SHORT CASES
With FAQs
dr.nyeinkohein@gmail.com
Nyein Ko Hein
Contents
Topics
Pages
1. CVS ………………..…………………………………………... 2
2. Respiration ………….………………………………………….23
3. Abdomen ……………….……………………………………… 30
4. Neuro ……………..……………………………………………. 39
Paraparesis ………………………………………………. 41
Hemiparesis ……………………………………………… 42
Cerebellar ………………………………………………… 48
Facial palsy ………………………………………………. 51
Ptosis ……………………………………………………... 55
Myasthemia gravis ………………………………………. 58
Parkinsonism …………………………………………….. 65
Wrist drop ………………………………………………… 67
Foot drop …………………………………………………. 72
5. Miscellaneous ..……………………………………………….. 78
Fundoscopy ……………………………………………… 78
Thyroid …………………………………………………… 87
SS …………………………………………………………. 89
RA hands ………………………………………………… 91
Ankylosing spondylitis …………………………………... 96
Psoriasis ………………………………………………….. 98
Vitiligo …………………………………………………….. 100
Acromegaly ………………………………………………. 102
Neurofibromatosis ……………………………………….. 103
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CVS Short Cases
MS, MR, AS, AR, ASD, VSD, TR, Prosthetic Valves
1. General (Dyspnoea, Cyanosis, Fever, Eyes, Face, Mouth, Neck, Legs + Pulses, Hands)
2. Pulse (Radial +/- Carotid) + Peripheral (Character, Equality, Delay)
If Collapsing Pulse (+), Find out Peripheral Signs of AR
3. BP +/- Both sides
4. JVP (Differentiate) +/- HJR (Time with Carotid)
5. Precordium Inspection (Apex, Pulses, Scars)
6. Palpation (Apex, Character, Thrills, Palpable P2, Parasternal Heaving)
If TR suspected, Palpate Pulsatile Liver
7. Auscustate HR + Position, Resp (M (S1), T, A (S2), P (S2), LSE, +/- S3, Murmurs, Radiations
If Scar (+), Listen with bear ears first
8. Aetiology, Complication (HF, IE)
Presentation
1. MS
On G/E, Patient is not dyspnoeic and orthopnoeic. Malar flush is present. PR is 80 bpm,
Irregular, Low volume and Normal character. BP is 120/80 mmHg. JVP is elevated.
O/E of Precordium, (Left lateral thoracotomy scar is present). Apex beat is at Left 5th ICS
within MCL and Tapping in character. There is Left parasternal heaving present.
On Auscultation at Mitral area, S1 is loud with variable intensity. S2 is normal. There is
opening snap followed by Rumbling MDM, Grading 3/6, best heard at Left lateral position at
the end of expiration by using Bell of the stethoscope without Radiation. At Pulmonary area,
S1 is normal, there is loud P2. At AA and TA, S1 & S2 are normal with no added sounds.
No basal crepts and No pedal oedema. No peripheral stigmata of IE.
Dx: Mitral Stenosis most probably due to Rheumatic in origin complicated by Atrial Fibrillation
and Pulmonary Hypertension without features of HF and IE.
2. MR
On G/E, Patient is not dyspnoeic and orhtopnoeic. PR is 80 bpm, Regular, Normal volume
and character. BP is 120/80 mmHg. JVP is not elevated.
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O/E of Precordium, No scar. Apex beat is displaced to Left 6 th ICS outside the MCL and
Heaving in character. There is no LPS Heaving and thrill.
On Auscultation at MA, S1 is soft and S2 is normal. There is PSM, Grading 3/6, loudest in
Expiration and Radiates to the axilla. S1 & S2 are normal with no added sounds at TA, AA,
PA.
No basal crepts and No pedal oedema. No peripheral stigmata of IE.
Dx: Mitral Regurgitation most probably due to Rheumatic in origin without Features of HF, IE,
3. MS + MR
Dx: Mixed Mitral Valvular Heart Disese, MS and MR with features of dominant MR, most
probably due to Rheumatic in origin, Complicated by AF and Pulmonary Hypertension without
Features of HF, IE.
4. Prosthetic Mitral Valve
On G/E, Patient is not dyspnoeic and orthopnoeic. PR is 80 bpm, Regular, Normal volume
and character. BP is 120/80 mmHg. JVP is not elevated.
O/E of Precordium, There is Midline sternotomy scar. Apex beat is displaced to Left 6 th ICS
outside the MCL and Heaving in character. There is no LPS Heaving and thrill.
A prosthetic click can be heard with unaided ear which coincides with the S1.
On Auscultation at MA, there is prosthetic click at S1 and S2 is normal. There is PSM,
Grading 3/6, loudest in Expiration and Radiates to the axilla. S1 & S2 are normal with no
added sounds at TA, AA, PA.
No basal crepts and No pedal oedema. No peripheral stigmata of IE. No anaemia is noted.
Dx: Mitral Valve Replacement underlying Mitral Regurgitation most probably due to
Rheumatic in origin without Features of HF, IE. Prosthetic valve appears to be functioning
well.
5. AS
On G/E, Patient is not dyspnoeic and orthopnoeic. PR 80 bpm, regular. Low volume and
Slow-rising in character. BP is 120/100 mmHg (Narrow pulse pressure). JVP in not elevated.
O/E of Precordium, Apex beat is at Left 6 th ICS outside the MCL, Heaving in character
associated with Systolic thrills at AA. There is no LPS heaving.
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On Auscultation of AA, S1 is normal, S2 is soft with soft aortic component. There is Harsh
ESM best heard at AA during Expiration and radiates to the carotids. Normal S1 and S2 with
no added sounds at MA, TA, PA.
No basal crepts and No pedal oedema. No peripheral stigmata of IE.
Dx: Aortic Stenosis most probably due to Rheumatic in origin without features of HF, IE.
6. AR
On G/E, Patient is not dyspnoeic and orthopnoeic. PR is 80 bpm, regular. Large volume with
Collapsing character associated with Dancing Brachialis and Carotids (Corrigan’s sign). BP
120/50 mmHg, Wide pulse pressure. JVP is not elevated.
O/E of Precordium, There is no scar. Apex beat is at Left 6 ICS outside the MCL with Heaving
in character. There is no thrills and no LPS heaving.
On Auscultation at LLSE, EDM, Grading 3/6, is present best heard with leaning forward
position during Expiration without Radiation. Normal S1 and S1 with no added sounds are
heard at MA, TA, PA, AA.
Other Peripheral signs of AR, Quinke’s sign, De Musset’s sign, Muller’s sign, Douziez signs
are not noted.
No basal crepts and No pedal oedema. No peripheral stigmata of IE.
Dx: Aortic Regurgitation most probably due to Rheumatic in origin (Bicuspid Aortic valve,
Syphilis, AS, Takayasu) without features of HF, IE.
7. Prosthetic Aortic Valve
On G/E, Patient is not dyspnoeic and orthopnoeic. PR is 80 bpm, regular rhythm. Regular
volume and character. BP is 120/80 mmHg. JVP is not elevated.
On examination of Precordium, There is a midline sternotomy scar. A prosthetic click can be
heard with unaided ear.
Apex beat is at Left 5th ICS within MCL normal in character. There is no thrills and no LPS
heaving.
On Auscultation at AA, S1 is normal followed by ESM and Prosthetic click at S2.
Normal S1 and S2 with no added sound are heard at MA, TA, PA.
No basal crepts and No peripheral stigmata of IE.
Dx: Aortic Valve Replacement with Prosthetic valve most probably due to Rheumatic in origin
without features of HF, IE. Prosthetic valve appears to be functioning well.
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8. VSD
On G/E, Patient is not dyspnoeic, orthopnoeic and cyanotic. There is no clubbing. PR is 80
bpm, regular, normal volume and character. BP is 120/80 mmHg. JVP is not elevated.
On examination of Precordium, there is no scar. Apex beat is at Left 5th ICS within the MCL,
normal in character. There is LPS heaving and thrill.
On Auscultation, S1 is mixed with a loud (harsh) PSM throughout the precordium, loudest at
LLSE, grading 4/6 without radiation. S2 is normal. S1 and S2 are normal with no added
sounds at MA, TA, AA, PA.
No basal crepts and No peripheral stigmata of IE.
Dx: VSD with Left to Right shunt without features of HF, IE. Absence of clinical signs of
Pulmonary Hypertension and LV enlargement suggesting Haemodynamically insignificant
shunt.
9. ASD
On G/E, Patient is not dyspnoeic, orthopnoeic and cyanotic. No clubbing. PR is 80 bpm,
regular. Volume and character is normal. BP is 120/80 mmHg. JVP is not elevated.
On examination of Precordium, there is no scar. Apex beat is at Left 5th ICS within MCL.
There is no LPS heaving. Systolic thrill is present at upper Pulmonary area.
On Auscultation at PA, S1 is mixed with Ejection click and ESM, Grading 4/6, without
radiation. There is fixed wide splitting of S2. S1 is normal and fixed wide splitting of S2 at MA,
TA, AA.
No basal crepts and No peripheral stigmata of IE.
Dx: ASD with Left to Right shunt without features of HF and IE. Absence of clinical signs of
pulmonary hypertension suggesting a Haemodynamically insignificant shunt.
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Frequently Asked Questions (Most Answers from Gautam Mehta OST)
Mitral Stenosis
MDM
1. MS
2. Left Atrial Myxomas
3. LA Thrombus
4. Severe MR (Increased forward flow across mitral valve)
5. TS
Causes
1. Rheumatic Fever
2. Congenital MS
3. Rheumatoid Arthritis
4. SLE
5. Carcinoid $
Severity of MS
Clinically
1. Early opening snap
2. Increasing length of murmur
3. Signs of pulmonary hypertension
4. Signs of pulmonary congestion
5. Graham-Steell murmur (Functional PR)
6. Low pulse pressure
Echo
Normal mitral valve orifice 4-6 cm2
Symptomatic
<2
Mild
>1.5
Moderate
1-1.5
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Severe
<1
Complications
1. LA enlargement
2. AF
3. LA thrombus formation
4. Pulmonary hypertension
5. Pulmonary oedema
6. Right heart failure
ECG
1. AF
2. Left atrial hypertrophy (Bifid P waves in lead II) if in sinus rhythm
3. Left atrial dilatation (Inverted or Biphasic P waves in V1-V2) if in sinus rhythm
CXR
1. Double right heart border (LA enlargement)
2. Splaying of the carina
3. Pulmonary congestion
4. Prominent pulmonary arteries (pulmonary hypertension)
Procedures
1. Closed commisurotomy
2. Open commisurotomy
3. Mitral valve replacement
Criteria for Balloon Valvuloplasty
1. Mobile valve (Loud S1 and Opening snap)
2. Minimal calcification of valve and subvalvular apparatus
3. Absence of MR
4. Absence of LA thrombus (TOE)
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Indications for Surgery
1. Pulmonary congestion
2. Pulmonary hypertension
3. Haemoptysis
4. Recurrent thromboembolic events despite therapeutic anticoagulation
Prosthetic Valves
1. Mechanical prostheses
a. Starr-Edwards valve: Ball and cage (High incidence of Haemolysis)
b. Medtronic-Hall valve: Tilting disc valve
c.
Bjork-Shiley valve: Single tilting disc valve with lamina flow
d. St. Judes valve: Double tilting disc valve
2. Xenografts: Porcine/ Pericardial valve
3. Homografts: Cadaveric Aortic/ Pulmonary valves
Bioprosthetic Valves For
1. Patients where anticoagulation would be contraindicated
2. Life expectancy shorter than predicted lifespan of prosthesis (~10 years)
3. Age >70 yr (Rate of degeneration is slow)
AF Treatment (From Davidson)
Rhythm Control in most successful in
1. AF <3 months
2. Young patients
3. No important structural heart disease
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Mitral Regurgitation
PSM
1. MR
2. TR (At LLSE, louder in inspiration: Carvallo’s sign)
3. VSD
MR
Acute
1. IE
2. Rupture of chordae tendineae (IE, Acute rheumatic fever, Ischaemia)
Chronic
1. Rheumatic fever
2. MVP
3. IE
4. LV dilatation (Function MR)
5. Marfan’s $
6. Ehlers Danlos $
7. Papillary muscle dysfunction (Ischaemia or Degenerative disease of chordae)
8. Cardiomyopathies (Dilated)
Severity of MR
Clinically
1. Soft S1
2. S3
3. S4 in sinus rhythm
4. Displaced apex beat
5. Precordial thrill
6. Mid-diastolic flow murmur
7. Widely split S2
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8. Signs of pulmonary congestion
9. Signs of pulmonary hypertension
Echo (From R R. Baliga)
1. Mild: Regurgitation Fraction <30%, Regurgitant orifice area <0.2 cm2
2. Moderate: Regurgitation Fraction 30-49%, Regurgitant orifice area 0.2-0.39
3. Severe: Regurgitation Fraction ≥50%, Regurgitant orifice area >0.4
Additional criteria: LA size enlarged, LV size enlarged
MR vs TR
Clinical Features
MR
TR
Pulse
Normal/ Jerky if severe
Normal
JVP
No association
Systolic ‘v’ wave
Palpation
Apical systolic thrill, Heaving
Parasternal systolic thrill,
displaced apex
Parasternal heaving
PSM loudest at Apex, during
PSM loudest at LSE, during
Expiration, Radiate to Axilla
Inspiration, No radiation
No
Pulsatile hepatomegaly
Auscultation
Hepatomegaly
ECG
1. AF
2. Left atrial hypertrophy (Bifid P waves in lead II) if in sinus rhythm
3. Left atrial dilatation (Inverted or Biphasic P waves in V1-V2) if in sinus rhythm
CXR
1. Double right heart border (LA enlargement)
2. Splaying of the carina
3. Pulmonary congestion
4. Prominent pulmonary arteries (pulmonary hypertension)
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Indications for mitral valve surgery
1. Symptomatic (NYHA III/IV) despite OMT
2. Asymptomatic: f/u every 6 months with Echo (LV size and function): if LVEF <60% or LV
End-systolic diameter >45 mm
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Aortic Stenosis
ESM
1. AS
2. HOCM
3. Supravalvular AS (William’s $)
4. PS
Gallavardin Phenomenon

