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PACES > PACES Station 3 > Flashcards

PACES Station 3 Flashcards

1
Q

Presenting Cardiac Cases

A

No stigmata of endocarditis
Pulse rate is…, regular/irregular, volume, character
Venous pressure
On examination of chest…

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2
Q

Clinical Features of Aortic Stenosis

A

Slow rising pulse, low volume (severe)
Venous pressure not elevated
Undisplayed heaving apex
Soft second heart sound
Fourth heart sound (not in AF), forced atrial contraction
Ejection systolic murmur, louder in expiration and radiating to carotids

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3
Q

Causes of aortic stenosis

A

Common:

  • bicuspid aortic valve
  • degenerative calcification
  • rheumatic valve disease
  • congenital

Rare:

  • Infective endocarditis
  • Hyperuricaemia
  • Pagets disease of bone
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4
Q

Differential Diagnosis for Ejection Systolic Murmur

A

Aortic stenosis
HOCM
Supravalvular aortic stenosis (Williams syndrome)

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5
Q

Classifying severity in Aortic Stenosis

A

Aortic valve area:

  • normal 3-4cm2
  • mild >1.5cm
  • moderate 1-1.5cm2
  • severe <1cm

Pressure gradient:

  • encorporates aortic valve area, cardiac output and heart rate
  • severe is mean gradient >50mmHg
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6
Q

What is aortic sclerosis?

A

Mild thickening/calcification of trileaflet aortic valve
Absence of outflow obstruction
Affects 1/4 over 65s
Progressive and overtime leads to stenosis
Inc risk of MI and cardiovascular mortality
Atherosclerosis as common aetiology

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7
Q

Clinically differentiating aortic stenosis and sclerosis

A

Normal pulse volume and character in sclerosis

Localised murmur without radiation

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8
Q

Causes of reversed splitting of second heart sound

A 
Severe aortic stenosis
LBBB
HOCM
PDA
WPW B
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9
Q

Complications of aortic stenosis

A 
LVF
Sudden death
Pulmonary HTN
Arrhythmia - AF and VT
Heart block
IE
Systemic emboli
Haemolytic anaemia
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10
Q

Management of asymptomatic patient

A

Ask to report symptoms of angina, palpitations, syncope and breathless
Regular screening
If become symptomatic may warrant valve replacement

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11
Q

Mechanism of Angina in AS

A

May have normal angio

but hypertrophied left ventricle has decreased blood flow reserve so sensitive to ischaemic injury

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12
Q

Mechanism of Syncope in AS

A

low cardiac output state

arrhythmia

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13
Q

Investigation of AS

A

ECG: LVH, left atrial hypertrophy (bifid Pwaves in II), LAD, conduction abnormalities
CXR: rib notching (sign of coarctation), calcification of valve, cardiomegaly (late), prominent pulmonary arteries (pHTN)
Echo: LV function, aortic valve area
Angio: exclude coronary artery disease as cause of symptoms, all being considered for replacement need

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14
Q

Indications for Aortic Valve Replacement in AS

A

Symptomatic severe >50mmHg
Asymptomatic moderate/severe undergoing other cardiac surgery e.g. bypass, other valve

Asymptomatic Severe AS plus any of the following:
- LV dysfunction
- abnormal BP response to exercise
- VT
Valve area <0.6
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15
Q

Williams Syndrome

A

Rare genetic condition: elfin facies, cardiovascular anomalies, mental retardation, sensorineural deficit, high calcium

Cardiac anomalies include supravalvular aortic stenosis, pulmonary stenosis, MR

Deletion in elastin gene chr 7

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16
Q

Role of statins in AS

A

Atherosclerotic process
Use of statins to slow progression

However recent study (SALTIRE) did not show statins to significantly slow progression calcific aortic stenosis

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17
Q

Clinical Features of Mitral Stenosis

A

Irregular low volume pulse (often in AF)
Elevated JVP
Malar flush (low cardiac output state)
Undisplayed tapping apex
Loud first heart sound (if mobile and pliable leaflets)
Opening snap and mid diastolic rumbling murmur heard best in expiration in left lateral position
Features of CCF
Early diastolic murmur at left sternal edge - graham steell murmur of pulmonary regard

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18
Q

Causes of Mitral Stenosis

A 
Rheumatic fever
Congenital
RA
SLE
Carcinoid syndrome
Fabrys disease
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19
Q

Causes of mid-diastolic rumbling murmur

A

Left atrial mass (myxoma)
Left atrial thrombus
Severe MR (inc flow across valve)

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20
Q

Pathophysiology of Mitral Stenosis

A

Normal area 4-6cm2
<2.5cm2 impedes free flow over blood and leads to increased left atrial pressure
Critical stenosis if <1cm2 leads to pulmonary congestion and mimics left ventricular failure but with preserved LV contractility

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21
Q

Clinical Markers of Severe Mitral Stenosis

A 
Early opening snap
Increased length of murmur
Signs of Pulmonary HTN
Signs of Pulmonary congestion
Graham-Steel murmur (PR)
Low pulse pressure
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22
Q

Complications of mitral stenosis

A 
Left atrial enlargement
AF + left atrial thrombus
Pulmonary HTN
Pulmonary oedema
RHF
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23
Q

Differential Diagnosis for Malar Flush

A 
Mitral stenosis
Hypothyroidism
Cold weather
Carcinoid syndrome
SLE
SS
Irradiation
Polycythaemia
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24
Q

Management of Mitral Stenosis

A

Asymptomatic in sinus - endocarditis prophylaxis, regular follow up with echo
Manage AF
Symptomatic - diuretics, as surgery worsens then for surgery

Surgery: closed/open commisurotomy, mitral valve replacement
Indications - pulmonary HTN, haemoptysis, recurrent thromboembolic events despite anticoag

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25
Q

Criteria for Valvuloplasty in Mitral Stenosis

A

Mobile valve
Minimal calcification
No MR
No left atrial thrombus

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26
Q

Cause of Hoarse Voice in Mitral Stenosis

A

Enlarged left atria compresses recurrent laryngeal nerve leading to vocal cord paralysis
(Ortners syndrome)
OR
Hypothyroidism from amiodarone used to treat AF

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27
Q

Clinical Features of Prosthetic Aortic Valve

A 
No features of endocarditis
Prosthetic click after carotid pulse 
Midline sternotomy scar, check for any venous harvest scars re:CABG
Ejection systolic murmur
Anaemia?

