signs: jaundice, skin pigmentation, xanthelasma, xanthomata, hepatosplenomegaly
- Complications: those of cirrhosis, osteoporosis is common
- Malabsorption of fat-soluble vitamins (A, D, E,K ) due to cholestasis and decreased bilirubin in the
gut lumen results in osteomalacia and coagulopathy; HCC – check AFP twice yearly)
Tests:
- Blood: increased alk phos, increase gamma GT and mildly increased AST and ALT
o Late disease: increased bilirubin, decreased albumin and increased prothrombin time
o 98% are AMA m2 subtype positive, e.g. in a titre of 1:40
o Other autoantibodies may occur in low titres
o Immunoglobulins are increased (esp: IGM), TESH and cholesterol increase or the same
- Ultrasound: excludes extra hepatic cholestasis
- Biopsy: not usually needed (unless drug-induced cholestasis or hepatic sarcoidosis, need excluding-
look for granulomas around the bile ducts and cirrhosis)
o Liver granuloma differential is sarcoidosis

KIDNEY

ACUTE KIDNEY INJURY:

Acute kidney injury (AKI), previously termed acute renal failure, describes a reduction in renal function
following an insult to the kidneys. In years gone by the kidneys were very much a neglected organ in acute
medicine - the recognition of decreasing renal function was often slow and action limited. Around 15% of
patients admitted to hospital develop AKI.

Whilst most patients with AKI recover their renal function there are many patients who will have long term
impaired kidney function due to AKI. As well as long-term morbidity, AKI may also result in acute
complications including death. Whilst exact figures are difficult to calculate NICE estimate that inpatient
mortality of AKI in the UK might typically be 25-30% or more.

What causes AKI?

Causes of AKI are traditionally divided into prerenal, intrinsic and postrenal causes

Prerenal

Think of what causes big problems in other major organs. In the heart a lack of blood (ischaemia) to the
myocardium causes a myocardial infarction. In a similar fashion 85% of strokes are causes be ischaemia to
the brain. The same goes for the kidneys. One of the major causes of AKI is ischaemia, or lack of blood flowing
to the kidneys.

Examples
• hypovolaemia secondary to diarrhoea/vomiting
• renal artery stenosis

Intrinsic

The second group of causes relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the
kidneys themselves. This may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.

Examples
Glomerulonephritis
Acute tubular necrosis (ATN)
Acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome

Postrenal

The third group relates to problems after the kidneys. This is where there is an obstruction to the urine
coming from the kidneys resulting in things 'backing-up' and affecting the normal renal function. An example
could be a unilateral ureteric stone or bilateral hydroneprosis secondary to acute urinary retention caused by
benign prostatic hyperplasia.

Examples
• kidney stone in ureter or bladder
• benign prostatic hyperplasia
external compression of the ureter

Who is at an increased risk of AKI?

One of the keys to reducing the incidence of AKI is identifying patient who are at increased risk. NICE support
this approach and have published guidelines suggesting which patients are at greater risk.

Risk factors for AKI include:

• chronic kidney disease
• other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
• history of acute kidney injury
• use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II
receptor antagonists [ARBs] and diuretics) within the past week
• use of iodinated contrast agents within the past week
• age 65 years or over
• oliguria (urine output less than 0.5 ml/kg/hour)
neurological or cognitive impairment or disability, which may mean limited access to fluids because of
reliance on a carer

Preventing AKI

By identifying patients at increased risk of AKI (see above) it may be possible to take steps to reduce the risk.
For example, patients who are at risk of AKI and who are undergoing an investigation requiring
contrast are usually given IV fluids to reduce the risk. Certain drugs such as ACE inhibitors and ARBs may
also be temporarily stopped.

What happens when kidneys stop working?

It's best to work backwards and think about what kidneys actually do. The kidneys are primarily responsible
for fluid balance and maintaining homeostasis. Therefore two of the key ways AKI may be detected are:
• a reduced urine output. This is termed oliguria and is defined as a urine output of less than 0.5
ml/kg/hour
• Fluid overload
• A rise in molecules that the kidney normal excretes/maintains a careful balance of. Examples
include potassium, urea and creatinine

Symptoms and signs

Many patients with early AKI may experience no symptoms. However, as renal failure progresses the
following may be seen:
• Reduced urine output
• Pulmonary and peripheral oedema
• Arrhythmias (secondary to changes in potassium and acid-base balance)
• Features of uraemia (for example, pericarditis or encephalopathy)

Detection

One of the most common blood tests performed on the wards is 'urea and electrolytes' or 'U&Es'. This returns
a number of markers, including
• Sodium
• Potassium
• Urea
• Creatinine

NICE recommend that we can use a variety of different criteria to make an official diagnosis of AKI. They state:
Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following
criteria:
• A rise in serum creatinine of 26 micromol/litre or greater within 48 hours
• A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7
days
• A fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults

Urinanalysis
• All patients with suspected AKI should have urinanalysis

Imaging
• If patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction
they should have a renal ultrasound within 24 hours of assessment.