Due to calcified ascending aorta in elderly patients, ESM is heard loudest over the Apex.
Causes
1. Bicuspid aortic valve (in young)
2. Degenerative calcification (in elderly)
3. Rheumatic heart disease
4. Congenital
Severity of AS
Clinically
1. Low volume pulse
2. Slow-rising pulse
3. Narrow pulse pressure
4. Heaving apex
5. Systolic thrill
6. Reversed splitting of S2
7. Late systolic peak of long murmur
8. Soft of Absent aortic component of S2
9. S4
10. Signs of pulmonary hypertension
11. Signs of pulmonary congestion
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Echo
Normal
3-4 cm2
Mild
>1.5
Moderate
1-1.5
Severe
<1
Complications
1. LV Failure
2. Sudden death
3. Arrhythmia (AF & VT)
4. Heart block
5. IE
6. Systemic embolic complication
7. Pulmonary hypertension
8. Haemolytic anaemia
9. IDA (Heyde’s $: Occult GI bleeding from colonic angiodysplastic lesions)
ECG
1. LVH
2. LV Strain pattern
3. LAH (Bifid P waves in lead II)
4. LA dilatation (Inverted or Biphasic P waves in V1-V2)
5. LAD
6. Conduction abnormalities (LBBB, 1st degree heart block)
CXR
1. Post-stenotic dilation of proximal ascending aorta (especially in bicuspid aortic valve)
2. Rib notching (Coarctation of aorta with bicuspid aortic valve)
3. Calcification of aortic valve
4. Cardiomegaly
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5. Pulmonary congestion
6. Prominent pulmonary arteries (Pulmonary hypertension)
Echo
1. LV size and function
2. Aortic valve area
CAG
To exclude CAD
Before doing AV replacement
Indication for AV Replacement
Symptomatic patients
1. Symptomatic severe AS (Mean gradient >50 mmHg)
Asymptomatic patients
1. Moderate/Severe AS undergoing other cardiac surgery
2. Severe AS AND any of following
a. LV systolic dysfunction (Mean gradient >40 mmHg)
b. Abnormal BP response to exercise
c.
VT
d. Valve area <0.6 cm2
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Aortic Regurgitation
EDM
1. AR
2. PR
Bounding Pulse
1. Anaemia
2. Fever
3. Pregnancy
4. Thyrotoxicosis
5. AR
6. PDA
7. AV fistula
8. Severe bradycardia
9. Severe MR
Carotid vs JVP
Clinical Features
Carotid Pulse
JVP
Waveform
Single
Double
Respiratory variation
No
Inspiration causes reduction
Patient’s position
No effect
Lying will raise
Hepato-jugular reflex
No effect
Will raise
Palpation
Palpable
Not
Compression
Not abolish
Abolish
Causes
Acute AR
1. Aortic dissection
2. IE
3. Ruptured sinus of Valsalva aneurysm
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Chronic AR
1. Bicuspid aortic valve
2. Hypertension
3. Rheumatic fever
4. Aortitis (Syphilis, Takayasu, Ankylosing spondylitis)
5. RA
6. SLE
7. CTD (Marfan, ED$, Pseudoxanthoma elasticum, Osteogenesis imperfect)
Eponymous Signs of AR
1. Corrigan’s sign: Visible carotid pulsations in neck
2. Quinke’s sign: Capillary pulsations in fingernails
3. De Musset’s sign: Head nodding with each heart beat
4. Muller’s sign: systolic pulsation of uvula
5. Traube’s sign: (Pistol shot femoral) Booming sound heard over the femoral artery
6. Duroziez’s sign: To and fro systolic and diastolic murmur produced by compression of
femoral artery and auscultating proximally (Diastolic M2 (+) (Diastolic M2 (+) ￫ Moderate)
7. Becker’s sign: Visible pulsations in the retinal arteries and pupils
8. Rosenbach’s sign: Systolic pulsation of the liver
9. Gerhard’s sign: Systolic pulsation in the spleen
10. Hill’s sign: Popliteal systolic pressure > Brachial systolic pressure (>60 mmHg): Moderate
11. Mayne’s sign: >15 mmHg drop in diastolic pressure with arm elevation
Severity of AR
Clinically
1. Wide pulse pressure
2. Long duration of the decrescendo diastolic murmur
3. S3
4. Austin Flint murmur (without Tapping apex beat, Loud S1, & Opening snap)
5. Signs of pulmonary hypertension
6. Signs of LV failure
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Echo (From R R. Baliga)
1. Mild: Regurgitant Fraction <30%, Regurgitant orifice area <0.1 cm2
2. Moderate: RF 30-49, ROA 0.1-0.29
3. Severe: RF >50, ROA ≥0.3
Additional criteria: LV size increased
Investigations
ECG
1. LVH +/- Strain pattern (especially if co-existent AS)
CXR
1. Valvular calcification
2. Cardiomegaly
3. Pulmonary congestion
4. Prominent pulmonary arteries (pulmonary hypertension)
Indications for Surgery
Symptomatic patients
1. Severe AR and symptoms of HF
2. Severe AR with Angina
Asymptomatic patients
1. LVSD (EF <50%)
2. LV End-systolic diameter >55 mm or End-diastolic diameter >75 mm
3. Aortic root dilatation ≥50 mm (Irrespective of degree of AR)
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Ventricular Septal Defect
PSM
1. MR
2. TR (At LLSE, louder in inspiration: Carvallo’s sign)
3. VSD
Causes
1. Congenital
Maternal factors
↳
DM
↳
Alcohol consumption (Fetal alcohol $)
↳
Phenylketouria
Aneuploid $
↳
Down’s (Trisomy 21)
↳
Edward’s (Trisomy 18)
↳
Patau’s (Trisomy 13)
↳
Di George (Deletion 22q11)
↳
Deletion 4q, 5p, 21, and 32
2. Acquired
Ischaemia (Post MI)
Iatrogenic (RV pacing with septal puncture, complication of alcohol septal ablation)
Classification
1. Perimembranous (Infra-cristal) 80%
2. Muscular (Trabecular) 5-20%
3. Supra-cristal (Outlet)
4. Posterior (Inlet)
Complications of VSD
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1. IE
2. Pulmonary hypertension
3. LV dysfunction
4. AR (Perimembranous or Supra-cristal defects)
5. Ventricular arrhythmias
6. Eisenmenger’s $
Investigations
CXR
1. Small defects: Normal heart size and pulmonary vascular markings
2. Large defects with pulmonary hypertension
a. Cardiomegaly
b. Increased pulmonary vascular markings with prominent main pulmonary arteries
with Decreased pulmonary markings in outer 1/3 of lung fields (Peripheral
pruning)
c.
Enlarged LA (Left atrial appendage and double right heart border)
ECG
1. Small defects: No associated ECG changes
2. Large defects
a. LVH
b. Biventricular hypertrophy as Large equiphasic mid-precordial voltage (>50 mm) in
V2-V4 (Katz-Wachtel phenomenon)
c.
RVH in Eisenmenger’s $
d. LAH (Bifid P waves in II)
e. LA dilatation (Biphasic P waves in V1)
Indications for VSD closure
1. Increasing Pulmonary:Systemic blood flow (Qp:Qs >2:1)
2. LV dilatation
3. LV dysfunction
4. Recurrent endocarditis
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5. Development of AR
6. Acute rupture of interventricular septum (following MI)
Contra-indications for VSD closure
1. Irreversible severe pulmonary hypertension
If evidence of pulmonary reactivity with vasodilator challenge (+) or
Lung biopsy findings consist with reversible pulmonary arterial changes,
Closure may be undertaken even in Eisenmenger’s $.
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Atrial Septal Defect
Widely split S2
1. ASD
2. VSD
3. MR
4. PS
5. RBBB
Types of ASD
1. Ostium secundum (at foramen ovale) (~70%)
2. Ostium primum (Anterior and Inferior aspect) (15%)
3. Sinus venosus (at Upper atrial septum and Junction of RA and IVC) (15%)
4. Coronary sinus (1%)
Complications
1. Atrial arrhythmias (AF is most common)
2. Pulmonary hypertension
3. Eisenmenger’s $
4. Paradoxical embolism
5. IE
6. Recurrent chest infections
ASD with MS
1. Lutembacher $ (Congenital ASD with Acquired rheumatic MS)
2. Iatrogenic ASD in patient with MS who has had Mitral valvotomy via transeptal puncture
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Investigations
CXR
1. Increased pulmonary vascular markings with prominent main pulmonary arteries
2. Decreased pulmonary marking in outer 1/3 of lung fields (Peripheral pruning)
3. Enlarged LA (Left atrial appendage and double right heart border)
ECG
1. Incomplete RBBB
2. LAD (Ostium Primum defects)
3. RAD (Ostium Secundum defects)
4. Inverted P waves in Inferior leads (Sinus venosus defects)
5. RVH
6. RAH (P pulmonale)
7. LA enlargement (Biphasic P waves in V1-V2)
Indications for ASD closure

Increasing Pulmonary:Systemic blood flow (Qp:Qs >2:1)
Contraindication

If there is irreversible severe pulmonary hypertension (Eisenmenger’s $)
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Respiration Short Cases
Pleural Effusion, Consolidation, Collapse, COPD/Asthma, ILD with PH
1. General (Fever, Eyes, Face, Neck veins, Dyspnoeic, Cyanotic/Pink, Effort, Clubbing, Stain,
Wasting, Bounding Pulse, HPOA, Oedema)
Anterolateral
2. Inspection (m/m, Flatten, Scars/Aspiration/Radiation marks, Inhaler)
3. Palpation (Trachea + Tug, Apex, Chest Wall Expansion, VF, Local rib tenderness)
4. Percussion (Supra/Clavicular/Infra, ICS, Axilla, Lateral) (6-8-11)
5. Auscultation + Bear Ears + Loud P2 (VBS, BBS, Crepts + Post-tussive, VR)
Posterior
6. Inspection (Aspiration Marks)
7. Palpation (L/N, Expansion)
8. Percussion & Auscultation
9. HF, RF, PEFR
Presentation
1. Pleural Effusion
On G/E, Patient is not breathless at rest. Patient does not appear cachectic and nutritional
status is good. Fingers are not clubbed. There is no evidence of nicotine staining. There are
no peripheral stigmata of rheumatological disease. There is no feature of venous congestion.
There is no palpable lymphadenopathy.
Trachea is at midline. Apex is not displaced.
O/E of Chest, Chest wall movement reduced on Right lower zone.
There is no scar. Aspiration mark is noted at Right posterior axillary line. There is no radiation
mark.
On Percussion, there is stony dullness on the right side started from 4 th ICS and downward
Anteriorly, Laterally and Posteriorly.
On Auscultation, Breath sounds are reduced in Right lower zone with area of BBS above the
area of dullness. There is no pleural rub.
VF and VR are also reduced in Right lower zone.
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There is no sign of peripheral oedema.
Dx: Right sided Moderate Pleural Effusion probably caused by pulmonary TB without features
of Respiratory Distress
2. CA Lung
On G/E, Patient is breathless at rest with Productive cough. He appears to be cachectic.
There is no feature of venous congestion. Fingers clubbing with features of HPOA are
present. There is nicotine staining of the fingers. Lymph nodes are palpable in Left
supraclavicular fossa.
Trachea is at midline. Apex is not displaced.
O/E of Chest, Chest wall movements reduced on the left middle and lower zones.
There is no scar, aspiration mark and radiation mark. There is no chest wall tenderness.
On Percussion, there is stony dullness on the Left side started from 4 th ICS and downward
Anteriorly, Laterally and Posteriorly.
On Auscultation, Breath sounds are reduced in Left middle and lower zones with area of BBS
above the area of dullness. There is no pleural rub.
VF and VR are also reduced in Left middle and lower zones.
There is no sign of peripheral oedema.
Dx: Left sided Moderate Pleural Effusion most probably due to Carcinoma of Left Lung with
Features of Respiratory Distress and HPOA.
3. Consolidation: Trachea Midline, Dullness, BBS, Coarse crepitations, Pleural rubs, Increased
VR (Bacterial pneumonia)
4. Collapse: Trachea deviated to affected side, Dullness, Reduced/Absent Breath sounds and
VR.
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Frequently Asked Questions (Most answers from Gautam Mehta)
Pleural Effusion
Dullness at lung base (From R R. Baliga)
1. Pleural effusion (Stony dull, Trachea may be deviated to opposite side in large effusions)
2. Pleural thickening (Trachea midline, Breath sounds will be heard)
3. Consolidation (Trachea midline, VR increased, BBS and associated crackles)
4. Collapse (Trachea deviated to affected side, Absent Breath sounds)
5. Raised hemidiaphragm
Causes
1. Exudate (Protein >30 g/L)
a. Bronchogenic carcinoma
b. Secondaries in pleura (P’ from Lung, Breast, Ovary, Pancreas)
c.
TB
d. Pneumonia
e. Empyema
f.
Sub-phrenic abscess
g. Pulmonary infarction
h. RA
i.
SLE
j.
Lymphoma (in young patients)
k.
Mesothelioma
2. Transudate (Protein <30 g/L)
a. Nephrotic $
b. Heart failure
c.
Liver failure
d. Hypothyroidism
Light’s Criteria for Exudate
1. Pleural fluid protein : Serum protein >0.5
2. Pleural fluid LDH : Serum LDH >0.6 or
3. Pleural fluid LDH >2/3 of ULN of Serum
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Blood stained Pleural Effusion
1. Malignancy
2. TB
3. Pulmonary embolism
4. Chest trauma
TB Pleural Effusion
Mostly due to hypersensitivity reaction to M. TB
1. AFB stains (+) in (<10%)
2. Culture (+) in (65%)
3. Pleural Biopsy & Culture yield (90%)
CXR