Any features of heart failure to suggest valve is functioning well

Any complications of anticoagulation visible

NG Double click suggests -Starr-Edwards ball and cage prosthesis

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28
Q

Indications for Aortic Valve Replacement

A

Severe AS gradient >50mmHg and symptomatic

Asymptomatic AS moderate/severe but needs CABG anyway
Severe AS with LV dysfunction, abnormal BP in exercise, VT, valve area <0.6cm2

Symptomatic severe AR
Asymptomatic AR undergoing surgery anyway
AR with severe LV dysfunction (EF<50%)

Other:
IE failed medical therapy
Enlarging aortic root diameter
Acute severe AR - ruptured valsalva aneurysm

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29
Q

Different types of prosthetic valve

A

Mechanical
-starr-edwards ball and cage - high incidence of haemolysis
Medtronic-Hall - tilting disc valve

Xenografts
-porcine or pericardial

Cadaveric

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30
Q

Indications for Bioprosthetic Valve over Metallic

A

Where anticoag is contraindicated
Shorter life expectancy
>70 years as rate of degeneration slower in this age group

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31
Q

Complications of prosthetic valve

A 
Thromboembolism
Anticoag complications
Valve dysfunction
Endocarditis
Haemolysis
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32
Q

Causes of anaemia in patient with prosthetic valve

A

Blood loss secondary to anticoag
Haemolysis
Endocarditis

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33
Q

Clinical Features of Prosthetic Mitral Valve

A 
No stigmata of endocarditis
Pulse features
Anaemia
Prosthetic click coincides with first heart sound (with carotid pulse) or 2 clicks (Starr-Edwards)
Midline sternotomy scar
Any features of pulmonary HTN
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34
Q

Indications for Mitral Valve Replacement

A

Stenosis with pulmonary congestion, pHTN, haemoptysis or recurrent thromboembolic events

Regurg with LV dysfunction, EF<60%

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35
Q

Clinical Features of Mitral Regurg

A 
No features of endocarditis
Pulse blah blah
Displaced and thrusting apex
Pan systolic murmur radiating to axilla
Any signs of pulmonary HTN/congestion
- if present then loud pulmonary component of second heart sound
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36
Q

Causes of MR

A 
Rheumatic fever
Mitral valve prolapse
IE
LV dilatation (functional MR)
Marfans
Ehlers-Dalos
OI
RA
SLE
Cardiomyopathy
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37
Q

Mechanism of Functional MR

A

In LV dysfunction get dilatation of mitral valve annulus and lateral displacement of papillary muscles

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38
Q

Clinical Signs of Severe MR

A 
Features of pulmonary HTN
Features of pulmonary congestion
Displaced apex
Third heart sound 
Soft first heart sound
Precordial thrill
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39
Q

Differential Diagnosis for Pansystolic Murmur

A

Mitral regurgitation
Tricuspid regurgitation - pulsatile liver, no radiation to axilla, louder left sternal edge
VSD - heard throughout precordium, smaller defect = louder murmur

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40
Q

Management of MR

A

Asymptomatic

  • annual echo
  • endocarditis prophylaxis

Manage AF

Manage HF - diuretics, ACEi, beta blocker

Indications for surgery:
NYHA III despite optimum medical therapy
EF falls below 60% consider

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41
Q

Clinical Features of Aortic Regurgitation

A 
No features of endocarditis
Large volume collapsing pulse
Wide pulse pressure
JVP not elevated
Displaced, thrusting apex
Early diastolic murmur at left sternal edge loudest with patient leaning forward in expiration

Corrigans sign - visible carotid pulsation
Quinkes sign - capillary pulsation in fingernails
De Mussets sign - head nodding with each heart beat

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42
Q

Causes of AR

A 
Bicuspid aortic valve
HTN
Rheumatic fever
Aortitis - Takayasus, ank spond, Reiters, psoriatic arthropathy
RA
SLE
CTD: marfans, ehlers-danlos

Acute causes: dissection, IE, ruptured sinus of valsalva aneurysm

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43
Q

Clinical Signs of Severe AR

A 
Wide pulse pressure
Long duration murmur
Third heart sound
Austin-Flint murmur
Signs of pHTN
Signs of LVF
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44
Q

What is an Austin-Flint Murmur

A

Low frequency mid-diastolic murmur heart at apex caused by aortic regarg jet on anterior mitral valve leaflet (mimics MS)

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45
Q

Causes of collapsing/bounding pulse

A 
AR
Anaemia
Fever
Pregnancy
Thyrotoxicosis
PDA
AV fistula
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46
Q

Role of vasodilators in AR

A

reduce systolic BP as HTN will increase wall stress

ACEi/nifedipine recommended for symptomatic patients

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47
Q

Clinical Features of Mitral Valve Prolapse

A

Late systolic crescendo-decresendo murmur loudest at left sternal edge

Hx: palpitations, atypical chest pains, fatigue, dyspnoea, anxiety

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48
Q

Causes of Mitral Valve Prolapse

A

Primary

Secondary to :
Marfans - high palate, arachnodactyly, pectus excavatum
Ehlers-Dalos - blue sclera, hyper extensible skin, purpura/poor skin healing
Pseudoxanthoma elasticum - pluck chicken skin
OI: blue sclera, hearing aids
PCKD: scars, RRT
SLE

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49
Q

Complications of Mitral Valve Prolapse

A 
Stroke
Chordal rupture
Endocarditic
Arrhythmia (long QT)
Sudden death
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50
Q

Pathophysiology of mitral valve prolapse

A

Collagen dissolution results in myxomatous degeneration. Stretching of leaflets and chordae tendinae

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51
Q

Differential diagnosis for Mitral Valve Prolapse Murmur

A

AS
PS
HOCM
Trivial MR

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52
Q

Management of MVP

A

Reassure asymptomatic
Endocarditis prophylaxis in those with audible click/murmur
Treat arrhythmia
Treat atypical chest pain with simple analgesia and beta blockers