MAP Equation and nuber needed for adequate renal perfusion:

- MAP= ((2xdiastolic)+systolic) divided by 3
- Renal filtration gradient: MAP- 2 x IAP (<7)
o Intraabdominal pressure rising (HTN) reduces arterial flow, increased IVC pressure
o Oliguria is present at IAP 15mmHg
o Anuria is present at 25 mmHg

Management

The management of AKI is largely supportive. This means patients require careful fluid balance to ensure
that the kidneys are properly perfused but not excessively to avoid fluid overload. It is also important to
review a patient's medication list to see what treatments may either be exacerbating their renal dysfunction
or may be dangerous as a consequence of renal dysfunction. The table below gives some examples of common
drugs:
Treatments which are not recommend include the routine use of loop diuretics (to artificially boost urine
output) and low-dose dopamine (in an attempt to increase renal perfusion). There is however a role for loop
diuretics in patients who experience significant fluid overload.

Raid Progressive Glomerulonephritis

Acute Tubular Necrosis

NEPHROTIC SYNDROME:

Triad of:
• 1. Proteinuria (> 3g/24hr) causing
• 2. Hypoalbuminaemia (< 30g/L) and
• 3. Oedema

Loss of antithrombin-III, proteins C and S and an associated rise in fibrinogen levels predispose to thrombosis.
Loss of thyroxine-binding globulin lowers the total, but not free, thyroxine levels.

Minimal change disease

- In children/young adults- Minimal change glomerulonephritis

o Nearly always presents as nephrotic syndrome, accounting for 75% of cases in children and
25% in adults
o The majority of cases are idiopathic and respond well to steroids

The majority of cases are idiopathic, but in around 10-20% a cause is found:
• Drugs: NSAIDs, rifampicin
• Hodgkin's lymphoma, thymoma
• Infectious mononucleosis

Pathophysiology
T-cell and cytokine mediated damage to the glomerular basement membrane → polyanion loss
The resultant reduction of electrostatic charge → increased glomerular permeability to serum
albumin

Features
• Nephrotic syndrome
• Normotension - hypertension is rare
• Highly selective proteinuria*
• Renal biopsy: electron microscopy shows fusion of podocytes

Management
• Majority of cases (80%) are steroid responsive
• Cyclophosphamide is the next step for steroid resistant cases

Prognosis is overall good, although relapse is common. Roughly:

 • 1/3 have just one episode
• 1/3 have infrequent relapses
• 1/3 have frequent relapses which stop before adulthood

*Only intermediate-sized proteins such as albumin and transferrin leak through the glomerulus

NEPHRITIS:

Typically presents with nephritic syndrome (haematuria, hypertension)

Rapidly progressive glomerulonephritis - aka crescentic glomerulonephritis

• rapid onset, often presenting as acute kidney injury
• causes include Goodpasture's, ANCA positive vasculitis

IgA nephropathy - aka Berger's disease, mesangioproliferative GN

typically young adult with haematuria following an URTI

presentation: proteinuria / nephrotic syndrome / chronic kidney disease

Rapidly progressive glomerulonephritis

Rapidly progressive glomerulonephritis is a term used to describe a rapid loss of renal function associated
with the formation of epithelial crescents in the majority of glomeruli.

Causes
• Goodpasture's syndrome
• Wegener's granulomatosis
• Others: SLE, microscopic polyarteritis

Features
Nephritic syndrome: haematuria with red cell casts, proteinuria, hypertension, oliguria
Features specific to underlying cause (e.g. haemoptysis with Goodpasture's, vasculitic rash or sinusitis
with Wegener's)
HEMOLYTIC UREMIC SYNDROME:
- Progressive failure linked with microangiopathic hemolytic anemia (intravascular hemolysis and red
cell fragmentation)
- Endothelial damage triggers thrombosis, platelet consumption and fibrin strand deposition, mainly
in the renal micovasculature
o The strands cause mechanical destruction of passing RBC’s and THROMBOCYTOPENIA AND
AKI RESULT
- Triad:
o Thrombocytopenia
o Non-Immune hemolytic anemia
o Acute renal failure
- Causes:
o 90% are from the E.Coli strain 0157
§ VTEC (spread from person to person or through food and water)
o Shigella dysenteriae (GI pathogens)
- Signs:
o Decreased UO
o Weakness, lethargy
o Bloody diarrhea
o Pallor, purpura
o Epistaxis
o Odema
- Ix and results:
o Blood Film:
§ Fragmented RBC- schistocytes
o Cultures:
§ Blood cultures negative
§ Stool culture positive- MC&S
o Renal:
§ Hematuria and proteinuria
§ Urea increased, smaller increase in creatinine
o Thrombocytopenia and Hb with normal PT and aPTT