It needs at least 200 mL to be detectable
Indications for Pleurodesis
1. Recurrent Malignant effusion
2. Recurrent pneumothoraces
Use: Doxycycline, Bleomycin, Talc
Lung Fibrosis
Apical
1. Berylliosis
2. Radiation
3. EAA (Farmer’s lungs)
4. ABPA, Ankylosing Spondylitis
5. Sarcoidosis
6. TB
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7. Silicosis
Basal
1. Idiopathic pulmonary fibrosis
2. Rheumatological diseases (except An Spond)
3. Drugs (Methotrexate, Amiodarone)
4. Asbestosis
Carcinoma of Lung
Risk Factors
1. Smoking (SCLC, SCC)
2. Asbestos (Adeno)
3. Arsenic
4. Coal tar
5. Radiation
Classification
1. Small cell lung cancer (SCLC) 20%
2. Non-small cell lung cancer (NSCLC) 80%
a. Adenocarcinoma 50%
i. Bronchoalveolar carcinoma (Subtype of Adenocarcinoma)
b. Squamous cell carcinoma (SCC) 30% (Epidermoid CA, often Cavitating)
c.
Large cell carcinoma (Undifferentiated CA)
Staging (TNM) (Tx/is-T4, N0-N3, M0-M1)
Stage I:
Confined to lung (5-years survival 75%)
Stage II and III: Confined to chest (Larger and More invasive tumours as III)
Stage IV:
Spread beyond the chest (5-years survival <1%)
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Paraneoplastic $ (Non-metastatic, common in SCLC)
Endocrine
1. SIADH (Ectopic ADH)
2. Cushing $ (Ectopic ACTH)
3. Hypercalcaemia (Ectopic PTH-related peptide) (SCC)
4. Hyperthyroidism (Ectopic TSH)
5. Hypoglycaemia (Ectopic IGF)
Neurological
1. LEM$ (Pre-synaptic V-gated Ca2+ channel antibodies)
2. Subacute cerebellar degeneration (Anti-Yo or Anti-purkinje)
3. Sensory neuropathy (Anti-Hu)
4. Limbic encephalopathy (Anti-Hu and Anti-Yo)
Musculoskeletal
1. PM/DM
2. Clubbing
3. HPOA (SCC)
Cutaneous
1. Acanthosis nigricans
2. Gynaecomastia (Ectopic HCG) (SCC)
3. Thrombophlebitis
4. Thrombosis (Trousseau $) (At least 2 different sites, common in Adeno CA)
5. Ichthyosis
6. Hypertrichosis
7. Herpes zoster
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Pancoast Tumour
Apical lung tumours that erode Ribs and Brachial plexus (C8-T1), Cervical sympathetic
nerves, and Ganglions. This results in Ipsilateral wasting of small muscles of hand, Ipsilateral
sensory disturbances in C8-T1 dermatomes and Ipsilateral Horner’s $.
Management
Surgery: NSCLC
Chemo: SCLC, it can also be used in NSCLC (Alone/ Adjuvant to Surgery/ + Radio)
Radio: SCLC and NSCLC
Contraindication for Surgical Resection

FEV1 <1.5 L
Indications for Radiotherapy
1. Bone pain
2. Bronchial obstruction
3. Dysphagia
4. Haemoptysis
5. SVCO
6. Pancoast’s tumour
Causes of Lung Collapse
1. Malignancy
2. Extrinsic compression by hilar lymphadenopathy
3. TB
4. Mucus plug (Asthma, COPD, Bronchiectasis)
5. Foreign body
6. Malpositioned ET tube
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Abdomen Short Cases
Hepatosplenomegaly, Ascites, ADPKD, Renal Transplant
1. Visual Survey
2. General Examination
Head: Fever, Pallor, J, Mouth & Teeth, Parotid
Neck: JVP, Epitrochlear + Cervical L/N
Back & Chest: Spider naevi, Tattoo, Gynaecomastia, Sternal tenderness, Axilla hair
Hands: Leukonychia, Clubbing, Dupuytren, Erythema, Tattoo, Flap
(Renal transplant: Fistula, BP)
Legs: Clubbing, Oedema, DVT
3. Inspection (Abd Shape, Mass, Veins, Scars, Aspiration marks, Hernia, Pubic Hair)
4. Palpation (Tender?) (Superficial, Deep, Ballotable Kidneys, Inguinal L/N)
5. Percussion (Liver, Spleen, Mass, Ascites)
6. Auscultation (Bowel sound, Rub, Bruit)
7. Thalassaemia: Palpate Spine, Check Paraparesis
8. Ask PR exam, Testicular atrophy
ADPKD: BP
Presentation
1. Hepatosplenomegaly underlying Thalassaemia
On G/E, Patient has Frontal bossing, Depressed nasal bridge, Malar prominence suggestive
of Thalassaemic face. Eyes show Moderate pallor and Mild jaundice. There is no palpable
lymphadenopathy and Sternal tenderness. No spider naevi.
There is no finger clubbing. No leukonychia. Skin colour is slate-grey especially on face and
hands.
O/E of Abdomen, Localized distention of right and left upper quadrants. It moves with
respiration. There is no scar, No dilated veins and No aspiration marks.
Moderate Hepatomegaly is present measuring about 5 cm below the right costal margin, not
tender, sharp edge with smooth surface.
Huge Splenomegaly is present measuring about 8 cm below the left costal margin, not tender,
splenic notch is palpable, sharp edge with smooth surface.
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Both Kidneys are not ballotable and there is no ascites.
There is no liver bruit and splenic rub.
There is no flapping tremor.
Spine is normal and no spine tenderness.
Dx: Moderate Hepatomegaly and Huge splenomegaly due to Chronic Haemolytic Anaemia
most probably β Thalassaemia Major
2. Hepatosplenomegaly underlying Lymphoproliferative/Myeloproliferative Disorder
On G/E, Patient is anaemic. There is no jaundice. There are no stigmata of chronic liver
disease and no evidence of rheumatological disease. There is widespread lymphadenopathy
and excoriation marks to suggest pruritus. There is hepatosplenomegaly with liver edge
palpable 3 cm below the costal margin and splenic edge palpable 4 cm below the costal
margin. There is no ascites or peripheral oedema. There is no venous hum. There are no
signs of hepatic encephalopathy.
Dx: Hepatosplenomegaly with widespread lymphadenopathy. In the absence of stigmata of
chronic liver disease and portal hypertension, the most likely cause is lymphoproliferative
disorder (Lymphoma)
If there is no lymphadenopathy, consider Myeloproliferative disorder (CML, Myelofibrosis, ET,
PRV)
3. Splenomegaly underlying COL with Portal Hypertension
On G/E, Patient has mild anaemia and moderate jaundice. Spider naevi are present on upper
part of chest and back.
There is no palpable lymphadenopathy. Finger clubbing and leukonychia are present.
O/E of abdomen, it is markedly distended with dilated veins on abdominal wall. There is no
aspiration mark. Liver is not palpable and Moderate splenomegaly is present, splenic edge
palpable 6 cm below the costal margin. Fluid thrills and shifting dullness (+). There is no
peripheral oedema. There is no splenic rub. There is no signs of hepatic encephalopathy.
Dx: Moderate splenomegaly and ascites with features of chronic liver disease underlying COL
most probably due to chronic alcoholism without features of Hepatic encephalopathy.
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4. ADPKD
On G/E, Patient has no anaemia. There is no sign of chronic liver disease. No palpable
lymphadenopathy. There is no finger clubbing.
O/E of Abdomen, it is distended with fullness in the flanks. There is irregular, non-tender liver
edge palpable 3 cm below the costal margin. There is no evidence of splenomegaly. There
are bilateral flank masses. These masses are ballotable, it is possible to palpate above these
masses, and overlying percussion note is resonant. There are no signs of uraemia or
encephalopathy. There is no evidence of RRT.
Dx: Polycystic Kidney Disease with apparently normal renal function
5. Renal Transplant
On G/E, Patient has anaemia and no jaundice. No features of CLD. There is no gum
hypertrophy. No finger clubbing. No pedal oedema.
O/E of Abdomen, there is a 7 cm scar healed by primary union. Localized distension at RIF is
seen and a rounded mass is palpable at there. It is not tender. (In addition, there are bilateral
masses in the flanks which are bimanually palpable and ballotable with a nodular surface).
Percussion note is dullness on RIF mass. There is no palpable hepatosplenomegaly. No
ascites. No pedal oedema.
AV Fistula is present on left forearm with palpable thrill. There is no recent needle puncture
mark. No flapping tremor.
Dx: Transplanted kidney at RIF with underlying PKD in situ. Renal function appears to be
normal.
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Frequently Asked Questions (Most answers from Gautam Mehta)
Hepatosplenomegaly
Hepatosplenomegaly (From Macleod)
1. Chronic Malaria
2. Chronic Haemolytic Anaemia (Thalassaemia)
3. Myeloproliferative disorders (CML, Myelofibrosis)
4. Lymphoma
5. Amyloidosis
6. COL with Portal Hypertension
Tender Hepatomegaly
1. Viral Hepatitis
2. Alcoholic Hepatitis
3. Malignancy
4. Hepatic Congestion
5. Vascular liver disease (Budd-Chiari $, Sickle cell disease)
Hepatomegaly without Splenomegaly
1. Malignancy: P’ or S’
2. Cirrhosis (ALD, NAFLD, PBC)
3. Hepatic Congestion (RHF, Constrictive pericarditis, Restrictive CM)
4. Alcoholic Hepatitis
5. Infectious disease (Viral hepatitis, Leptospirosis, Amoebic liver abscess)
6. Infiltration (Amyloidosis, Sarcoidoisis, Gaucher)
7. Vascular liver disease (Budd-Chiari $, Sickle cell disease)
8. Polycystic liver disease
Massive Splenomegaly (>8 cm) (From Freeman)
1. Chronic Malaria
2. MPD (CML, Myelofibrosis, PRV)
3. Kala-azar (Visceral leishmaniasis)
4. Gaucher
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Moderate Splenomegaly (4-8 cm)
1. Chronic Malaria
2. MPD (CML, Myelofibrosis, PRV)
3. Lymphoproliferative disorders
4. Haematological (Thalassaemia, ITP, Acute Leukaemia, Hereditary Spherocytosis)
5. COL
Mild Splenomegaly (<4 cm)
1. MPD
2. LPD
3. Infections (CMV, EBV, SBE, Leptospirosis, Meloidosis, Typhoid, Brucellosis, Acute
malaria)
4. Infiltrative (Amyloidosis, Sarcoidosis)
5. Endocrine (Acromegaly)
6. CTD (SLE, Felty’s $)
7. Chronic haemolytic anaemia (Thalassaemia, ITP, AL, HS)
Causes of Cirrhosis
1. Chronic Alcoholism
2. HBV
3. HCV
4. NASH
5. Autoimmune Hepatitis
6. PBC
7. Haemochromatosis
8. Metabolic (Wilson’s disease)
Features of Chronic Liver Insufficiency
1. Jaundice
2. Spider naevi
3. Ascites
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Features suggestive of Alcoholic Liver Disease
1. Parotid swelling
2. Florid spider naevi
3. Dupuytren’s contracture
4. Palmar erythema
5. Gynaecomastia
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Polycystic Kidney Disease
Causes of bilateral renal cysts
1. Multiple simple cysts
2. Tuberous sclerosis
3. Von Hippel Lindau $
4. Mackel-Gruber $
5. Laurence-Moon-Bardet-Biedl $
6. Trisomy 13 (Patau $), 18 (Edward $), and 21 (Down $)
Single palpable kidney
1. PKD (with only one palpable kidney)
2. Hydronephrosis
3. Hypertrophy of a single functioning kidney
4. RCC
Bilateral palpable kidney
1. Bilateral renal cysts
2. Bilateral hydronephrosis
3. Amyloidosis
4. Bilateral RCC (in VHL $)
USG diagnostic criteria for PKD
1. <30 yrs: At least 2 cysts in 1 kidney or 1 cyst in each kidney
2. 30-59 yr: At least 2 cysts in each kidney
3. ≥60 yr: At least 4 cysts in each kidney
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Left Kidney vs Spleen
Clinical Features
Spleen
Left Kidney
Move with respiration
Superficially and diagonally
Deeply and vertically
Ballotable
No
Yes
Palpate above
No
Yes
Percussion
Dull
Usually resonant
Transplanted Kidney
Differential diagnosis of Right/Left iliac fossa mass
1. Transplanted kidney
2. Colonic CA
3. Fecal mass
4. Appendicular mass
5. Ovarian tumour
6. Lymphadenitis
Common disease leading to transplant
1. DM
2. Hypertension
3. GN
Advantages of RT over HD
1. Free of HD
2. Cost effective in long-term
3. Free of diet and fluid restriction
4. Improve survival
5. Improve QoL
6. Improve anaemia
7. Improve bone disease
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HLA Matching for RT
1. DR
2. B
3. A
SEs of Ciclosporin
1. Hypertrichosis
2. Hypertrophy of gum
3. Hypertension
4. Hyperglycaemia
5. Hypercholesterolaemia
6. Hyperkalaemia
7. Nephrotoxicity
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Nervous System Examination
Stroke, Para/Quadriparesis, Cerebellar, MND
1. General (Body built, Posture, Facial asymmetry, Ptosis, Squint, Urinary catheter)
2. Inspection (Wasting, Fasciculation, Wrist drop, Foot drop, Spine + Palpation)
3. Tone, Clonus, Power, Reflexes (+ Hoffman, +/- Reinforce)
If Cervical myelopathy (C5-6) is suspected: Check Inversion of biceps and supinator Reflexes
4. Plantar reflex
(In Para/Quadriparesis, Percuss lower abdomen for Bladder distension).
5. Sensory (Pinprick, Proprioception, Vibration)
6. Cerebellar (Heel-Chin test)
7. Romberg & Gait
8. Stroke
Pronator drip
Visual Field
Speech
Aetiology: Carotid Bruit, AF, Murmurs
9. Para/Quadriparesis
Aetiology: Examine Spine, Saddle anaesthesia
Complications: Pressure Sores
10. Cerebellar
Finger-nose, Rebound, Dysdiadochokinesia, Nystagmus
11. Ask Fundoscopy
12. Ask BP, RBS, Right/Left handed
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Sensory Levels
Macleod 13th Ed. Page. 267
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Presentation
1. Spastic Paraparesis
The patient has wasting of lower limbs with contractures. There is bilateral pyramidal
weakness, motor power 3/5 on both lower limb, with hypertonia, hyperreflexia, ankle clonus
and extensor plantar responses. Sensation is impaired in the lower limbs with a sensory level
at the level of T9.
Cerebellar and dorsal column features are intact.
There is no spinal deformity or tenderness. There is a surgical scar over the thoracic spine.
Dx: Spastic Paraparesis with sensory cut off level due to a lesion at the T9 level of the spinal
cord. The presence of surgical scar suggests previous surgery for trauma or spinal pathology
like tumour. The presence of wasting and contracture suggests this has been longstanding.
2. Spastic Quadriparesis
Patient has wasting of both upper and lower limbs bilaterally. There is no fasciculation. There
is pyramidal weakness on both sides, motor power 4/5 on ULs and 3/5 on LLs affecting both
proximal and distal parts. There is hypertonia, hyperreflexia, ankle clonus and extensor
plantar responses on both sides. Sensory impairment is noted up to C4 level of spinal cord
and above.
Cerebellar and Dorsal column features are intact.
There is no deformity and tenderness of cervical spine. There is no scar.
Dx: Spastic Quadriparesis with sensory impairment up to C4 level of spinal cord and above. It
is most probably due to cervical myelopathy above C4 level of spinal cord. Muscle wasting
suggests this has been longstanding.
3. Right sided cerebellar syndrome
O/E of ULs, there is Dysdiadochokinesis, impaired finger-nose testing with dysmetria and
intention tremor on the right side. Rebound phenomenon is present.
O/E of LLs, there is an impaired heel-shin test on the right side. Both plantar responses are
flexor.
Hypotonia is noted in both upper and lower limbs. Muscle power and reflexes are normal.
There is a nystagmus with a fast component to the right. There is loss of smooth pursuit
(broken pursuit).
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The gait is broad-based and ataxic with a tendency to fall to the right. Romberg’s test is
negative.
The speech is slurred and has an explosive (staccato) character.
Cranial nerves are intact.
Dx: Right sided Cerebellar syndrome
4. Right sided hemiparesis with Right facial palsy
On G/E, patient has right sided facial palsy. There is extensor posturing of right lower limb.
There is hypertonia, hyperreflexia and weakness in a pyramidal distribution in the right lower
limb, motor power 4/5. The right plantar response is extensor. There is reduced sensation
(pinprick and fine touch) in the right lower limb. Cerebellar signs are intact.
There is flexor posturing of the right upper limb. Pronator drip and Hoffman’s sign are positive
in right upper limb.
Visual field is normal. There is no aphasia.
There is no AF, carotid bruit and cardiac murmurs.
There is a right circumducting gait.
Dx: Right Hemiparesis with Right UMN Facial Palsy most probably due to left cerebral infarct
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Frequently Asked Questions (Most answers from Gautam Mehta)
Spastic Quadri/Paraparesis
Spasticity