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53
Q

Clinical Features of Pulmonary HTN

A 
Raised JVP with prominent a wave and giant v wave
Pulse ? AF, ? slow due to rate control
Undisplayed apex
Parasternal heave
Loud pulmonary component of S2
Pan systolic murmur if functional TR
Sacral and pedal oedema
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54
Q

Definition of Pulmonary HTN

A

Mean pulmonary artery systolic pressure of >25mmHg at rest

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55
Q

Causes of Secondary Pulmonary HTN

A
  1. Increased pulmonary venous pressure:
    - LV dysfunction
    - Mitral/aortic valve disease
  2. Decreased area of pulmonary vascular bed
    - PE
    - ILD
    - Collagen vascular disease
  3. Chronic Hypoxia
    - COPD
    - ILD
    - OSA
    - Neuromusclar disease
  4. Left to right shunt
    - ASD/VSD
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56
Q

Primary Pulmonary HTN

A

Rare disease effecting children and young adults with pHTN without demonstrable cause
1/10 are familial
Associated with CTD and HIV

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57
Q

Investigations for Pulmonary HTN

A 
ECG for evidence of Right heart strain/left
ABG
CXR: prominent vasculature, oligaemic lung fields, may have large heart or evidence of lung pathology suggesting underlying cause
Echo
CTPA/VQ to exclude clot
Lung functions
HRCT - ILD
Right and left heart catheterisation
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58
Q

Treatment of secondary pulmonary HTN

A 
Treat underlying cause
Diuretics for congestive symptoms
LTOT
Anticoag if VTE
Vasodilator therapy - prostacyclins
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59
Q

Treatment of Primary Pulmonary HTN

A

Diuretics for congestive symptoms to reduce preload to right heart
Anticoag
Vasodilators - nifedipine, prostacyclin analogues
Surgery - atrial septostomy (create right to left shunt)
Transplant

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60
Q

Clinical Features of VSD

A

Parasternal thrill
Pan systolic murmur all over chest, loudest at left sternal edge
Absence of pulmonary HTN or LV enlargement suggests it is haemodynamically insignificant

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61
Q

Causes of VSD

A

Congenital:
Maternal factors - diabetes, PKU, alcohol consumption
Aneuploid syndromes eg trisomy 21, digeorge deletion 22

Acquired:
Post MI
Iatrogenic

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62
Q

Classification of VSD

A

Perimembranous - most common

Supra-cristal, infundibular - rare

Muscular

Posterior

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63
Q

Complications of VSD

A 
IE
Pulmonary HTN
Aortic regurgitation
LV dysfunction
Eisenmengers
Arrhythmia
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64
Q

Mechanism of spontaneous closure of VSD

A

Hypertrophy of muscular septum
Formation of fibrous tissue
Sub aortic tags

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65
Q

Investigations of VSD

A

CXR - large defect cardiomegaly and features of pulmonary HTN
ECG - large defect LV hypertrophy
Echo - location, size and direction of shunt, function and pressures

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66
Q

Management of VSD

A

Small - reassure, prophylaxis, encourage living normal life

Larger - prophylaxis, diuretics for symptoms, treat LV dysfunction, closure if no contraindications

Contraindications to VSD closure - severe irreversible pulmonary HTN

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67
Q

Clinical Features of ASD

A

Fixed splitting of second heart sound
Ejection systolic murmur at upper left sternal edge

Absence of pulmonary HTN suggests haemodynamically insignificant shunt

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68
Q

Types of ASD

A

Ostium secundum
Ostium primum
Sinus venosus ASD
Coronary sinus ASD

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69
Q

Mechanism of widely split S2 in ASD

A

Left to right shunt

Increased right heart volume so slower for P2 to close

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70
Q

Complications of ASD

A 
Arrhythmia
Pulmonary HTN
Eisenmengers
IE
Paradoxical embolism
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71
Q

Clinical Features of Coarctation of Aorta

A

Developed upper torso compared to lower torso
Pulse differential?? left diminished in correction proximal to left subclavian artery (pre ductal - infantile)
Vigorous carotid pulsation
Bruit and thrills over collaterals of scapula
Ejection systolic murmur
Left thoracotomy scar if repaired

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72
Q

Different types of coarctation

A

Infantile - pre ductal - proximal to origin of left subclavian, heart failure in infancy

Adult - post ductal, presents between 15-30 years of age

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73
Q

Cardiac conditions associated with coarctation

A 
Bicuspid aortic valve
PDA
VSD
Mitral valve anomaly
Transposition of Great Vessels
Hypo plastic left heart
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74
Q

Non-cardiac associations with coarctation

A

Turners syndrome
Berry aneurysm
Haemangiomas
Renal abnormalities

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75
Q

Where do collaterals arise in long standing coarctations

A

Internal mammary to external iliac

Spinal and intercostal arteries to descending aorta (rib notching)

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76
Q

Complications of coarctation

A

HTN
Endocarditis
Hypoplastic limbs depending on site and severity
LV dysfunction

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77
Q

Clinical Features of PDA

A 
No features of endocarditis
Large volume collapsing pulse
Parasternal heave
Left subclavian thrill
Continous machinery murmur in left subclavicular area

IF features of pulmonary HTN/congestion then haemodynamically significant

Also comment on any cyanosis/clubbing

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78
Q

Pathophysiology of PDA

A

Derived from 6th aortic arch
As fetes diverts blood from pulmonary artery into systemic circulation, promoted by prostaglandin E2

Functional closure 15hrs after birth due to breathing and increased pO2

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79
Q

Causes of PDA

A 
Prematurity
Low birth weight
Maternal NSAID use (prostaglandins antagonist)
Maternal rubella
High altitude
Fetal alcohol syndrome
Maternal phenytoin
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80
Q

Main complications of PDA

A 
LV dysfunction
IE
Pulmonary HTN
Eisenmengers
Ductal aneurysm/rupture
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81
Q

Clinical Features of Pulmonary Stenosis

A

Ejection systolic murmur with prominent a wave in JVP (not elevated), parasternal heave
Louder in inspiration (unlike aortic stenosis)
Signs of right heart failure without pulmonary congestion