Goodpasture’s Syndrome:
- P/C:
o Pulmonary then renal syndrome
- Ix and Findings:
o CXR: Infiltrates due to pulmonary hemorrhage often in lower zones
o Kidney biopsy: cresentic glomerulonephritis
- Tx:
o Supportive management of shock
o ACE, ARB and dialysis for CKD
o Plasmapheresis corticosteroid (vigorous immunosuppression)
-

Diabetes Insipidus:
- Diabetes insipidus is characterised by a high plasma osmolality and a low urine osmolality

Diabetes insipidus (DI) is characterized by impaired water resorption by the kidney as a result of lack of
ADH secretion by the posterior pituitary (cranial DI) or reduced sensitivity of the kidneys to the action
of ADH (nephrogenic DI). Biochemistry reveals a high/borderline high plasma osmolarity (patient always
feels thirsty and tries to replace the lost fluid to lower plasma osmolarity) with an inappropriately low
urine osmolarity (the patient complains of production of large amounts of very dilute urine as a result of
reduced water resorption in the kidney). Note the wide normal reference range of urine osmolality which is
dependant on the state of hydration. A urine osmolality of >700 mOsm/kg excludes diabetes insipidus.

The water deprivation test is used to confirm diagnosis. In normal physiology an increase in urine
osmolarity (ADH working normally to maintain homoeostasis) will occur in response to water deprivation.
This acts to maintain a normal plasma osmolarity. However, in cranial DI patient there is a rise in plasma
osmolarity with production of low osmolarity urine until exogenous ADH (vasopressin) is given. In
nephrogenic DI patients, the same plasma and urine osmolarity changes occur but there is no
response to the exogenous vasopressin.

Diabetes insipidus (DI) is a condition characterised by either a deficiency of antidiuretic hormone, ADH,
(cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).

Causes of cranial DI
• Idiopathic
• Post head injury
• Pituitary surgery
• craniopharyngiomas
• histiocytosis X
• DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and
Deafness (also known as Wolfram's syndrome)

Causes of nephrogenic DI
Genetic: the more common form affects the vasopression (ADH) receptor, the less common form results
from a mutation in the gene that encodes the aquaporin 2 channel
Electrolytes: hypercalcaemia, hypokalaemia
Drugs: demeclocycline, lithium
Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis

Features
• Polyuria
• Polydipsia

Investigation
• High plasma osmolality, low urine osmolality.
• A urine osmolality of >700 mOsm/kg excludes diabetes insipidus.
• Water deprivation test

HEART EMERGENCIES:
SEVERE PULMONARY ODEMA:

Causes:
- Cardiovascular, usually left ventricular failure (post-MI or ischemic heart disease)
o Also valvular disease, arrhythmias, and malignant hypertension
- ARDS from any cause
o E.g. trauma, drugs, malaria
o Then look for predisposing factors e.g. trauma, post-op,sepsis
o Is aspirin overdose or glue-sniffing likely?
- Fluid overload
- Neurogenic
o E.g. head injury

Differential diagnosis:
- Asthma/COPD, pneumonia and pulmonary odema are often hard to distinguish, especially in the
elderly, where they may co-exist
- If the patient is extremely unwell and you are not sure, consider treating all three (e.g. with
salbutamol nebulizer, furosemide IV, diamorphine, amoxicillin)

Symptoms:
- Dyspnea, orthopnea (e.g. paroxysmal), pink frothy sputum
- NB: note drugs recently given and other illnesses (recent MI/COPD or pneumonia)

Signs:
 - Distressed, pale, sweaty, increased pulse, tachypnea, pink frothy sputum, pulsus alternanas, JVP
increased, fine lung crackles, triple/gallop, wheeze (cardiac asthma), Usually sitting up and leaning
forward
- Quickly examine for possible causes

Investigations:
- CXR
o Cardiomegaly, signs of pulmonary odema, look for shadowing (usually bilateral), small
effusions at costophrenic angles, fluid in the lung fissures and Kerley B lines (linear
opacities)
- ECG
o Signs of MI, dysrhythmias
- U&E, troponin, ABG
- Consider echo
- Plasma BNP may be helpful if diagnosis in question (high negative predictive value)