This is defined as an increase in muscle tone due to hyperexcitability of the stretch of
reflexes, and velocity-dependent increase in tonic stretch reflexes.
Rigidity

Rigidity represents a constant increased tone throughout the range of movement and is
independent of velocity.
Transverse Myelitis

This is a broad term used to describe acute inflammation of cord. Inflammation tends to
involve the cord diffusely at one or more levels, affecting all spinal cord function, with
resultant bilateral motor, sensory, and sphincter deficit below the level of the lesion.
Sensory loss of Vertebra level vs Spinal cord level (Minus to Reverse)

Upper cervical vertebra (C1-C4): Same level of spinal cord

Lower cervical (C5-C7): Add 1 to get level of spinal cord

Upper thoracic (T1-T6): Add 2

Lower thoracic (T7-T12): Add 3
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Causes of Spastic Quadri/Paraparesis
Ref: Therapeutic Manual
1. With sensory involvement
a. Definite sensory level
i. Compressive lesions
a. Vertebra (Trauma, PID, Metastasis, TB etc.)
b. Meninges (Tumours, Abscess)
c.
Spinal cord (Ependymoma, Glioma, Metastasis)
ii. Non-compressive lesions
a. Acute transverse myelitis*
b. NMO (Devic’s disease)
b. Proprioception loss
i. B12 deficiency (SCDC)
ii. Taboparesis
iii. Friedriech’s ataxia
c. Dissociated sensory loss
i. Brown-sequard $
ii. Central cord $
a. Trauma
b. Syringomyelia
c.
Intrinsic cord tumours
iii. Anterior spinal artery $ (Watershed area of Adamkiewicz T8-L2)
2. Without sensory involvement
a. MND
b. Hereditary spastic paraplegia
c.
Parasagittal meningioma (may be cortical sensory loss)
Causes of Transverse Myelitis*
1. Bacterial infections (Lyme, Mycoplasma, TB, Syphilis)
2. Viral infections (HSV, VZV, CMV, EBV, HIV, HAV, Influenza)
3. Demyelination (MS, NMO/Devic’s disease)
4. Radiation myelopathy
5. Anterior spinal artery occlusion
6. Vasculitis
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Spastic Paraparesis Causes and Features
Causes
Multiple sclerosis
Sensory signs
Dorsal column signs
Other features to look for
Cerebellar signs in the ULs,
Eye signs, Pseudoathetosis
Cord compression (Tumours)
Sensory level
Absence of signs above the
level of lesion
Trauma
Sensory level
Scars, Deformity
MND
None
Fasciculations (limbs and
tongue), Bulbar involvement,
Wasting of small muscles of
hands
Syringomyelia
Anterior spinal artery occlusion
Dissociated loss (preserved
LMN weakness in ULs,
posterior column and loss of
Wasting of small muscles of
spinothalamic)
hands, Horner’s $
Dissociated loss (preserved
Irregular pulse (AF): a cause of
posterior column and loss of
embolic phenomena
spinothalamic)
Subacute combined
Dorsal column signs,
Absent ankle jerks and
degeneration
peripheral neuropathy
extensor plantars: anaemia,
jaundice, glossitis,
splenomegaly
Taboparesis
Dorsal column signs
Absent ankle jerks and
extensor plantars: Argyll
Robertson pupils
Tropical spastic Paraparesis
Friedreich’s ataxia
Dorsal column signs,
Afro-Caribbean patient:
peripheral neuropathy
Proximal > Distal weakness
Dorsal column signs
Cerebellar signs: pes cavus,
kyphoscoliosis
Cervical myelopathy
Dorsal column signs
Neck pain, Lhermitte’s signs,
Inversion of biceps and
supinator reflexes,
Pseudoathetosis
Hereditary spastic Paraparesis
None
ULs normal
Parasagittal tumour
Cortical sensory loss
Papilloedema, history of
headache
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Non-traumatic causes
1. Processes affecting the spinal cord or blood supply directly:
a. MS
b. Transverse myelitis
c.
Spinal AV malformation
d. Syringomyelia
e. HIV myelopathy
f.
Other myelopathies
g. Spinal cord infarction
2. Compressive lesions affecting the spinal cord
a. Spinal epidural abscess
b. Spinal epidural haematoma
c.
Discitis
d. Neoplasm
e. Metastatic
Hemiparesis
Causes
1. CVA (Ischaemic, Haemorrhagic, or Thrombosis)
2. Tumour
3. Demyelination
4. Abscess
5. Venous sinus thrombosis
6. Post-ictal (Todd’s paresis) (Not >1-2 days)
Arterial Supply
1. Anterior cerebral artery: predominantly affect the Leg
2. Middle cerebral artery: Arm and Face
3. Posterior circulation (Vertebrobasilar artery): Cerebellum and Brain stem
4. If ACA + MCA ￫ Check Carotids ￫ ≥70% stenosis ￫ Endartectomy
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Clinical Syndromes
1. TACS: (Hemiparesis + Aphasia + Hemisensory + Hemianopia)
2. PACS (Hemiparesis) or (Aphasia/Neglect) or (Hemiparesis + Aphasia)
3. LACS (Hemiparesis) or (Hemisensory) or (Hemiparesis + Hemisensory)
4. POCS (Cerebellar + Cranial + Hemianopia)
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Cerebellar
1. ULs (Hypotonia, Dysdiadochokinesia, Finger-nose test)
2. Rebound phenomenon
3. LLs (Heel-shin test, Pendular Knee jerk)
4. Nystagmus
5. Speech (Ask name) (Scanning/Explosive dysarthria)
6. Gait (Broad based, Tendency to fall affected side)
7. Romberg test (Eyes open)
8. Aetiology:
Unilateral:
↳
Isolated – CVA (AF), SOL (Fever),
↳
Associated – Ptosis, RAPD, INO, 5+6+7+8 CNs, Neurofibromatosis,
Tremor+Rigidity+Bradykinesia, Contralateral Pain+Touch+Temp
Bilateral:
↳
Fever, Jaundice, KF Ring, Parotid swelling, Gum Hypertrophy, Neurofibromatosis,
Tremor+Rigidity+Bradykinesia, Clubbing, Pendular Knee Jerk/Absence of Ankle Jerk,
Pes Cavus, Telangiectasia.
Ask: Visual Fields, Fundoscopy (Papilloedema, OA)
Presentation
1. On examination of the upper limbs, hypotonia is noted on right side. There is
dysdiadochokinesis, impaired finger-nose testing with dysmetria and intention tremor on the
right side. Rebound phenomenon is present on right side.
On examination of the lower limbs, hypotonia is noted on right side. There is impaired heelshin test on the right side. Pendular knee jerk is also noted on right side.
On examination of eyes, there is a Nystagmus with fast component to the right.
Speech is slurred, scanning and explosive character.
Gait is broad-based and ataxic with tendency to fall to the right. Romberg’s test is negative.
Dx: Right Cerebellar syndrome.
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FAQs
Causes of Unilateral cerebellar $
1. Isolated
a. CVA
b. SOL in posterior fossa (Absess or Tumour)
2. Associated
a. CN
i. CPA tumours and/or neurofibromatosis
ii. Lateral medullary $ (Wallenberg): PICA occlusion
3. Ataxic hemiparesis
4. Parkinsonism with MSA
5. Demyelinating such as MS
Causes of Bilateral cerebellar $
1. Acquired
a. Infection: Lymes, HIV, Syphilis, CJD
b. Metabolic: Wilson, Hypothyroidism
c.
Drugs: Alcohol, Phenytoin, Carbamazapine, Lithium
d. MSA
e. NF 2 with bilateral CPA tumour
f.
Bilateral strokes
g. Paraneoplastic (Anti-Hu Ca Lungs or Anti-Yo Ovary)
2. Hereditary
a. Friedreich’s ataxia
b. Ataxia telangiectasia
Vermis Lesion
1. Midline tumour, Paraneoplastic
2. Signs: Truncal ataxia, Abnormal heel-toe walk test, cerebellar speech
Cerebellar signs with spastic paraparesis
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1. Friedreich’s ataxia
2. Spinocerebellar ataxia
3. Arnold-Chiari malformation
4. Syringobulbia
5. MS
Syndrome containing Cerebellar Signs
1. Lateral medullary $ (Wallenberg):
↳
PICA occlusion
↳
Ipsilateral cerebellar signs
↳
Contralateral spinothalamic sensory loss
↳
Ipsilateral 5th, 9th, 10th, 11th palsy
↳
Ipsilateral Horner’s $
↳
Vesibular disturbance
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Nyein Ko Hein
Facial Palsy
1. Wrinkle, Frown, Close eyes, Blow, Show teeth, Whistle
2. Complications (Cornea, Conjunctiva, Chronicity; Synkinesia)
3. Level of Lesion & Aetiology
Parotid: Scar
Vesicles in Ears,
Mastoid (Scar, Inflammation)
Facial Canal (Chorda tympani: Taste, Stapedius: Hyperacusis, Geniculate: Tears)
CP Angle → Associations: 8th, 6th, 5th, Cerebellar (Millard Gubbler, Foville)
Cerebral: UMNL Facial Palsy
Mononeuritis: WARDS PLC
4. Ask (Taste, Tears)
5. Test (Sugar, Serology, RA, ANA, p/cANCA)
Presentation
1. This patient has right sided facial weakness affecting the upper and lower parts of the face.
Bell’s sign is positive on right side. There is no hearing defect. There is no opthalmoplegia.
The facial sensation is normal. There is no cerebellar sign. The parotid gland is not enlarged
and is normal to palpation. There is no tenderness over the parotid gland and preauricular
area. There is no vesicle noted in external auditory meatus.
Dx: Right LMN Facial Nerve Palsy (Bell’s palsy)
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Frequently Asked Questions (Most answers from Gutam Mehta)
Facial Palsy
Causes of Bell’s (LMN) palsy
1. Idiopathic (>95%)
2. Structural lesion
a. Brainstem: Demyelination, Stroke, Tumour
b. CP angle: Acoustic neuroma
c.
Middle ear: Infection
d. Parotid gland: Infection, Tumour, Surgery
3. Mononeuritis multiplex
a. Wegner, Churg-Strauss, PAN, SLE, RA, Sjogren, Amyloid, Sarcoid, DM, Lyme,
Leprosy, Lymphoma (WARDS PLC)
Bilateral LMN facial palsy
1. Bilateral CPA tumour as in NF 2
2. Bilateral Bell’s palsy
3. Bilateral parotid enlargement (Sarcoid)
4. GBS, MND
5. Leprosy, Lyme
Bell’s phenomenon