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82
Q

Causes of Pulmonary Stenosis

A

Congenital
Rheumatic
Carcinoid
Noonans

Congenital rubella - supravalvular

TOF - subvalvular

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83
Q

Grading pulmonary stenosis

A

Area
Severe <0.5cm2

Transvalvular gradient
severe >80mmHg

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84
Q

Noonans Syndrome

A

Autosomal dominant/sporadic
Male phenotypic form of Turners but karyotype XX/XY

MSK: short stature, webbed neck, wide spaced nipples

Cardiac: pulmonary stenosis, Hypertrophic cardiomyopathy, ASD/VSD

Facies: triangular, ptosis, strabismus, high nasal bridge

Haem: vWF, coag defects

Small genitalia, undescended testes

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85
Q

Watsons Syndrome

A

Noonans + Neurofibromatosis

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86
Q

Clinical Features of Tetralogy of FAllot

A 
Central cyanosis
Clubbing
Diminished left radial pulse
Smaller left arm
Thoracotomy scar
Parasternal heave
Loud ESM (pulm)+ early diastolic murmur (aortic)
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87
Q

What are the components of TOF

A

VSD
Pulmonary infundibular stenosis
Right ventricular hypertrophy
Overriding aorta

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88
Q

Complications of TOF

A 
Cyanotic spells
Endocarditis
RHF
Polycythaemia
Paradoxical emboli
Cerebral abscess
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89
Q

Causes associated with TOF

A

Catch22 digeorge
Fetal alcohol syndrome
Maternal PKU

90
Q

Black-Taussig shunt

A

Palliative procedure used in TOF (not common anymore)
Anastomosis of subclavian artery and pulmonary artery thus bypassing right ventricular outflow obstruction

Would have thoracotomy scar and absent left radial pulse, otherwise healed

91
Q

Clinical Features of Eisenmengers

A

Central cyanosis and pulmonary HTN!!!
Clubbing

Features of underlying defect e.g. VSD, ASD, PDA

92
Q

What happens to VSD murmur in Eisenmenges

A

As right to left shunt develops, pressure equalises and murmur disappears.
A murmur in VSD and eisenmengers is likely functional TR

93
Q

Hypertrophic Cardiomyopathy

A 
Jerky pulse with double carotid impulse
Prominent a waves
Double apical impulse, undisplaced, heaving
Reversed splitting S2
4th heart sound
Pansystolic/ESM (LV outflow obstruction)
94
Q

Difference between Hypertrophic Cardiomyopathy and HOCM

A

HCM common, only with evidence of LV outflow gradient is HOCM

95
Q

Genetics of HCM

A

Autosomal dominant, 50% familial.

Over 200 distinct mutations identified, multiple chromosmes

96
Q

Complications of HCM

A 
Heart failure (diastolic in early)
AF
Arrhythmia
Sudden death
Angina
Endocarditis
97
Q

Markers of Poor Prognosis in HCM

A 
History of syncope
Family hx of sudden death
Non sustained VT on Holter
Marked LV wall thickness
Drop in BP during exercise
98
Q

reasons for Angina in HCM despite normal angio

A

Increased muscle mass
Decreased capillarity density
Abnormal intramural coronal arteries
Increased myocardial O2 consumption

99
Q

Investigations of HCM

A

ECG: LV hypertrophy, LAD, LA dilatation - bifid p waves in V1-V2, Q was in II, III and avF, ST/T wave changes, AF

CXR: cardiomegaly in late, large left atrial appending and double right heart border

Echo: LV hypertrophy, asymmetry septal hypertrophy, dynamic LV outflow obstruction, diastolic/systolic dysfunction

Exercise treadmill: ischaemia, inducible arrhythmia

Holter; arrythmias

100
Q

Conditions associated with HCM

A

WPW

Friedrichs ataxia

101
Q

Management of HCM

A

Endocarditis prophylaxis, education, screening

Without outflow obstruction:

  • no therapy if asymptomatic
  • if symptoms then beta blocker or verapamil, diuretics, ACEi, treat AF, ICD for ventricular arrthmias
With outflow obstruction
All get beta blockers
Treat AF, diuretics
ICD 
Alcohol septal ablation - controlled septal MI by injecting alcohol into septal arteries to reduce obstruction, alternative to surgical myomectomy. - risk of VSD/heart block.
102
Q

Clinical Features of Parkinsons Disease

A

Expressionless facies (hypomimia)
Bradkinesia - ask to open and close hands repeatedly or tap foot
Reduced blink rate
Soft speech (hypophonia)
Blepharoclonus - eye lid tremor when eyes gently closed
Tremor 4-6Hz, resting, pill rolling often asymmetric, enhanced by mental activity
Lead pipe rigidity - inc tone throughout passive movement
Cog wheeling
Forward stooping posture with lowered head and flexed knees and elbows
Shuffling small steps gait with reduced arm swing
May have loss of postural reflexes
Look for features of parkinson plus incl gaze palsy
TO end: measure postural BP, MMTS, handwriting and assess skin (seb dermatitis)

103
Q

What is Parkinsonism?

A

Movement disorder characterised by bradykinesia and at least 1 of tremor, rigidity and postural instability

104
Q

Causes of Parkinsonism

A 
Idiopathic
Drugs: valproate, metoclopramide, prochlorperazine
Tumour of basal ganglia
Lewy Body Dementia
Dementia pugilistica
Normal pressure hydrocephalus
Wilsons
Anoxic brain injury
Parkinsons plus:
-MSA, PSP, Corticobasal degeneration
105
Q

Aetiology of Idiopathic Parkinsons Disease

A

Neurodegenerative condition caused by disruption of dopaminergic neurotransmission in basal ganglia. Loss of production in substantia nigra and presents of cytoplasmic inclusions (lewy bodies) also seen in LBD and Alzheimers

106
Q

Distinguishing between PD and Parkinsonism

A

PD - asymmetric at first, progressive, good response to levodopa
Parkinsonism - rapid progression, symmetrical and responds badly to levodopa

107
Q

Parkinsons Plus: Multiple Systems Atrophy

A

Parkinsonism with autonomic failure, cerebellar dysfunction and pyramidal signs.