Management of Acute Heart Failure:

- Sit the patient upright
- Oxygen: 100% if no preexisting lung disease
- IV access and monitor ECG
o Treat any arrhythmias, e.g. AF
- Investigations whilst continuing treatment
- Diamorphine 1.25-5mg IV slowly
o Caution in liver failure and COPD
- Furosemide 40-80mg IV slowly
o Larger doses required in renal failure
- GTN spray 2 pulls SL or 2x0.3mg tablets LS
o Don’t give if systolic blood pressure <90mmHg
- Necessary investigations, examination and history
- If systolic BP>100mmHg, start a nitrate infusion, e.g. isosorbide dinitrate 2-10mg/h IVI; keep systoliv
B >90mmHg
- If the patient is worsening-
o Further dose of furosemide 40-80mg
o Consider CPAP- improves ventilation by recruiting more alveoli, driving fluid out of alveolar
spaces and into vasculature (get help before initiating!)
o Increase nitrate infusion if able to do so without dropping systoliv BP <100
o If systolic BP<100mmHg, treat as cardiogenic shock

Management:
- Begin treatment before investigations
- Monitoring progress:
o Pulse, BP, cyanosis, respiratory rate, JVP, urine output, ABG
- Once stable and improving:
o Daily weights, aim reduction of 0.5kg/day, check obs at least QDS
o Repeat CXR
o Change to oral furosemide or bumetanide
o If on large dose of loop diuretic, consider the addition of thiazide (e.g. bendroflumethiazide
or metolazone 2.5mg daily PO)
o ACE-I if LVEF <40%
§ If ACE-I contraindicated, consider hydralazine and nitrate (may also be more
effective in African-Caribbeans)

CARDIOGENIC SHOCK:
- This has a high mortality and is very difficult to treat
- Ask a senior physician to help
- Cardiogenic shock is a state of inadequate tissue perfusion primarily due to cardiac dysfunction
- It may occur suddenly or after progressively worsening heart failure

Causes:
- Myocardial infarction
- Arrhythmias
- Pulmonary embolus
- Tension pneumothorax
- Cardiac tamponade
 - Myocarditis: myocardial depression (drugs, hypoxia, acidosis, sepsis)
- Valve destruction (endocarditis)
- Aortic dissection

Management:
- if the cause is myocardial infarction, prompt revascularization (acute angioplasty or fibrinolysis) is
vital
- Manage in Coronary Care Unit or ICU
- Investigation and treatment may need to be done concurrently
- See for details of management
- Investigations:
o ECG, U&E, troponins/cardiac enzymes, ABG, CXR, echocardiogram
o If indicated CT thorax (aortic dissection/PE) or V/Q scan
- Monitor:
o CVP, BP, ABG, ECG, urine output
o Do a 12-lead ECG every hour until the diagnosis is made
o Consider a CVP line and an arterial line to monitor pressure, if these are in situ consider
using PICCO, LIDCO or other measures of cardiac output and volume status
o Catherterize for accurate urine output

Cardiac Tamponade:
- Essence:
o Pericardial fluid collects è intrapericardial pressure risesèheart cannot fillèpumping
stops
- Causes:
o Trauma, lung/breast cancer, pericarditis, myocardial infarct, bacteria (e.g. TB),
o Rare: increased urea, radiation, mycodema, dissecting aorta, SLE
o Also coronary dissection (secondary to PCI) and/or ruptured ventricle
- Signs
o Falling BP, a rising JVP, and muffled heart sounds (Beck’s triad)
o JVP increased on inspiration (Kussmaul’s sign), pulsus paradoxus (pulse faces on inspiration)
o Echocardiography may be diagnostic
o CXR: globular heart, left heart border convex or straight, right cardiophrenic angle <90
degrees, ECG: electrical alternans
- Prompt pericardiocentesis
- While awaiting this, give 02, monitor ECG, and set up IVI

Management of Cardiogenic Shock

o This may be very difficult
o Oxygen: titrate to maintain arterial saturations of 94-98% (88-92% if COPD)
o Diamorphne 1.25-5mg IV for pain and anxiety
o Investigations and close monitoring
o Correct arrhythmias, U&E abnormalities or acid base disturbances
o Optimize filling pressure with clinical assessment of pulse, BP, JVP/CVP (if in ICU consider
using PICCO, LIDCO, transesophageal Doppler or Swan-Gantz catheter to estimate cardiac
output and fluid balance)
§ Underfilled?
• Give plasma expander 100mL every 15 min IV
• Aim MAP 70mmHg, CVP 8.10mmHg
§ Well/overfilled?
• Inotropic support, e.g. dobutamine 2.5-10ug/kg/min IVI
• Aim MAP 70mmHg
o Look for and treat any reversible cause
MI or PE- consider thrombolysis’surgery for acute