Upward movement of eyeball with incomplete closure of the eyelid in attempt to close the eye.
Facial synkinesias

Attempt to move one group of facial muscles results in movement of another group.
Route of Facial Nerve
1. Nucleus at Midbrain close to VI CN
2. Exit Pons with VIII CN via CP angle
3. Enter Facial canal and enlarge to form Geniculate ganglion
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4. Gives 2 branches:
↳
Greater superficial petrosal branch to Lacrimal glands and
↳
Nerve to Stapedius
5. Chorda tympani (taste from anterior 2/3 of tongue) joins VII CN in Facial canal
6. Exit skull via Stylomastoid foramen
7. Pass through Parotid and Give 5 branches:
↳
Temporalis: Frontalis, Corrugator, Upper part of Orbicularis oculi
↳
Zygomatic: Lower and Lateral Orbicularis oculi
↳
Buccal: Upper part of Orbicularis oris, Buccinator, Levator anguli oris
↳
Mandibular
↳
Cervical: Platysma
Treatment
1. High dose steroid (PO 60 mg OD for 5 days) within 1st week
2. PO Acyclovir within 1st week
3. Corneal protection (Tape, Lubricant)
Complications of Bell’s palsy
1. Persistent facial weakness
2. Corneal abrasions
3. Pain and/or sensory disturbances in distribution of facial nerve (TZBMC)
4. Aberrant reinnervation causing Crocodile tears, Jaw-eyelid synkinesia
5. Hemifacial spasm
Eponymous syndromes
1. Millard Gubbler
↳
Occlusion of basilar artery branches in the pons
↳
Ipsilateral VI, VII CN palsy
↳
Contralateral Hemiplegia
2. Foville’s $
↳
Pontine lesion
↳
Ipsilateral VII CN palsy, Horizontal gaze palsy
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↳
Contralateral Hemiparesis, Hemisensory loss & INO
3. Ramsay Hunt $
↳
Reactivation of latent VZV in Geniculate ganglion
↳
Ipsilateral facial palsy, Loss of taste, Tinnitus, Dry eyes
4. Weber
↳
Occlusion of paramedian branches of basilar or posterior cerebral arteries.
↳
Infarction of ½ of Midbrain
↳
Ipsilateral III CN palsy
↳
Contralateral UMNL VII CN palsy, Hemiplegia
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Ptosis
1. Unilateral or Bilateral Ptosis, Enopthalmos/Proptosis, Sweating
2. Primary Gaze: Squint, Down & Out
3. Pupils: Dilated, Small, Normal, LR, AR, RAPD
4. Visual Acuity: Diplopia
5. EOM: Diplopia, Pain, Nystagmus
6. MG: Fatigability Test
7. Eye Ball Bruit
8. 5th CN: Sensory, Motor, Jaw Jerk
9. Ask Corneal Reflex: Tumours
10. Aetiology:
a. Muscular: Myopathic Facies, Grip (DM, OM, CPEO) (Bilateral)
b. Neuromuscular: Fatiguability, Proximal Muscle Weakness & Nasal Speech (MG)
(Uni/Bilateral)
c.
Nerve (Only for Small Pupil, Horner $)
1st Order Neuron (Midbrain-T1): MS, Stroke, Syringomyelia
2nd Order (T1-SCG): Pancoast, Sx/Trauma, L/N
3rd Order (SCG-CM): Carotid Aneurysm
Nerve Thickening, Vasculitis
11. Associations
a. Pronator Drip: Contralateral → Weber + 7th UMN, Bilateral → MS
b. Contralateral Involuntary Movements → Benedikt
c.
DANISH: Contralateral → Claude, Bilateral → MS
12. Ask: (Sweating, Adrenaline Eye-drop) RBS, NCS, MRI, Skin & Nerve Biopsy, VDRL & TPHA
Presentation
1. On examination eyes, there is partial ptosis of right eye. No squint in primary gaze position.
Pupils are equal and normal in size, normal LR and AR. Visual acuity is intact.
There is no opthalmoplegia. There is no eye ball bruit.
Dx: Right sided 3rd cranial nerve palsy
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FAQs
Causes of isolated 3rd nerve palsy
1. Brainstem
a. MS, Infarct, haemorrhage, tumour, abscess
b. Nuclear lesions
c.
Fascicular lesions
i. Weber’s (+ Contralateral hemiplegia) – base of midbrain
ii. Benedikt’s (+ Contralateral hemiplegia, Cerebellar, Tremor) – tegmentum of
midbrain and red nucleus
iii. Northnagel (+ Contralateral cerebellar) – tectum of midbrain
2. Peripheral
a. Subarachnoid portion – PCA aneurysm, meningitis, infiltrative
b. Cavernous sinus lesions – tumours, thrombosis, inflammation, ischaemia
c.
Orbital tumour (meningioma, hemagioma), Grave, Inflammation
d. Mononeuritis multiplex
e. Miller Fischer gradient of GB$
f.
MG
Causes of bilateral ptosis
1. Nerve
a. Bilateral 3rd nerve palsy
b. Bilateral Horner’s (Syringomyelia)
c.
Tabes dorsalis
d. Miller Fisher $
2. Neuromuscular
a. MG
3. Muscular
a. Dystrophia myotonica
b. Ocular myopathy
c.
CPEO
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Course and Anatomy of 3rd CN
1. Nuclear portion at midbrain (Ipsi: Lateral, Contra: Medial, Central Caudal, Parasympathetic
Edinger Westphal)
2. Fascicular intraparenchymal portion – close to the red nucleus, emerges from cerebral
peduncle
3. Fascicular subarachnoid portion – meninges, pass between superior cerebellar and posterior
cerebellar arteries parallel to posterior communicating artery.
4. Pass through cavernous sinus and enter into orbit via superior orbital fissure
5. It divides into superior and inferior division
6. Superior division innervates levator palpibrae superioris and SR, Inferior division to MR, IR,
IO, EW fibres to Cillary ganglion.
Causes of dilated pupils
1. 3rd nerve palsy (surgical)
2. OA
3. Holmes Adie (Myotonic pupil)
4. Mydiatric eye drops
5. Sympathetic overactivity
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Myasthenia Gravis
1. General Quick Survey
2. Eyes (Ptosis, Pupils, Vision, EOM)
3. Fatigability
4. Nasal Speech
5. Neck flexion/Extension
6. Sternotomy scar
7. Proximal muscle weakness
8. LL Reflexes
9. Severity: Resp. Rate, Cyanosis, Cough Intensity
10. Treatment: SEs (Cushingoid)
11. Autoimmune associations (Anaemia, Addison, Grave, Vitiligo)
12. Ask BP, RBS
Presentation
1. This patient has variable ptosis accentuated by sustained upgaze. There is variable
strabismus, opthalmoplegia and diplopia.
Patient has lack of facial expression and Myasthenic snarl on smiling.
Weakness of neck muscles is also noted. There is no sternotomy scar.
Voice is weak with nasal character.
Examination of limbs shows proximal weakness with fatiguability.
Deep tendon reflexes are normal.
Dx: Myasthenia Gravis without Features of respiratory distress and associated autoimmune
disorders.
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FAQs
Differentials (Therapeutic Manual)
1. LEM$
2. Botulism
3. Drug induced MG (Penicillamine)
4. Congenital Myasthenia
5. CPEO
6. Miller-Fisher $ (Areflexia, Ataxia, Opthalmoplegia AAO)
7. Metabolic and Toxic Myopathies
8. Snake bite (Cobra, Kraits)
9. Brain stem disease
Clinical Classification
1. Ocular MG (15%)
2. Generalized MG (85%)
Subtypes
1. AChR/MuSK Seropositive/Seronegative
2. Thymoma/No Thymoma
3. Ocular (2 yrs)/Generalized
4. Congenital (Possible MG but tests negative)
Osserman Grading (From R R. Baliga)
I.
Focal (Ocular)
II.
a. Mild generalized, Slow progress, No crisis, Drug response
b. Moderate generalized, Severe skeletal and bulbar, No crisis, Less Drug response
III.
Acute respiratory crisis, Poor drug response, High incidence Thymoma and Mortality
IV.
Late Severe, Takes 2 years from I to II, Respiratory crisis, High Mortality
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MGFA Classification
1. Any ocular muscle weakness
2. Mild generalized weakness*
3. Moderate generalized weakness*
4. Severe generalized weakness*
5. MG crisis needed for intubation with or without mechanical ventilation
*a. Axial predominant
*b. Bulbar predominant
Associated Diseases (HLA B8 DR3)
1. Hyperthyroidism or Goitre (13%)
2. Other Autoimmune diseases
(RA, SLE, Sjogren, Sarcoid, Pernicious anaemia, Diabetes, PM, Pemphigus, UC)
Pathophysiology
Autoantibody against nAChR on Post-synaptic membranes of NMJ, impair NM transmission.
1. Complement-mediated destruction of nAChRs
2. Damage with loss of normal folds of PSM
3. Functional blockage of nAChRs
4. Accelerated endocytosis and breakdown of nAChRs
5. Cross-linking 2 adjacent nAChRs by Anti-AChR antibody
Factors exacerbating MG
1. Physical exertion, Hot temperature, Emotional upset, Infection, Surgery, Menstruation,
Pregnancy, Hyperthyroidism, Hypokalaemia
2. Drugs
a. Antibiotics: Aminoglycosides, Quinolones, Macrolides, Tetra
b. CCB, β Blockers
c.
Steroid, D-penicillamine
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d. Antiarrhythmics: Quinidine, Procainamide, Licocaine
e. NMBA: Succinylcholine, Suxamethonium, Pancuronium
f.
Phenytoin
g. Quinine, CQ
Tests for MG
1. Fatigability test (Count 1-50)
2. Ice pack test (Sensitivity 80%, Specificity 100%) (Ptosis improves 2 mm after 2 mins)
3. Cogan’s lid twitch (Downward for 10-20 sec)
4. Peek sign (Close eyes for 20-30 sec)
5. Sleep test (30 mins)
6. Tensilon test (Edrophonium) (Sen 80-90%, Spec 98%)