108
Q

Parkinson’s Plus: Progressive Supranuclear Palsy

A 
Abnormal vertical then horizontal gaze
Prominent falls
Speech and swelling difficulties
Frontal symptoms - apathy, cognitive decline, depression
More axial than limb rigidity
109
Q

Parkinsons Plus: Corticobasal degeneration

A

High cortical abnormalities - limb apraxia and sensory loss - (alien limb)
Myoclonus
Dementia

110
Q

Differentiating tremor of parkinson vs BET

A

Essential tremor - symmetrical, worse with voluntary movements, accompanied by voice or head tremor, large writing

PD - asymmetrical, postural component but prominent tremor at rest, micrographia

111
Q

Management of Parkinsons Disease

A

Watch and wait till symptoms need treating

  1. Dopaminergics - levodopa, Dopamine agonist (Bromocriptine), MAO-B inhibitors (Selegilline)
    Cause motor fluctuations, dyskinesias
  2. Anticholinergics
  3. COMT inhibitors (entacapone)
    decrease GI breakdown of levodopa thus reducing off time and increasing on time
  4. Subcut apomorphine
112
Q

Postural hypotension in PD

A

Can be due to disease process and pharmacotherapy - can use fludrocortisone / midodrine

113
Q

Surgical therapies available in PD

A

Thalmotomy
Pallidotomy
Subthalmotomy
Deep brain stimulation - will have something like a pacemaker

114
Q

Clinical Features of Charcot-Marie-Tooth Disease (lower limb)

A

Lower limbs:

  • distal wasting (especially anterolateral muscle compartment leading to inverted champagne bottle)
  • check for scars to suggest traumatic cause of foot drop
  • Palpable popliteal nerve
  • bilateral pes Casus and clawing of foot (high arch doesn’t flatten when weight bear)
  • Symmetrical distal weakness and bilateral foot drop (check shoes for signs of orthotics/scuff marks)
  • Absent deep tendon and planters
  • Stocking sensory loss (later on)
  • High stepping gait
  • Rombergs positive as sensory ataxia

Motor+sensory neuropathy with pes cavus and or palpable nerves = CMT

115
Q

Clinical Features of C-M-T Upper Limb

A

Distal wasting of upper limbs
Wasting of small muscle hands (guttering)
Hyperextension of MCPs and flexion at IPs resulting in claw hand
Absent deep tendon reflexes
Symmetrical glove distribution of sensory loss
May have postural tremor

116
Q

Pathogenesis of Pes Cavus in CMT

A

Weakening of anterior tibialis and perineal muscles. Posterior muscles antagonised and pull harder. Imbalance results in deformity

117
Q

Causes of Pes Cavus

A

Unilateral:

  • malunion of previous fracture
  • burns
  • poliomyelitis
  • spinal trauma/tumour

Bilateral:

  • CMT
  • Freidrichs ataxia
  • Spinal muscular atrophy
  • CP
  • Spinal cord tumours
118
Q

Different types of CMT (HSMN)

A

Hereditary sensory motor neuropathies. A heterogenous group with multiple underlying genetic mutations
1 - demyelination, autosomal dominant, palpable nerves
2 - axonal degeneration
3 - demyelinating, infantile onset and more severe

119
Q

Why are pain and temperature usually unaffected in CMT

A
  • carried by unmyelinated fibres and most CMT is process of demyelination
120
Q

Histology of nerves in CMT

A

Onion bulb appearance
As a result of demyelination, schwann cells proliferate and form concentric arrays of remyelination. Get build up of thick layers of abnormal myelin

121
Q

Management of CMT

A 
Symptomatic
MDT
Patient education and advice
Exercise to maintain function  - physic
Walking aids
Orthotics for foot drop
OT
Analgesia for neuropathic pain
Orthopaedic surgery
122
Q

Clinical Features of MND

A

Dysarthria
Nasal quality speech
Wasted flaccid tongue with prominent fasciculations
Palatal paralysis
Normal eye movements (oculomotor nerves not involved)
Upper limbs: proximal and distal wasting with fasciculations, hypertonia and hyperreflexia, normal sensation
Lower limbs: as above + angle clonus and bilateral extensor plantars

To finish assess respiratory function

123
Q

What is MND?

A

Progressive disorder characterised by neuronal loss at all levels of motor system
Physical signs therefore include upper and lower motor neurones

4 different types

  • Amyotrophic lateral sclerosis - both upper and lower
  • Progressive muscular atrophy - predominantly lower
  • Primary lateral sclerosis - predominantly upper
  • Progressive bulbar palsy - predominantly bulbar or pseudobulbar
124
Q

Pathophysiology of MND

A

Unclear. Theories include

Excitotoxicity hypothesis: amino acid neuromodulators such as glutamate become toxic at supra physiological concentrations. These trigger calcium influx stimulating cascade resulting in free radical formation and neuronal death

Free radical hypothesis:

125
Q

Diseases that mimic MND

A

UMN & LMN:

  • syringomyelia (also may have horners)
  • cervical myelopathy - no bulbar signs

UMN: spinal tumours, HIV myelopathy

LMN:

  • chronic inflammatory demyelinating polyneuropathy
  • Spinal muscular atrophy
  • Old polio
126
Q

Prognosis in MND

A

Worse in older age at onset, female, bulbar onset

Mean age onset 60
Mean survival 3-5years from onset

127
Q

Management of MND

A

MDT - supportive

  • Symptom control, QOL
  • planning for palliative care early
  • anticholinergics for drooling
  • dietary advice/PEG feeding
  • SALT for communication difficulties
  • Quinine/diazepam for fasciculations and cramps
  • Baclofen and physic for spasticity
  • Consider NIV fro respiratory support

Riluzole - disease modifying effects, 3 month increased survival, doesn’t help symptoms

128
Q

Clinical Features of Cerebellar Syndrome

A

Ataxic on side of lesion
Ipsilateral dysdiadochokinesia, dysmetria and intention tremor which worsens closer to target
Rebound phenomenon - failure of displaced arm to find original position when eyes closed
Impaired heel shin test
Hypotonia
Nystagmus with fast component to side of lesion
Broad based gait with tendency to fall to side
Slurred speech with staccato character

All features ipsilateral

Features of underlying cause
MS - internuclear ophthalmoplegia
Alcohol - liver disease, peripheral neuropathy
Friedrichs ataxia - pes Casus
Paraneoplastic - bilateral signs, clubbing, horners, anti Hu (SLCL), anti Yo (gynae and breast)