Shock and Sepsis:

Sepsis:
- Disregulated immune response to a host infection
- +/- organ dysfunction

SIRS Criteria:
- Temperature
o Over 38
 o Under 36- being hypothermic is worse than increased temperature
- Respiratory Rate
o >22-24
o Hypercapnia
- Heart Rate
o Tachy
- White Cell
o Less than 4 or greater than 12
o Neutrophils greater than 80%

Sepsis:
- SIRS plus infection

Q-SOFA:
- SOFA score was an ICU guideline originally
- 3 can predict the need for ICU
- 2/3 Q-SOFA would be more likely to need ICU
o Confusion
o Hypotension
o Tachypnea

Sources of infection:
1. Most common source of infection in all age groups is Urinary tract infections
a. Confusion in elderly patients
b. Flank pain, vomiting, spiking temperatures- pyelonephritis (systemically unwell)
c. STI in young age group with urinary tract infections
i. Young men tend not to get UTIs unless there is a structural abnormality or a STI
- Long lines, indwelling devices, can also be a source
o Peripheral lines are rarely a source of infection
o Can cause local cellulitis and thrombolitis but less likely to cause a systemic source
o Clear entry site does not always mean it is not a source of infection
2. Respiratory tract
a. Dyspnea, productive cough, pain
3. Intraabdominal source
a. Pain, guarding, fever, rigors
b. Obstructive jaundice in the background of infection
i. Cholecystitis
4. CNS- Meningitis
a. Potentially and so quickly lethal- a lot of people may be treated
b. Non-blanching rash- meningicoccus gives you this but meninigitis does not
5. Skin, soft tissue infection
a. Cellulitis, red, tenderness to touch
b. Necrotising fasciitis
i. Rapidly spreading
ii. Bullae, crepitus (gas or air in the soft tissues)
iii. Disproportionate pain
iv. Fernier’s gangrene- necrotizing fasciitis affecting the perineum, genital area
6. Heart – infective endocarditis
a. New murmur
b. Prosthetic valves
c. IVDU

Treatment:
- Antimicrobial coverage:
o Indwelling devices:
§ Gram positive coverage- MRSA, MSSA
§ Flucloxacillin, Vancomycin, Daphthomycin,
o Cellulitis:
§ Strep pyogenes
§ Benzyl-penicillin, flucloxacillin
o Necrotizing fasciitis
§ Often polymicrobial
§ Anerobes, strep, gram negative, clostridium perfinges etc
§ Metronidazole, gentamycin, vancomycin, tazozem
§ Broad coverage
 o Urinary tract infection:
§ E. coli – gram negative bacteria
§ Staph. saprofyticus
§ Treatment: ciprofloxacin, ampicillin, co-amoxiclav, metronidazole- anaerobes
§ Trimethoprin is more associated with community, non- acutely unwell patients
§ Aminoglycosides are often used in combination therapy- gentamycin etc
o Respiratory tract infection:
§ Strep pneumonae, staph, klebsiella, h. influenza, pseudomonas
(immunocompromised, Hospital acquired, CF)
§ Treatment: tazozem for pseudomonas (world wide shortage, however), amoxicillin,
co-amoxiclav, clarithromycin if the bug does not have a cell wall for the penicillin to
work on
o Meningitis
§ Third generation cephalosporins, vancomycin
o Infective endocarditis:
§ Staph aureus, prosthetic valve- strep, staph epidermidis, HACEK organisms
§ IVDU: can get everything causing it, fungal etc

Supportive therapy:
- Antimicrobials
- Fluid therapy
o Beyond 2/2 and a half litres of fluid you should think of something else
§ Boluses of crystalloids
o Fluid challenge—if they do not respond you should be doing vasopressors
- Vasopressors
o Noradrenaline, adrenaline

Shock 1:

MAP = CO xSVR
- Mean arterial pressure is equal to the cardiac output multiplied by systemic vascular resistance
CO = Heart Rate v Stroke Volume
- Stroke Volume is Preload x Contractility
Body wants to maintain MAP such that, if the CO falls, it will compensate by increasing SVR
- And Vice Versa

Classic Models of Shock:

- Distributive- SVR
o Tone or how constricted the blood vessels are
o Diastole
- Cardiogenic- CO
o Think of CO as systole
- Hypovolemic- CO
- Obstructive – CO