CPR facility and Inj. Atropine in hand

Initial IV 1-2 mg. If no response after 60 sec, give 8-9 mg
SEs: Bradycardia, Hypotension, Resp depression, Arrhythmia
Positive: if weakness improve (Ptosis, Nasal voice, Strabismus)
False positive: MND (ALS), LEM$, GBS, Botulism, Polio, Myositis
Hering’s law

When ptotic eyelid is lifted manually, other eyelid becomes ptotic.
Investigations
1. (Seropositive) Anti-AChR antibody (+) in 80-90%
(Seronegative) Ocular MG
2. Anti-MuSK antibody (+) in 30-40% of Seronegatives, usually in Female, Neck, Bulbar, Resp.
3. Striated muscle antibody (+) in 80% of Thymomatous MG, and 30% of Non
4. CT/MRI (Chest): Thymic hyperplasia (70-80%), Thymoma (10%)
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Differences between MG and LEM$
MG
LEM$
Antigenic target
Post-synaptic nAChR
Pre-synaptic V-gated Ca2+
Diplopia
Common
Rare
Ptosis
Common
Rare
Tendon reflexes
Normal
Reduce (↑with Exercise)
Weakness
Proximal (UL > LL)
Proximal (LL > UL)
Autonomic dysfunction
No
Yes (Cholinergic)
Associations
Autoimmune disease
SCLC (60%)
Female : Male
2:1
1:2
Repetitive nerve stimulation
Decrement (3Hz stimulation)
Increment (20Hz)
Single fiber EMG
Normal
Decreased amplitude
Treatment
AChEI, Immunotherapy
Treat tumour,
3, 4-diaminopyridine
Plasma pheresis

For MG Crisis or Pre-op preparation

2-4 L per exchange, 5-6 times within 1-2 weeks

Effect lasts only for 6-8 weeks

CI: Vascular instability, Systemic sepsis, Venous access problems
Immunoglobulin

Alternative to Plasma exchange

For MG Crisis or Preparation before Thymectomy and early Post-op

IV 0.4 g/kg/day for 5 days

CI: Hypercoagulable states, Renal failure
Thymectomy
Aim:
1. To remove source of Ag stimulation (B cells and Immunomodulation)
2. To prevent local invasion of Thymoma
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Indications (VC must be >20 mL/kg)
1. Thymoma
2. Anti-AchR antibody (+)
3. <45 years
4. Generalized MG <7 years
Improvement noted 1-10 years after surgery (Baliga)
Beneficial in 85% and 35% goes into drug-free remission
Acute Crisis
Cholinergic Crisis (SLUDGE BBBB)
1. Small pupils, Sweating, Salivation
2. Lacrimation
3. Urination
4. Diarrhoea
5. GI upset
6. Emesis
7. Bradycardia, BP↓, Bronchorrhoea, Bronchoconstriction
8. Confusion
Stop Pyridostigmine and Monitor
Myasthenic Crisis
1. Exacerbation of myasthenia leading to paralysis of Respiratory and Bulbar muscle that
require an urgent respiratory support.
Stop exacerbating factors, Stop Pyridostigmine (↑Bronchorrhoea), PE/IVIG
Clinical assessment of Myasthenic crisis
1. Rapid, Shallow breathing
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2. Paradoxical breathing
3. Inability to count 1-25 in single breath
4. ↓Strength of cough
5. Stridor in life-threatening upper airway obstruction
Indication for Intubation
1. VC <1L (≤15 ml/kg)
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Parkinsonism
1. Inspection (Front, Sides): Masked Face, Infrequent Blink, Ask to Close Eye (Bell?)
2. Voice (Name)
3. Tremor (Pill-rolling)
4. Rigidity (Cogwheel) [Distraction]
5. Bradykinesia [Distraction]
6. Glabellar tap (Mayerson sign)
7. Parkinson Plus (Vertical gaze palsy, Jaundice, KF Ring, Cerebellar, Pyramidal)
8. Walk (Stooped posture, Reduced arm swing, Short strike Shuffling, Festinating gait)
9. Ask Hand-writing, Pull test, BP
Presentation
1. This patient has a mask-like, expressionless face with infrequent blinking and low-volume,
monotonous speech.
There is continuous pill-rolling tremor of hands with lead-pipe rigidity at the elbows and
cogwheel rigidity of wrists.
There is bradykinesia with decreased amplitude of movements.
Tremor, rigidity and bradykinesia are more marked on right side.
Hand writing shows micrographia.
There is no cerebellar and pyramidal sign. There is no gaze palsy.
On standing, he has stooped posture, difficult to start and stop walking. He walks with
hesitant, shuffling, narrow-based gait with reduced arm-swinging.
Dx: Parkinsonism most probably due to idiopathic Parkinson’s disease with walking difficulty.
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FAQs
Parkinsonism

It is a movement disorder characterized by bradykinesia and at least one of

Resting tremor, Rigidity, and Postural instability
Causes
1. Idiopathic (PD) – the most common cause
2. Drugs: Chlorpromazine, Metoclopramide, Valporate, Methyldopa
3. Tumours of the basal ganglia
4. Lewy body dementia
5. Wilson’s disease
6. Normal pressure hydrocephalus
7. Post-encephalitis
8. Anoxic brain damage
9. Toxins: CO, MPTP (Methyl Phenyl Tetrahydropyridine), Mangnese
10. Parkinson Plus $
a. PSP (Steel-Richardson-Olzewski $) (Supranuclear gaze palsy + Cognitive impair)
b. MSA (Parkinsonism + Cerebellar + Autonomic)
c.
Corticobasal degeneration
Lewy bodies

Spherical, eosinophilic, cytoplasmic inclusions: primary component is α-synuclein, found in
brainstem and cortex.

PD, Lewy body dementia, Alzheimer
Essential tremor

Symmetrical and worse with voluntary movement, often accompanied by a voice and head
tremor (titubation).

Writing exacerbates tremor and script becomes larger and irregular.
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Wrist Drop (Radial nerve palsy)
1. Inspection: Wasting, MCPJ Extension (IPJ Preserved), Wrist extend
If No sensory loss & Radial Deviation (+) → Consider Posterior Interosseus N. lesion
2. Power (MCPJ, Wrist, Brachioradialis, Triceps) (Site of Lesion)
3. Reflexes (Triceps)
4. Screen:
Thumb Abduction + Oschner’s Clasping Test for Median
Finger Abduction + Froment’s Sign for Ulnar
5. Sensory: 1st Dorsal Interosseous, Anatomical Snuffbox
6. Function
7. Aetiology: Inspect Forearm, Elbow, Arm, Axilla, Shoulder, Neck, Nerve thickening, Gum Line
8. Ask: Injury h/o, RBS, NCS
Presentation
1. This patient has wrist drop on the right. There is weakness of extension at the wrist and at the
MCP joints. Extension at IPJ is normal. Finger abduction and adduction is normal.
There is weakness of forearm supination and elbow flexion with forearm held in between
supination and pronation.
The tricep motor power as well as tricep jerk is intact.
There is sensory loss over the first dorsal interosseous.
There is a scar noted at medial aspect of arm.
Dx: Right radial nerve palsy most likely site of lesion is in the middle third of humerus (spiral
groove).
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FAQs
Course and Anatomy of Radial nerve
1. It originates from the posterior cord of the brachial plexus, innervated by C5-T1 spinal roots.
2. In the axilla, it gives of branch to tricep muscle and 3 sensory branches that supply the skin
over triceps and posterior forearm.
3. It then wraps around the middle third of the humerus and travels down the spiral groove.
4. After exiting the spiral groove, it supplies brachioradialis and extensor carpi radialis longus
then divides into posterior interosseous and sensory branches.
5. Posterior interosseous nerve supplies supinator muscle and extensor carpi ulnaris, then dives
into supinator muscle through the fascia, under the arcade of Frohse, to supply wrist and
finger extensors.
6. Sensory branch arises at elbow and travels down the forearm to become superficial at wrist.
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Sensory Levels
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Macleod 13th Ed. Page. 267
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Causes of Radial nerve palsy
1. C7-8 root
a. Trauma
b. Cervical spondylosis
c.
Cervical rib
2. Axilla
a. Trauma
b. Compression (Crutch)
3. Spiral groove
a. Trauma
b. Compression (Saturday night palsy)
c.
Lead poisoning, Leprosy, Mononeuritis
4. Proximal forearm
a. Trauma
b. Subluxation of the radius
c.
Elbow synovitis
d. Tumour (Lipoma)
e. Supinator muscle hypertrophy (Entrapment neuropathy)
5. Wrist
a. Trauma
b. Compression (Tight bracelet or handcuffs)
Level of Lesion
1. C7-8 root – Radial deviation preserved, Sensory loss on C7-8 dermatones
2. Axilla – All gone including triceps and triceps reflex
3. Humerus
a. Upper 1/3 – All is lost
b. Middle 1/3 – Triceps and Triceps reflex preserved
c.
Lower 1/3 – Triceps and Brachioradialis preserved
4. Elbow
a. Triceps and Brachioradialis preserved
b. PIN – Sensory normal
5. Forearm (PIN) – Sensory normal
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Foot Drop
1. Inspection: Foot drop, Wasting, Fasciculation
2. Power
a. Dorsiflexion (-) → Deep Peroneal Nerve Palsy
b. Eversion (-) → Superficial Peroneal
c.
Dorsiflexion & Eversion (-) → Common Peroneal
d. Inversion & Plantar-flexion (-) → Posterior Tibial Nerve Palsy
e. Inversion & Eversion (-) with Plantar-flexion (+) → L5 Root
f.
All (-) → Posterior Tibial + Common Peroneal/ Sciatic/ Plexus/Roots
g. Knee Flexion (Weak) → Sciatic/ Cerebral, Cord (Bilateral)
h. Hip Abduction & Internal Rotation (Weak) →L4-5 Root/ MND (Bilateral)
i.
Straight Leg Raising Test → Sciatic
3. Tone
a. (↑) → Cerebral, Cord (Bilateral)
b. (↓) → MND (Bilateral)
4. Reflexes
a. Ankle (-) → Sciatic, Peripheral Neuropathy/ Friedrich’s Ataxia (Bilateral)
b. Ankle, Others, Extensor Plantar (↑) → Cerebral, Cord (Bilateral)
5. Sensory
a. Between 1st and 2nd Toes (-) → Deep Peroneal
b. Lateral Compartment (-) → Superficial Peroneal
c.
Both (-) → Common Peroneal
d. Glove & Stocking Pattern → Peripheral Neuropathy (Bilateral)
e. Knee & Thigh (-) → Sciatic
f.
L4-5 Dermatomes (-) → L4-5 Root
g. Cut-Off (+) → Cord (Bilateral), Other Leg → Brown Sequard $
h. Normal → Cerebral, Parasagittal/ MND (Bilateral)
6. Aetiology:
Unilateral: Injury, Hyper/Hypo-pigmented Skin Lesions, Rashes, Joints, Nerve Thickening, CA
Bilateral: Pes Cavus, Spine, Transverse Myelitis
7. Gait: High Stepping, Stand on Heel/Toes (-), Hemiplegic → Cerebral
8. Function: Walking Aids
9. Ask: RBS, Fundus, NCS
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Presentation
1. This patient has high stepping gait with a right foot drop. There is a scar over the neck of the
right fibula. There is wasting of anterolateral compartment of right calf with weakness of ankle
dorsiflexion and eversion. Ankle inversion is spared. There is weakness of dorsiflexion of first
toe. The ankle jerk is preserved. There is loss of sensation over the lateral calf and dorsum of
the foot.
Dx: Right common peroneal nerve palsy.
FAQs
Course of Common peroneal nerve
1. L4-S3 nerve roots become sciatic nerve (L4-S2 for Common peroneal, L4-S3 for Tibial)
2. The sciatic nerve splits at or slightly above the popliteal fossa to form the tibial and common
peroneal nerves.
3. Common peroneal nerve winds around fibula from posterior to lateral, (where it is vulnerable
to injury), and divides into the superficial and deep peroneal nerves.
4. Superficial peroneal nerve supplies peroneus longus and brevis (everters) and sensation to
anterolateral part of leg and medial and lateral dorsal foot.
5. Deep peroneal nerve supplies tibialis anterior, extensor digitorum longus, extensor hallucis
longus and peroneus tertius (ankle and toe dorsiflexors) and sensation to the first dorsal web
space.
Causes of common peroneal nerve palsy
1. External compression
a. Plaster cast
b. Tourniquets
c.
Leg crossing
d. Prolong squatting (strawberry picker’s palsy): peroneus longus muscle
2. Trauma
a. Direct trauma to nerve
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b. Fibular #
c.
Following total knee arthroplasty
3. Causes of Mononeuritis Multiplex (Leprosy is the commonest) WARDS PLC
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Sensory Levels
Macleod 13th Ed. Page. 267
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Ulnar nerve palsy
1. Inspection (Wasting, Dorsal guttering, Claw, Scar)
2. Power (Fingers, Thumb, Frogment’s sign)
3. Sensory
4. Aetiology (Nerve thickening, DM, Injury, Syringe)
Median nerve palsy
1. Inspection (Wasing thenar)
2. Power (LOAF, Pen touching, Ochsner’s Clasping)
3. Tinel’s sign
4. Sensory
5. Aetiology (Nerve thickening, DM, Injury, Syringe)
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Miscellaneous Short Cases
Fundoscopic Examination
1. External Eye Exam: Lids, Conjunctiva, Anterior Segment: Cornea, AC, Pupils/Iris, Lens
2. Evidence of Systemic Diseases: Arcus lipidus, Necrobiosis lipoidica, Foot ulcers (DM)
3. Visual Acuity: Far Vision (6 m/Counting Fingers/Light Perception), Near Vision (15 inches)
with or without Glasses
4. Structures in front of fundus:
↳
Red Reflex Both Eyes (Lens for Cataract)
↳
Vitreous for opacities (Asteroid Hyalosis, Preretinal/Subhyaloid or Subretinal
Haemorrhage, Fibrous Tissue or New Vessels)
5. Optic Disc 4C’s: Colour, Contour (Margin, Shape, Elevation), Cup-Disc Ratio (0.1-0.3),
Caliber of Vessels (A:V = 2:3), Vascularity, Blurring, Suffused and Elevated, Haemorrhages
6. Retinal Vessels: Calibre, Silver Wiring, AV nipping, Venous Engorgement, Pulsation
7. Four Quadrants
↳
Haemorrhages: Dots (Microaneurysms), Blots (Deep Haemorrhages), Flame-shaped
(Superficial Haemorrhages)
↳
Exudates: White/Yellow and Shiny with Well-defined Margin (Hard), Fluffy with Illdefined Margin Cotton wool spots (Soft/Infarct)
↳
New Vessels
↳
Photocoagulation Scars
8. Periphery of Retina: Ask patient to look Up/Down/Temporally/Nasally
9. Macula: (2 Disc Temporal) Ask to look at the Light.
10. If Optic Disc Swelling (+): Ask Test Visual Field (Central Scotoma), Enlarged Blind Spot, Red
Desaturation, Pupil Response if not dilated (Direct & Consensual, RAPD)
11. Ask Tenderness & Palpate Temporal region in Elderlies
12. Request: EOM, BP, RBS, Lipid Profile, Smoking Cessation Counselling
Presentation
1. Papilloedema
On examination of both eyes, optic discs appear hyperaemic with blurred margins. Retinal
veins are dilated and tortuous with loss of spontaneous pulsation. There are haemorrhages,
cotton wool spots and exudates around the disc.
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Dx: Papilloedema with preserved visual acuity
2. Diabetic Retinopathy
On examination of right eye, optic disc has normal colour with clear margin. There are
microaneurysms, dot haemorrhages, and hard exudates in superior temporal quadrant. In
particular, there are multiple large blot haemorrhages and cotton wool spots and venous
beading. There are leashes of new vessels in inferior temporal quadrant. Photocoagulation
scars are also seen in inferior temporal quadrant.
Hard exudate on the right macula with macula oedema associated with reduced visual acuity.
On examination of left eye, optic disc has normal colour with clear margin. There are
microaneurysms, dot haemorrhages, and hard exudates in inferior temporal quadrant. In
particular, there are multiple large blot haemorrhages and cotton wool spots. There are
leashes of new vessels in inferior temporal quadrant. Photocoagulation scars are also seen in
inferior temporal quadrant.
Dx: Proliferative diabetic retinopathy treated with laser photocoagulation in both eyes with
maculopathy affecting the right eye.
3. Hypertensive Retinopathy
On examination of the right eye, optic disc has normal colour with blurred and raised margins.
the retinal arterioles are tortuous, thickened, and narrowed with enhanced light reflex (silver
wire appearance). There is AV nipping at AV junctions. There are microaneurysms, dot and
blot haemorrhages, flame-shaped haemorrhages at superior temporal quadrant, cotton wool
spots, and hard exudates. There is papilloedema.
On examination of the left eye, there is silver wiring appearance of arterioles, AV nipping,
flame-shaped haemorrhages at inferior temporal quadrant. Papilloedema is also present.
Dx: Grade IV hypertensive retinopathy
4. Optic Atrophy
On examination of the right eye, optic disc colour is pale, margins are distinct. (If pupils are
not mydriated, there is loss of direct light reflex whereas consensual light reflex is preserved).
Visual acuity is reduced. Visual field testing reveals a central scotoma.
On examination of the left eye, the same as right eye or normal.
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Dx: Optic Atrophy
5. Central Retinal Artery Occlusion
On examination of the
6. Central Retinal Vein Occlusion
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FAQs
Papilloedema