Truncal features if vermis, limb ataxia if hemisphere

129
Q

Causes of Cerebellar Syndrome

A 
Demyelination (MS)
Alcohol cerebellar degeneration
Posterior fossa SOL
Brainstem lesion
Friedrichs ataxia
Ataxia telangiectasia
Hypothyroidism
VitE Deficiency
von-Hippel lindau
Arnold-chiari malformations
Drugs - phenytoin, carbamazepine, lithium, chemo
130
Q

Drugs causing cerebellar disturbance

A

Phenytoin
Carbamazepine
Lithium
Chemo agents

131
Q

Clinical Features of Myotonic Dystrophy

A

Myopathic facies - lifeless, lean and expressionless
Frontotemporal balding
Ptosis
Cataracts
Wasting of facial muscles, temporals, master, small muscles of hands
Difficulty opening eyes from firm closure
Distal wasting and weakness with impaired fine movement
Foot drop
Depressed deep tendon reflexes
High stepping gait

Other features you would like to look for:

  • Diabetes: skin prick, urinalysis, fundoscopy
  • Cardiomyopathy: signs of heart failure
  • Valvular heart disease: MVP
  • Arrythmias: AF
  • Conduction defects: do they have pacemaker
  • Hypogonadism
  • Goitre: nodular thyroid enlargement

May have family hx of respiratory complications following anaesthetic

132
Q

What is the genetic basis of myotonic dystrophy

A

Autosomal dominant
CTG repeat expansion in myosin protein kinase gene on chr 19
Expansion and anticipation

133
Q

Cardiovascular Complications of Myotonic Dystrophy

A 
ECG: prolonged PR, lon QTC, widened QRS
Arrhythmia: AF, SVTs, VT
Conduction defect: heart block
MVP
Cardiomyopathy
134
Q

GI Complications of Myotonic Dystrophy

A 
Diabetes
Dysphagia
Reflux
Hypo motility
Bacterial overgrowth
Malabsorption
Megacolon
135
Q

Respiratory Complications of Myotonic Dystrophy

A

Hypoventilation
Respiratory failure following anaesthesia
Pneumonia

136
Q

Drugs which can help in Myotonia

A

Phenytoin
Quinine
Procainamide (may worsen cardiac conduction)

137
Q

Causes of distal wasting and weakness

A

Myotonic Dystrophy
HMSN
Inclusion body myositis

138
Q

Common Causes of Sensori-motor neuropathy

A 
Alcohol
Diabetes
Hypothyroidism
Uraemia
Sarcoidosis
Vasculitis
Paraneoplastic
GBS
Drugs: Cisplatin, amiodarone, allopurinol, vincristine
139
Q

Causes of Sensory Neuropathy

A 
Alcohol
Diabetes
Hypothyroidism
Uraemia
Sarcoidosis
Vasculitis
B12 deficiency
Drugs; isoniazid, metronidazole, flecainide
140
Q

Small fibre neuropathy

A

Subtype of peripheral neuropathy where cold, pain and autonomic sensory nerves are involved buy large fibre vibration sense and proprioception are preserved

141
Q

Main causes of mono neuritis multiplex

A 
Diabetes
Polyarteritis nodosa
Churn-Strauss
Wegners
SLE
Sjogrens
Sarcoidosis
Lymphoma
Amyloidosis
142
Q

Investigations for patient with peripheral neuropathy

A

FBC, ESR, U&E, LFT, Glucose, TFTs, B12, folate, serum protein electrophoresis, autoimmune profile

Urine: glucose and pence-jones
Other: nerve conduction studies, CSF may be indicated, nerve biopsy, genetic testing

143
Q

Clinical Features of Common Peroneal Nerve Palsy

A

High stepping gait
Foot drop
Wasting of anterolateral compartment of calf
Weakness of ankle dorsiflexion and eversion
Weakness of dorsiflexion of first toe
Preserved ankle jerk
Loss of sensation over lateral calf and dorsum of foot
Look for scars to suggest traumatic cause

144
Q

Clinical Features of L5 root lesion

A

High stepping gait with foot drop
Weakness of hip abduction, dorsiflexion of first toe
Ankle inversion also involved (spared in peroneal nerve)
Loss of sensation to lateral calf, dorsum of foot and lateral thigh

Don’t forget to examine back for scars

145
Q

What is the course of the common peroneal nerve

A

Arises as terminal branch of sciatic on posterior aspect of distal thigh
Winds around neck of fibula then splits into superficial and deep
-Superficial supplies peroneus longus and braves and sensation to anterior lower leg and dorsum of foot
-Deep supplies tibialis anterior, extensor hallacus longus and sensation to 1st web of foot

146
Q

Causes of flaccid foot drop

A 
Muscle - myotonic dystrophy, trauma
NMJ - myasthenia gravis
LMN - MND, causes of motor neuropathy
Cauda equina tumour
L5 disc prolaps, neurofibroma
Common peroneal nerve palsy - often external compression/trauma
Sciatic nerve palsy
147
Q

Management of Foot Drop

A

Treat any underlying cause
Physio
Orthotics

148
Q

Clinical Features of Friedrichs Ataxia

A

Pes cavus
Kyphoscoliosis
High arched palate

Gait ataxia is common Pc

Cerebellar features: DANISH bilateral

Distal wasting of limbs in pyramidal distribution
loss of proprioception and JPS (degeneration of posterior columns)

Hearing aids/foot orthoses

Other features:
Diabetes in 10%
Optic atrophy - look at disc
Hypertrophic cardiomyopathy in 50% - double jerky apex, systolic murmur
Sensorineural deafness
149
Q

Genetics of Friedrichs Ataxia

A

Autosomal recessive, chr 9

Trinucleotide GAA expansion of protein frataxin involved in mitochondrial iron regulation. Shows anticipation

150
Q

Cardiac abnormalities in Friedrichs Ataxia

A

Arrhythmia
Conduction defects
Hypertrophic cardiomyopathy
Myocardial fibrosis

151
Q

Multiple Sclerosis Sites

A

Optic nerve - atrophy and RAPD
Brainstem - internuclear ophthalmoplegia, facial sensor loss and weakness, tremor
Cerebellum - ataxia, dysarthria
Spinal cord (corticospinal) - pyramidal weakness
Spinal cord (dorsal columns) - loss of vibrations and proprioception