Cardiogenic shock:
- Quintessential blood pressure is 120/80
- If someone has increased systemic vascular resistance but no change in the CO, then if they increased
SVR the diastolic tone and pressure will go up
- As this person begins to go into cardiogenic shock, then the pulse pressure becomes narrow and they
begin to lose the blood pressure
o Narrow pulse pressure is shock from cardiac output ** because the diastolic tone is
maintained through SVR but the CO falls and so does systole = e.g. 110/100
- SVR means something to peripheral dilation as well
o When a person goes into shock with a narrow pulse pressure, the vasoconstriction trying to
maintain the diastolic tone, there will be no blood flow to the extremities
o Narrow pulse pressure and a cutting off a blood vessels and thus clinically you will see cold
extremities
- Fall in CO
o HR: (cardiogenic)
§ Too fast or too slow
o Preload
§ Can be volume depleted (hypovolemic)
 • Diarrhea, diuresis, dehydration, hemorrhage
§ Obstructive: Conditions that don’t allow enough volume to get into the right side
ventricle- impair venous return
• Pericardial tamponade
• Tension pneumothorax
§ Obstructive: Left ventricle impaired filling
• Pulmonary HTN
• Pulmonary embolism
o Contractility (Cardiogenic)
§ CHF
§ MI
§ Myocardial contusion (severe trauma, not medicine)

Distributive Shock- Fall in SVR

- Pulse pressure begins to widen as the diastolic pressure falls
- Blood pressure will begin to fall ultimately
- Loss of systemic vascular resistance will show a wide pulse pressure and peripheral vasodilation
o Blood flow goes to the extremities when it shouldn’t, extremities will feel warm
o This is the shins and their forearms
- Reduced SVR
o Big differential here is Sepsis
o Can be anaphylaxis
o Spinal trauma- transecting the sympathetic
o Anaethesia
o Addison’s disease

Obvious overt shock:

- Systolic blood pressure less than 90
- MAP of less than 65
Occult shock:
- People who are not in frank obvious shock but you should consider taking to the unit even if the
numbers don’t say so
- Uncontrolled blood pressure in the outpatient department and on one instance they have a normal
BP- BP is suddenly lower than it should be
Shock index:
- HR > Systolic Blood Pressure

Vasopressor Activity:

MAP= CO X SVR

4 Different Categories of Vasopressors:

- Pure vasoconstrictors – causes of systemic vascular resistance other than sepsis
o Purely SVR
o Phenylephrine
o Vasopressin
o Epinephrine
- Inotropes (inoconstrictors)- Sepsis
o Contractility and SVR
o Dopamine
§ 5-10mg/kg – Inotropic (beta)
§ 10-20mg/kg=Constrictor (alpha)- mostly a vasoconstrictor compared to levophed
o Levophed- more of an inotrope and less of a vasoconstrictor
§ If you have to pick a vasopressor, pick levophed
• Safer in septic shock
- Inodilator- ideal for CHF – given in issue with contractility
o Lots of contractility
o Drop systemic vascular resistance
o Dobutamine
o Milrinone
- Pure vasodilator – for blood pressure to be brought down in hypertensive events
o CCB
o Betablocker
o Nitrites
If the problem is with preload or volume depleted:
- IV fluids
- Plasma

Endocrine Emergencies:

DIABETIC KETOACIDOSIS:
- Mechanism:
o Normally the body metabolizes carbohydrates, leading to efficient energy production
o Ketoacidosis is an alternative metabolic pathway, normally used in starvation states, it is far
less efficient and produces acetone as a byproduct (hence the characteristic fruity breath of
patients in ketosis)
o In acute diabetic ketoacidosis, there is excessive glucose, but because of the lack of insulin,
this cannot be taken up into cells to be metabolized so pushing the body into a starvation-like
state where ketoacidosis is the only mechanism of energy production
o The combination of severe acidosis and hyperclycemia can be deadly, so early recognition
and treatment is important
- Typical picture:
o Gradual drowsiness, vomiting and dehydration in type 1 diabetic (very rarely type 2)
§ Do glucose in all those with unexplained vomiting, abdo pain, polyuria, polydipsia,
lethargy, anorexia, ketotic breath, dehydration, coma or deep breathing (sighing
‘Kussmaul’ hyperventilation)
o Triggers: infection, e.g. UTI, surgery, MI, pancreatitis, chemotherapy, antipsychotics, wrong
insulin dose/non-compliance
- Diagnosis:
o Acidemia (blood pH <7.3)
o Hyperglycemi
o Ketonemia
- Tests:
o ECG
o CXR
- Urine:
o Dipstick and MSU
- Blood:
o Capillary and lab glucose
o Ketones
o U&E
o HCO3-
o Amylase
o Osmolality
o ABG/VBG
o FBC
o Blood culture
- Plasma Osmolarity= 2[Na+]+[urea]+[glucose] mmol/L
- Severe DKA:
o If one or more of the following features is present on admission, consider transfer to
HDU/ICU for monitoring and central venous access
§ Blood ketones >6mmol/L
§ Venous bicarbonate <5mmol/L
§ Venous/arterial pH <7.1
§ K <3.5 mmol/L on admission
§ GCS <12
§ O2 sats <92% on air (assuming no respiratory disease)
§ Systolic BP <60mmHg
§ Pulse >100 or <60 bpm
§ Ansion gap above 16
- Pitfalls in diabetic ketoacidosis:
o Plasma glucose: is usually high, but not always, especially if insulin is continued
o High WCC: may be seen in the absence of infection
o Infection: often there is no fever
§ Do MSU, blood cultures and CXR, start broach spectrum antibiotics (coamoxiclav),
early if infection is suspected
o Creatinine: some assays for creatinine cross-react with ketone bodies, so plasma creatiine
may not refect true renal function
 o Hyponatremia: is common, due to osmolar compensation for the hyperglycemia
§ Increased or normal sodium indicates severe water loss
§ As treatment commences Na+ rises aas water enters cells
§ Na+ is also low due to an artifact, corrected plasma [Na+]=Na+ + 2.4 (glucose -
5.5)/5.5
o Ketonuria:
§ Does not equate with ketoacidosis
§ Anyone may have up to ++ketonuria after an overnight fast
§ Not all ketones are due to diabetes- consider alcohol if glucose is normal
§ Always check venous blood ketones
o Recurrent ketoacidosis: blood glucose may return to normal long before ketones are
removed from the blood, and a rapid reduction in the amount of insulin administered may
lead to lack of clearance and return to DKA
§ This may be avoided by maintaining a constant rate of insulin, e.g. 4-5u/h IVI and
coinfusing glucose 10-20% to keep plasma glucose at 6-10mmol/L- the extended
insulin regimen
o Acidosis:
§ Without gross elevation of glucose, but consider overdose (aspirin) and lactic
acidosis
o Serum amylase: Is often raised (up to 10x) and non-specific abdominal pain is common,
even in the absence of pancreatitis
- Complications:
o Cerebral odema – get help if sudden CNS devline
o Aspiration pneumonia
o Hypokalemia
o Hypomagnesemia
o Ypophosphatemia
o Thromboembolism
OTHER DIABETIC EMERGENCIES:

Hypoglycemic coma:
- Usually rapid onset; may be preceded by odd behavior (e.g. aggression), sweating, increased pulses,
seizures
- Management:
o Give 20-30g glucose IV e.g. 200-300mL of 10% dextrose
o This is preferable to 50-100 mL 50% glucose which harms veins
o Expect prompt recovery
o Glucagon 1mg IV/IM is nearly as rapid as dextrose but will not work in drunk patients
o Dextrose IVI may be needed for severe prolonged hypoglycemia
o Once conscious, give sugary drinks and a meal
- Whipple’s triad:
o Hypoglycemic symptoms
o Serum glucose <4mmol/L
o Reversal of symptoms on glucose intake
- Symptoms:
o 3-4mmol/L: minor cognitive disturbances
o Neurogenic (adrenergic/sympathoadrenal activation)
§ Sweating
§ Tachycardia
§ Anxiety
o Neuroglycopaenic:
§ Weakness
§ Tiredness
 § Dizziness
§ Coma leading to death
- Risks:
o Medication changes/overdose/ethanol
o Infection
o Diet changes
o Metabolic changes over time
o Ailmentary problems
o Fasting
o Insulinoma
o Hepative disease, bost bariatric surgery
- Treat:
o Conscious:
§ 15g oral glucose/ check blood glucose in 15 min (if <4mmol/L, repeat)
§ Once BG is >4mmol/L give long acting carbohydrate
§ Treat but continue insulin with next meal
o Unconscious/Drowsy
§ 1mg glucagon IM
§ If does not correct within 10-15 min, give 25mL of 50% glucose IV stat
§ In alcoholics give pabrinex with glucose (Query Wernickes)

Hyperglycemic hyperosmolar non-ketotic coma (HONK):