Swelling of the optic nerve head as seen on fundoscopy.
Stages
1. Increase in venous caliber and tortuosity
2. Loss of spontaneous venous pulsation with vessels seeming to disappear suddenly on the
surface of the disc. Disc appears hyperaemic.
3. Blurring of the discs on nasal side
4. Whole disc becomes suffused and slightly elevated. The margins may disappear and vessels
seem to emerge form a mushy swelling. The optic cup is filled and there are haemorrahges
and exudates and cotton wool spots around the disc.
Causes
Raised ICP
1. BIH
2. Intracranial SOL (Tumour, Abscess, Haematoma)
3. Venous sinus thrombosis
4. Cerebral oedema
5. Hydrocephalus
6. Meningitis
7. Encephalitis
Others
1. Malignant hypertension
2. CRVO
Unilateral optic disc swelling
1. Venous sinus thrombosis
2. Grave’s opthalmopathy
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3. CRVO
4. Toxoplasmosis
5. AION
Foster-Kennedy $

Intracranial tumour press on the optic nerve causing ipsilateral OA, contralateral papilloedema
Difference between Papilloedema and Papillitis
Papilloedema
Papillitis
Unilateral/Bilateral
Bilateral
Unilateral
Visual acuity
Only affected late
Reduced
Colour vision
Red desaturation
Normal
Visual field
Enlarged blind spot
Central scotoma
Constriction of fields
Eye movements
Not painful
Painful
Marcus Gunn pupil (RAPD)
Absent
Present
Causes of Papillitis/ Optic Neuritis

Demyelination: MS, NMO (Devic disease)

Infections: Lyme, HIV, Viral encephalitis

Inflammation: Syphilis, Sarcoid
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Diabetic Retinopathy
Stages
1. Background retinopathy
Microaneurysms (dots), haemorrhages (blots) and hard exudates (lipid deposits)
2. Pre-proliferative retinopathy
Cotton-wool spots (retinal infarcts), haemorrhages, venous beading.
3. Proliferative retinopathy
New vessels formation
4. Maculopathy
Hard exudate around the macula causing clinically significant macular oedema: within 500 µm
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Macula

2 discs diameter temporal to the optic disc
Other ocular manifestations of DM
1. Cataracts
2. Rubeosis iridis (New vessels on iris)
3. Glaucoma (complicating from rubeosis iridis)
4. Visual changes (secondary to osmotic changes in the lens)
5. EOM paralysis secondary to Mononeuritis multiplex
6. Increased external eye infections
7. CRVO
8. CRAO (co-existent atherosclerosis)
9. Hypertensive retinopathy (co-existent hypertension)
Factors worsening DR
1. Poor glycaemic control
2. Hypertension
3. Anaemia
4. Diabetic nephropathy (proteinuria)
5. Hyperlipidaemia (increased risk of leakage and hard exudate)
6. Pregnancy (5% background retinopathy develop proliferative retinopathy)
7. Tight glycaemic control in patient with previous poor control
Indications for ophthalmologist referral
1. Macular involvement
2. Pre-proliferative retinopathy
3. Proliferative retinopathy
4. Advanced eye disease: Vitreous haemorrhage, retinal detachment, rubeosis iridis
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Hypertensive Retinopathy
Grading
1. Arteriolar thickening, tortuosity and increased reflectiveness (silver wiring)
2. 1+ Constriction of veins at arterial crossings (AV nipping)
3. 2+ Evidence of retinal ischaemia (flame-shaped or blot haemorrhages and cotton wool
exudates)
4. 3+ Papilloedema
Malignant or Accelerated phase hypertension

Rapid rise in BP leading to vascular damage (fibrinoid necrosis)

Usually with severe hypertension >200/130 mmHg + Grade 3/4 retinopathy
Hypertensive emergencies

Malignant hypertension with acute renal failure, heart failure or encephalopathy.
Optic Atrophy
Causes
Inherited
1. Leber’s hereditary optic neuropathy
2. Friedreich’s ataxia
3. DIDMOAD $
Acquired (* Common causes of Primary OA)
1. Post optic neuritis
2. MS*
3. Compression*: tumours of anterior visual pathways
4. Ischaemia: temporal arteritis, CRAO
5. Toxic: Methanol, tobacco, cyanide, arsenic, lead
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6. Drugs: Ethambutol, INH, Ccol, Quinine
7. Metabolic: B12 deficiency (SACD), Diabetes
8. Infiltration: Syphilis, Sarcoid, TB
9. Others: Trauma, Glaucoma*, Retinitis pigmentosa,
10. Post papilloedema (Secondary OA): yellow/grey disc with blurred margins
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Goitre
1. Thyroid: Inspection: Deglutition, Tongue protrusion
Ask Pain & Palpate Move with deglutition, Tenderness, Consistency, Thrills, Pulse, Margin
(Lateral, Upper, Lower, Isthmus)
Percussion: Retrosternal Extension of Goitre
Auscultation: Bruit
2. Eyes: Proptosis, Exophthalmos, Lids Retraction, Lids Lag, Vision, EOM, Diplopia
3. ULs: Tremor, Acropachy, Sweating, Pulse (Rate, Character), Proximal Myopathy
4. LLs: Pretibial Myxoedema, Proximal Muscle Weakness, Knee & Ankle Jerk
5. Associations: Fever, A+, Buccal Pigmentation, Vitiligo
6. Ask: BP, RBS, TFT
Presentation
1. Grave’s Disease
This patient looks anxious and he has diffusely enlarged thyroid gland. There is no
tenderness. There is no retrosternal extension. Thyroid bruit is heard at both upper poles.
Patient has bilateral exophthalmos associated with lid retraction and lid lag. Visual acuity is
normal. There is opthalmoplegia and resultant diplopia. Thyroid acropachy is present with
warm, moist and sweaty hands. Fine tremor of outstretched hands is noted. Pulse is 76 bpm
with regular rhythm. Proximal myopathy of both upper and lower limbs is present. There is no
pretibial myxoedema. Tendon reflexes are exaggerated. There is no feature of associated
autoimmune disorders.
Dx: Thyrotoxicosis due to Grave’s disease at partially treated state without features of
associated autoimmune diseases.
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FAQs
Features of Graves’ disease
1. Diffuse goitre with bruit
2. Graves’ opthalmopathy (Proptosis, Exophthalmos, Chemosis, Keratitis, Corneal ulceration)
3. Thyroid acropachy
4. Pretibial myxoedema
Causes of Proptosis
1. Graves’ disease
2. Cavernous sinus thrombosis
3. Carotico-cavernous fistula
4. Orbital cellulitis
5. Retro-orbital tumour
6. Trauma
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Systemic Sclerosis
1. Inspection: Hands: Fingers, Forearms, Arms, Chest
Face: Scalp, Forehead, Nose, Mouth 3 fingers, Ulcers, Pigmentations
2. Ask Pain & Palpate:
Fingers: Tight skin, Calcinosis, Coldness
Joints: Tenderness, Tinel’s sign
Functions: Handgrip, Unbuttoning/ Buttoning
Forearm, Arm, Chest, Proximal muscle weakness, pain and tenderness
3. Inspect & Palpate: Lower Limbs, Pedal oedema
4. Inspect, Palpate & Auscultate Abdomen
5. Auscultate: Chest & Back
6. Association: A+, J+, Buccal Pigmentation, Goitre, Vitiligo
7. Ask: BP, Raynaud, Nailfold capillaroscope
8. Ask: Dysphagia, DOE, Urine Output
Presentation
1. Skin over the face, upper and lower limbs appears smooth, shiny and tight. There is loss of
facial wrinkles, perioral puckering with restrictive mouth opening. There is telangiectasia of
the face. On examination of the hands, there is sclerodactyly with atrophic nails. There is
atrophy of soft tissues at the finger pulps. There are palpable nodules of calcinosis on some
fingers. There is salt and pepper skin pigmentation on her chest.
Dx: Diffuse cutaneous systemic sclerosis without features of pulmonary hypertension,
arthropathy and myositis.
FAQs
Diffuse scleroderma (Anti-Scl 70 topoisomerase 1, Anti-RNA polymerase

Diffuse involvement of skin: trunk and extremities

Early involvement of lungs, kidneys, gut and heart
Limited scleroderma (Anti-centromere antibody, ANA, RF)

Skin is affected only at extremities and/or face

CREST

Late involvement of lungs, pulmonary hypertension

Renal crises are rare
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Scleroderma sine scleroderma

Organ involvement without skin involvement
Systemic sclerosis (SSc)
ACR/EULAR 2013 Criteria (Definite SS if Score ≥9/24)
(1) Skin thickening

Skin thickening of fingers of both hands Proximal to MCP (9)

Skin thickening of whole fingers Distal to MCP (4)

Skin thickening of fingers, Puffy fingers (2)
(2) Telangiectasia (2)
(3) Finger tip lesions

Pitting scars (3)

Digital tip ulcers (2)
(4) Abnormal nailfold capillaries (2)
(5) Raynaud’s phenomenon (3)
(6) Scleroderma related Ab (Any ACMA, ATPI1, AScL 70, ARNA-P3) (3)
(7) PAH and/or ILD (2)
CREST

Calcinosis, Raynaud, Esophageal dysmotility, Sclerodactyly, Telangiectasia
Renal failure is the major cause of death.
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RA Hands
1. Inspection: Joints (Swelling, Deformities), Nails (Onycholysis, Infarct), Skin, Scars, Muscle
wasting, Nodules
2. Ask Pain and Palpation: Tenderness, Nodules, Tinel’s sign
Functions: Nerves (Radial, Median, Ulnar nerves), Grip, Fine movement, Joint movements
Muscle Tenderness
Proximal muscle weakness
3. Lower Limbs: Nails, Joints, Skin, Muscle wasting, Ask Pain and Palpate Tenderness (Jt, m/s)
4. Spine, SI Joints
5. Extra-articular: Fever, Eyes (A+, J+, Episcleritis), Heart, Lungs, Abd: Felty’s
6. Associations: MCTD (SLE, RA, SS, PM/DM, Sjogren’s $)
7. Proximal Myopathy: Lower Limbs, Gait
8. Ask: Dry Eyes/Mouth
9. Test: ESR/CRP
Presentation

There is a symmetrical deforming arthropathy of the small joints of the hands involving the
PIP and MCP joints with sparing of the DIP joints. There is spindling of the fingers due to soft
tissue swelling. There is palmar subluxation at the MCP joints and ulnar deviation of the
fingers. The deformities present include swan-neck deformities, Boutonniere’s deformities,
and Z deformity of the thumb.