152
Q

Examining the Eyes of Patient with MS

A

Internuclear ophthalmoplegia - impaired ipsilately adduction, flicking of other eye in abduction

Pale optic disc - atrophy

RAPD - loss of direct pupil response but consensual is intact

Central scotoma on red hat pin field testing

Reduced acuity

May also have cerebellar signs, pseudoathetosis etc

153
Q

Examining Upper/Lower Limbs in MS

A

Pyramidal weakness
Hypertonia, hyperreflexia

Dysdiadochokinesia, impaired finger nose testing and intention tremor

Pseudoathetosis when eyes closed
Rebound phenomenon

Impaired vibration and proprioception

Slurred speech, nystagmus etc if you have time

154
Q

Pathophysiology of MS

A

Idiopathic Demyelinating Disorder of CNS characterised by demyelinating plaques separated in both space and time. Inflammatory and autoimmune

155
Q

Different Categories of MS

A

Relapsing remitting
Secondary progressive
Primary progressive
Progressive relapsing

156
Q

What is Lhermittes sign?

A

Neck flexion results in rapid tingling and electric shows down spine into arms and legs. Indicates dorsal column involvement of c-spine.

Seen in - MS, cervical myelopathy, SACDC

157
Q

What is Internuclear Ophthalmoplegia?

A

Lesion in medial longitudinal fasciculus
Connects ipsilateral CNIII (medial rectus, adductor) to contralateral CNIV (lateral rectus, abductor)

Results in impaired ipsilateral adduction and nystagmus on abduction of contralateral eye

Causes: MS, brainstem lesions, Wernickes, SLE, miller fisher

158
Q

Investigations useful in confirming MS

A

T2 weighted MRI - periventricular white matter lesions

CSF if diagnosis is uncertain - oligoclonal bands - raised intrathecal IgG, lymphocytosis

Oligoclonal bands also seen in neurosarcoidosis, CNS lymphoma, SLE, GBS

159
Q

Management of MS

A

General: education, PT/OT, walking aids, visual aids

Acute attacks: IV methyl pred, plasma exchange

Prevention of relapses:

  • Beta interferon: reduced relapse in 33% but can cause flu like symptoms/myalgia
  • –licences for relapse remitting form after 2 relapses in 2 years
  • Glatirimer - competes with autoantibody
  • Mitoxantrone
  • Natalizumab

Symptomatic treatment

  • Spasticity - baclofen
  • Depression
  • Fatigue - amantadine, SSRIs
  • Pain - neuropathic
  • Bladder dysfunction - intermittent self cath, anticholinergics
160
Q

Clinical Features of Cervical Myelopathy

A

Upper Limbs: fasciculations, absent biceps, brisk triceps jerk, sensory loss in C5-C7 dermatome, wasting in C5-C7 dermatome,
Difficulty opening and closing grip in succession
Pseudoathetosis of fingers

Lower Limbs: spastic paraparesis with dorsal column signs
Ddx of friedrichs, MS, SACDC

161
Q

Pathophysiology of Cervical Myelopathy

A

Canal stenosis encroaches on cord leading to lower signs in arms proceeding to upper signs below level

Spondylosis most common but can occur in tumours or following trauma

162
Q

Cerebellar nystagmus

A

Horizontal nystagmus

Fast component towards side of lesion

163
Q

Vestibular nystagmus

A

Horizontal nystagmus
Fast component away from side of lesion.
Nystagmus suppressed by visual fixation and adapts to continued gaze

164
Q

CN III Palsy (oculomotor)

A

Ptosis
Divergent strabismus at rest
Eye fixed in down and out position
Fixed dilated pupil - means parasymp involved usually from extrinsic compression (surgical rather than medical)

165
Q

CN IV Palsy (trochlear)

A

Adducted eye can’t look down

Diplopia worse on looking down and away on affected side

166
Q

CN VI Palsy (

A

Convergent strabismus and impaired abduction

Diplopia maximal on gaze to that side

167
Q

Differential for opthalmoplegis which doesn’t fit into specifically III, IV or VI

A 
Myopathy
Muscular dystrophy
Myasthenia
Myositis
Trauma
168
Q

Main structures in cavernous sinus

A

CNs III, IV, VI, Va and Vb
Sympathetic carotid plexus
Carotid artery

169
Q

Causes of cavernous sinus syndrome

A 
Thrombosis
Aneurysm
Fistula
Tumour - primary or secondary
Trauma
Inflammation - Herpes zoster, TB, sarcoid, wegners
170
Q

Clinical features of cavernous sinus lesion

A 
Unilateral III, IV and VI nerve palsies
Sensory loss in Va and Vb
Loss of corneal reflex
Painful ophthalmoplegia
Proptosis
Visual loss
Papilloedema
171
Q

Clinical Features of Myasthenia Gravis

A

Variable ptosis accentuated by sustained upward gaze, improves following eye closure
Furrowing of forehead
Variable strabismus and diplopia
Bilateral facial muscle weakness, jaw weakness
Weak voice with nasal twang
Proximal weakness with fatiguability

Look for evidence of steroid use, thymectomy scar and other autoimmune conditions e.g. DM, RA, SLE, pernicious anaemia

172
Q

Pathophysiology of myasthenia gravis

A

Autoimmune disorder characterised by antibodies against nicotinic acetyl choline receptors on post-synaptic membrane of NMJ

Can be generalised or ocular

173
Q

Drugs which exacerbate myasthenia gravis

A 
Amino glycosides
Macrolides
Beta blockers
Phenytoin
Lignocaine
174
Q

Difference between MG and lambert-eaton

A

Lambert-Eaton assoc with SCLC, antibodies against pre-synaptic Ca channels, more limb than eye involvement

175
Q

Causes of False positive nAChR antibodies

A 
First degree relative with myasthenia
MND
Lambert-eaton
Autoimmune hepatitis
PBC
SLE
Penicillamine therapy
176
Q

Treatment options for Myasthenia Gravis

A

Acetyl cholinesterase inhibitors - symptomatic benefit not DMARD, can cause N&V, cramps, salivation

Immunosuppressive - steroids then azathioprine, cyclosporin. NB steroids may make weakness worse in first 10 days

Plasma exchange/IVIG

Thymectomy - MG occurs as a result of loss of tolerance to auto antigens. Thymic abnormalities common in these patients and can lead to remission. Always consider if have thymoma or young with thymic hyperplasia