- Typically those with type 2 diabetes are at risk for this
- This history is longer (e.g. 1 week), with marked dehydration and glucose >35mmol/L
- Acidosis is absent as there is no switch to ketone metabolism
- Osmolality is >340 mosmol/kg
- Occlusive events are a danger (e.g. focal CNS signs, chorea (a neurological disorder characterized by
jerky involuntary movements affecting especially the shoulders, hips, and face), DIC, leg
ischemia/rhabdomyolysis), DVT- give LMWH prophylaxis to all unless contraindication
o Rehydrate slowly with 0.9% saline IVI over 48h- typical deficits are 110-220mL/kg, i.e. 8-
15L for a 70kg adult
o Replace K+ when urine starts to flow
o Only use insulin if blood glucose not falling by 5mmol/L/h with rehydration or if ketonemia-
start slowly 0.05 u/kg/h
o Keep blood glucose at least 10-15 mmol/L for first 24 hours to avoid cerebral odema
o Look for the cause, e.g. MI, drugs or bowel infarct
- P/C:
o Glucose>40mmol/L, without significant acidosis and no ketones
o Serum osmolality 2 (Na+K)+ Serum Glucose+ Urea (>340mosol/kg)
o Longer history (1 week + marked dehydration)
o Predicipated by sugary drink/diuretics
o MARKED DEHYDRATION
- Diagnosis:
o Hyperglycemia (>30mmol/L)
o Total osmolality (>340mOsm/Kg)
o Serum bicarb >15mmol/L
o Urinary ketones <1+
- Treatment:
o Gradual normalization! Blood glucose at 10-15 mmol/L for the first 24 hours to avoid
cerebral odema
o O2 + CVP monitoring to guide fluid resus
§ Rehydrate slowly with 0.9% saline IVI over 48 hours (typical deficit 110-220ml/Kg-
ie. 8-15 L)
o NG tube if decreased conscounsess
o Urinary catheter (Replace K+ when urine starts to flow
o Prophylactic heparin if no contraindications- risk of DVT
o Look for the cause: MI, Drugs, bowel infarct
- What’s the risk in treatment?
o Rapid reduction in blood glucose can lead to cerebral odema
o Occlusive events are a danger- focal CNS, chorwea, DIC, leg ischemia, rhabdomyolysis

Lactic Acidosis:
- Rare but serious complication of DM with metformin use or septicemia
- Blood lactate: >5mmol.K
- Treat sepsis vigorously, maintain blood pressure and hence tissue perfusion
 - Stop metformin

Myxodema Coma:
- the ultimate hypothyroid state before death
- Signs and symptoms:
o Looks hypothyroid often >65 yrars, hypothermia, hyporeflexia, decreased glucose,
bradycardia, coma, seizures
o May have had radioiodine, thyroidectomy or pituitary surgery (signs of hypothyroidism)
o Patient may have seemed psychotic (myxedema madness) just before the coma (e.g.
precipitated by infection, MI, stroke or trauma)
- Examination:
o Goitre; cyanosis; BP decreased (cardiogenic), heart failyre, signs of precipitants
- Treatment: preferable ICU
o Blood for: T3, T4, TSH, DBC, U&E (Na+ often decreased), cultures, cortisol, glucose
o ABG for Pa02
§ High flow 02 if cyanosed
§ Ventilation may be needed
o Correct any hypoglycemia
o Give T3 (liothyronine) 5-20ug/12h IV slowly
§ Be cautious: you may precipitate manifestations of ischemia heart disease
§ Alternative regimens involve levothyroxine
o Give hydrocortisone 100mg/8h IV-vital if pituitary hypothyroidism is suspected (i.e. no
goitre, no previous radioidone and no previous thyroid surgery)
o If infection suspected, give antibiotic e.g. cefuroxime 1.5g/8h IVI
o Caution with fluid, rehydrate as needed but watch for cardiac dysfunction, BP may not
respond to fluid and inotropes may be needed
o Active warming (blankets and fluids) may be needed for hypothermia
§ Beware complications (hypoglycemia, pancreatitis
- Further management:
o T3 5-20 ug4-12 hours IV until sustained improvedment (around 2-3 days) then
levothyroxine 50 ug/24h PO
o Hydrocortisone + IV fluids as needed (hyponatremia is dilutional)

Hyperthyroid crisis (thyrotoxic storm):

- Signs and symptoms:
o Female: male 4:1
o Severe hyperthyroidism: increased temperature, agitation, confusion, coma, tachycardia, AF,
D&V, goitre, thyroid bruit, acute abdomen (exclude surgical causes), heart failure,
cardiovascular collapse
- Precipitants:
o Recent thyroid surgery or radioiodine, infection, MI, trauma
- Diagnosis:
o Do not wait for test results if urgent treatment is needed
o Do TSH, free T4 and free T3
o Confirm with technetium uptake if possible
- Treatment:
o Counteract peripheral effects of thyroid hormones
o Inhibit thyroid hormone synthesis
o Treat systemic complications
- If you are not making headway in 24 h consider thyroidectomy if you can find a good anesthetist and
surgeon
Rheumatology:
PFTs