There is generalized wasting of small muscles of the hand and use is restricted by weakness,
deformity and pain. There are nodules at the elbow, over the extensor tendons and in the
palm.

There are arteritic lesions in the nail-folds. The presence of erythema, warmth, pain and
swelling suggests that there is active inflammation at present.

There is no feature of associated autoimmune disorders.
Dx: Chronic Rheumatoid Arthritis Hands with deformity and functional limitation
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FAQs
Ref: ACR Guideline, OHCM9, Mehta, Davidson22, Freeman
RA Diagnosis Criteria (ACR/EULAR 2010)
A. Large: Shoulders, Elbows, Hips, Knees, Ankles. Small: +Wrist, Exclude DIPs, 1st CMJ, 1st MTP
B. Serology Low +ve ≤3 times ULN, High +ve >3 times ULN
D. Current clinically involved joint
Deformities
1. Swan-neck deformity: Hyperextension at PIP joint and flexion at MCP and DIP joints
2. Boutonniere’s deformity: Flexion at PIP joint and Hyperextension at MCP and DIP joints
3. Z deformity: Flexion at IP joint and Hyperextension at MCP joint
Severity
DAS 28 (TJC, SJC, GH, ESR)
1. High activity >5.1
2. Moderate 3.2-5.1
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3. Low 2.6-3.2
4. Remission <2.6
Rheumatoid Factor

IgM antibody against constant portion (Fc) of own IgG (Sensitivity 70%)

Up to 5% + in Normal population

20% + in people >65 yr
Anti-cyclic Citrulinated Peptide (Anti-CCP)

Sensitivity 70% in Early RA

Specificity 95%
Poor prognostic factors for RA
1. Functional limitation (FHS III/IV)
2. Extra-articular manifestation
3. Positive Rh factor and Anti CCP
4. Bony erosion by radiograph
Extra-articular manifestations of RA
1. Episcleritis, Scleritis, Scleromalacia, Keratoconjunctivitis sicca
2. Nodules at elbow (25%) and lungs
3. Lymphadenopathy
4. Vasculitis
5. Fibrosing alveolitis, Obliterative bronchiolitis
6. Pleural and Pericardial effusion
7. Raynaud’s, Carpal tunnel $, Peripheral neuropathy
8. Splenomegaly, Felty’s $ (5%, 1%)
9. Osteoporosis
10. Amyloidosis
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DDx of Rheumatoid nodules
1. Gouty tophi
2. Xanthomata
3. Bone tumours
4. Cutaneous sarcoidosis
Causes of Anaemia in RA
1. Anaemia of chronic disease
2. GI blood loss due to NSAIDs and Steroids
3. Folate deficiency due to methotrexate
4. Bone marrow suppression (Methotrexate, Sulphasalazine)
5. Felty’s syndrome
6. AIHA
7. Pernicious anaemia
Eye diseases in RA
1. Episcleritis, Scleritis, Scleromalacia, Keratoconjunctivitis sicca
2. Sjogren’s $
3. Opthalmoplegia due to Mononeuritis multiplex
4. Penicillamine-induced MG
5. Steroid-induced cataract
6. CQ-induced corneal deposits or retinopathy
Episcleritis vs Scleritis
1. Episcleritis: Painless
2. Scleritis: Painful with reduced vision
DMARDs
1. Prednisolone 2.5-10 mg OD
2. HCQ 200 mg OD
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Synthetic (sDMARDs)
Conventional synthetic (csDMARDs)
1. MTX 7.5-15 mg weekly (+ Folic Acid 5 mg weekly)
2. Leflunomide 60 mg OD 3 days f/b 20 mg OD
3. Sulfasalazine
Targeted synthetic (tsDMARDs)
1. Tofacitinib
Biological (bDMARDs)
1. TNFi (Infliximab, Etanercept)
2. Non-TNFi (Rituximab B-CD20, Tocilizumab IL-6)
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Ankylosing Spondylitis
1. General quick survey
2. Look from the side: Protuberant abdomen (Kyphosis)
3. Loss of cervical and lumbar lordosis with increased thoracic kyphosis, ? posture
4. Cervical movements (Look up, down, left, right. Rotate left, right)
5. Ask to stand with their back to the wall, assess occiput to wall distance. (Flesche’s test)
6. Lumbar spine movements (Bend forward, left, right. Rotate left, right)
7. Measure chest expansion at 4th ICS with patient’s hands behind their head. (<2.5 cm, Ñ >5)
8. Sacroilitis, Heel pain
9. Systemic manifestations: Anterior uveitis (red eyes), Apical lung fibrosis, AR
10. Alternatives: Psoriasis: Nails, Hairline
11. I would like to perform Modified Schober’s test to further assess spinal mobility. (<5 cm)
Presentation
1. This patient has a protuberant abdomen, and severe kyphosis with loss of cervical and
lumbar lordosis having “question mark” posture. There is decreased cervical and lumbar
spine movements in all directions. Increased occiput to wall distance and decreased chest
expansion is also noted. There is no features of Anterior uveitis, Apical lung fibrosis, AR,
sacroilitis and enthesitis. There is no evidence of psoriasis.
Dx: Ankylosing Spondylitis
FAQs
Ankylosing Spondylitis
1. Symptomatic sacroilitis (persistant pain and stiffness for >3 months) associated with morning
stiffness and improvement on exercise or worsening with rest.
Systemic manifestations (6 As)
1. Anterior uveitis 40%
2. Atlanto-axial subluxation
3. Apical pulmonary fibrosis
4. AR (MVP can also occur)
5. AV conduction defects 10%
6. Achilles tendonitis – enthesitis. Amyloidosis (rare cause)
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Knee and Hip joints are most commonly effected. 20-30%
Genetics

Male : Female 8:1

HLA-B27 95%

6% out of 8% patients with HLA-B27, develop AS. 80-fold
Seronegative arthritis (PEAR)
1. Psoriatic arthropathy
2. Enteropathic arthritis
3. AS
4. Reactive arthritis
Management
1. Risk of HLA-B27 in offspring 50%
2. These children have 1:3 risk of developing disease
3. Overall risk is 1:6
4. Physiotherapy, Swimming
5. Occupational therapy
6. Pharmaco: Analgesics, NSAIDs, Pulse corticosteroid,
7. DMARDs Methotrexate, SSZ have effect on peripheral disease but not on spine
8. Biological: Adalimumab, Etanercept
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Psoriasis
1. General survey
2. Inspection: Skin: Extensor surfaces, Scalp, Behind the ears, Navei (5 types)
Inverse psoriasis (flexor surfaces, intertriginous areas)
(Well demarcated, Salmon pink plaques with Silvery white scales)
Tiny punctate bleeding (Auspitz sign)
3. Nails: nail pitting, onycolysis 20% of uncomplicated, commonly with arthropathy
4. Psoriatic arthropathy (5 types)
5. Other systemic associations:
a. Musculoskeletal: Gout
b. Eyes: Conjunctivits, Uveitis
c.
CVS: AR
d. Respiratory: Apical lung fibrosis (rare)
6. Complications: J+, Fine Basal Crepts (Methotrexate)
Presentation
1. There are well-defined erythematous plaques with silvery white scales over the extensor
surfaces, scalp, navel, and behind the ears. There is nail pitting, and onycholysis. In addition,
there is an asymmetrical arthropathy of the hands mainly involving the DIP joints. Gouty tophi
are also noted on fingers.
Dx: Chronic plaque psoriasis and psoriatic arthropathy associated with chronic tophaceous
gouty arthritis.
FAQs
DDx of arthropathy
1. OA
2. RA
Genetics of psoriasis

HLA-B13, B17
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Types
1. Chronic plaque psoriasis (most common)
2. Pustular psoriasis (palmoplantar)
3. Guttate psoriasis (rain-drop shaped palques occur 2 week after sore throat, resolve 1-2 mths.)
4. Palmoplantar psoriasis
5. Erythrodermic psoriasis
Exacerbating factors
1. Trauma
2. Sunburn
3. Stress
4. Alcohol
5. Smoking
6. Streptococcal infection (guttate psoriasis)
7. Drugs (ACEI, β blocker, Anti-malarial, Lithium)
Koebner phenomenon
1. Psoriasis
2. Lichen planus
3. Vitiligo
4. Viral warts
5. Pemphigus, Pemphigoid
Treatment
1. General: Education, Avoid exacerbating factors
2. Topical: Emollients, Salicylic acid, Topical steroids
3. UVB phototherapy
4. Systemic: PUVA, Steroids, MTX, AZA, Cyclosporin
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Vitiligo
1. General quick survey
2. Inspection: Site, Size, Shape, Margin, Nature, Scalp, Hair
3. Palpation: Reduced Sensation
4. Aetiology: Nerve thickening, Hansen, Fungal (+ Nails), Albinism, Burns, Radiodermatitis
5. Association: Pernicious A+, J+, Buccal Pigmentation, Goitre
6. Ask: RBS (DM), Fatiguability (GBS)
Presentation
1. This patient has well-demarcated areas of depigmentation on the face, dorsal surfaces of
hands, extensor surfaces of the elbows and knees and dorsal surfaces of the feet.
Dx: is Vitiligo
FAQs
Differential Dx
1. Pityriasis versicolour (Malassezia furfur)
2. Tuberculoid leprosy
3. Ash-leaf spots of tuberous sclerosis
4. Discoid lupus erythematosus
5. Morphea
6. Lichen sclerosis
7. Naevus depigmentosus
Genetic: Family history of vitiligo (+) in up to 40%.
Histo: Partial or complete loss of melanocytes.
Associations
1. Alopecia areata
2. MAGIC S
Treatment
1. Corticosteroids (Topical and systemic)
2. Topical Tacrolimus ointments
3. Photochemotherapy (PUVA) Psoralen + UVA
4. Narrow-band UVB phototherapy
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5. Surgical: Punch grafts, Minigraft
6. Other measures: Micropigmentation (Tatoo), Depigmentation of normal skin if widespread.
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Acromegaly
1. Hands: Sweating, Doughy, Large, Spade-shaped, Fingers
Carpal Tunnel Syndrome
2. Face: Supraorbital Ridges
3. Nose & Lips: Large
4. Lower Jaw: Protrusion (Prognathism), Malocclusion & Splaying Teeth
5. Tongue: Macroglossia, Dental Impression on Tongue
6. Visual Field: Bitemporal Hemianopia
7. Neck: Goitre
8. Axilla: Skin Tags, Acanthosis Nigrican
9. Chest: Cardiomegaly, Gynaecomastia, Galactorrhoea
10. Abdomen: Hepatosplenomegaly, Mass
11. Joints: Arthropathy: OA, Chondrocalcinosis
12. Spine: Kyphosis
13. Ask: Old Photos, BP, RBS, Headache, Fundoscopy (Hypertensive Retinopathy, OA)
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Neurofibromatosis
1. General survey
2. Inspection: Skin: Fibromata (Axillary freckles), Café au lait spots, Eyes Lisch nodules.
3. Measure (>5/15 mm)
4. Association: Visual Acuity, V1 Sensation, Ask Corneal reflex (5), EOM (6, Cerebellar),
Hearing (8), Facial palsy (7)
Spine: Kyphoscoliosis
Renal bruit
5. Ask: Fundus, BP (RAS, Pheochromocytoma)
dr.nyeinkohein@gmail.com
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