177
Q

Clinical Features of Pancoast Syndrome

A

Horners
C8-T1 weakness (hand)
C8-T1 dermatomal weakness
Clubbing and tar staining (lung Ca)

178
Q

In a patient with wasting of hand(s) always look for

A 
Horners
Neurofibromas
Tongue fasciculations
Clubbing (Horners syndrome)
Pes Cavus (HSMN, Friedrichs, old polio)
inverted champagne legs
Spastic paraparesis (syringomyelia, cervical myelopathy, MND
179
Q

Innervation and action of hand muscles

A

All C8-T1 nerve root
Thenar muscles median
Interossei and digiti minimi ulnar

180
Q

Clinical Features of Syringomyelia

A

Kyphoscoliosis - median motor nuclei involvement which supplies paraspinal muscles
Surgical scars
LMN signs in upper limbs
UMN signs in lower limbs
Dissociated sensory loss - loss of pain and temp with preservation of JPS and proprioception

181
Q

What is syringomyelia?

A

development of fluid filled tubular cavity in central area of spinal cord. Most often develops in cervical or thoracic spinal cord

Causes include:

  • CSF blockage from Arnold-Chiari malformation
  • Spinal cord injury
  • Intramedullary spinal tumour
  • Idiopathic
182
Q

How to explain the clinical signs seen in syringomyelia?

A

At level of syrinx
- anterior horn cell affected thus damaging LMN
-decussating spinothalamic tracts affected through length of syrinx
Below level - corticospinal tracts affected at level thus UMN signs below level

183
Q

Causes of Dissociated Sensory Loss

A

Syringomyelia
Anterior spinal artery occlusion
Small fibre neuropathies

184
Q

Clinical Features of Ulnar Nerve Palsy

A

Wasting and weakness of small muscles of hand with sparing of thenar eminence
Extension deformity at MCP
Clawing of ulnar aspect of hand
Weakness of finger ab and adduction, weakness of thumb adduction only
reduced sensation on 5th finger and ulnar aspect of 4th

Most commonly caused by lesion at the elbow

185
Q

Causes of Ulnar Nerve Palsy

A

At elbow - fracture, arthritis, fibrous arch compression

At wrist - ganglion, tumour, fracture, aberrant artery, entrapment in guyons canal

186
Q

Clinical Features of Radial Nerve Palsy

A

Motor: wrist drop, weak extensors of wrist and MCPs, weak elbow flexion
Triceps intact

Sensory loss over first dorsal interosseous space

If lesion higher at humerus then also forearm sensory loss
If no sensory loss then likely pure motor branch

187
Q

Course of Radial Nerve

A

Posterior branch of brachial plexus

Wraps around humerus in spiral grove then divides into sensory and motor

188
Q

Causes of Radial Nerve Palsy

A

Axilla - trauma, compression
Spiral groove - trauma, saturday night palsy
Proximal forearm - trauma, sublux of radius, elbow synovitis, ganglion, tumour
wrist - trauma, compression

189
Q

Clinical Features of Median Nerve Palsy

A

Wasting of thenar eminence
Weakness of thumb
Sensory loss over palmar aspect of first 3 fingers
If spared over thenar eminence likely carpel tunnel (if not spared then lesion higher as palmar cutaneous branch involved)
Tinels
Phalens

Consider underlying cause: acromegaly, RA, trauma, hypothyroidism, amyloidosis, gout, DM, pagets

190
Q

Relative Afferent Pupillary Defect - Optic Atropy

A

Can have normal direct and consensual reflexes when tested separately

During swinging torch test, one appears dilated and the other constricted because the direct reflex of affected eye is weaker

Causes: optic neuritis/optic atrophy causes, retinal causes including central retinal artery/vein occlusion, severe ischaemic diabetic retinopathy

191
Q

Argyll Robertson pupils

A

Both pupils small and irregular accommodate but don’t react to light

Causes: neurosyphilis, diabetes, midbrain tumour/lesion, wernickes

192
Q

Myotonic Pupil

A

Dilated pupil which reacts slowly
Benign condition seen in middle aged females
when accompanied by arreflexia known as Holmes-Adie syndrome

193
Q

Causes of Miosis

A 
Argyll Robertson pupil
Horners
Opiates
Organophosphate poisoning
infancy/advanced age
194
Q

Clinical features of Horners Syndrome

A

Miosis
Partial ptosis (some innervation from III) which can be overcome with voluntary gaze
Normal eye movements
Ipsilateral anhidrosis if lesion central or pre-ganglionic

Look at neck: scars, masses, aneurysms

Hands: wasting, clubbing, nicotine staining, sensory loss etc to show pancoast tumour

Chest: apical lung signs, sternotomy scars, cervical rib

195
Q

Causes of unilateral ptosis

A

III nerve palsy
Horners
MG
Congenital

196
Q

Causes of bilateral ptosis

A 
MG
Myotonic dystrophy
Bilateral horners - syringomyelia
Nuclear III nerve palsy
Congenital
197
Q

Causes of Horners

A

Central (1st order neurone) - demyelination, brainstem tumour, basal meningitis

Peripheral (2nd order) - pan coast tumour, cervical rib, neurofibromatosis, LN, cardiothoracic surgery

Peripheral (3rd order) - internal carotid dissection, herpes zoster

198
Q

Clinical Features of Cerebellopontine angle lesion

A 
VI nerve palsy - unable to abduct eye
LMN weakness of face
Sensory loss in CN V
Wasting of jaw muscles (V)
Sensorineural hearing loss (unilateral)
May be involvement of IX-XII: hypophonia, neck muscle weakness, tongue deviation
199
Q

Causes of Cerebellopontine angle lesion

A 
Acoustic neuroma
Meningioma
Cholesteatoma
Haemangioblastoma
Granuloma
Metastases
200
Q

Clinical Features of Hemiparesis

A 
Flexural posturing
Dystonic
Pronator drift
Hypertonia
Hypereflexia
Reduced sensation
Circumducting gait
May be expressive dysphasia
Extensor plantars

Would also like to assess:
complete neuro exam, speech, visual fields, measure BP, assess pulse (AF)

201
Q

Common causes of hemiplegia

A 
CVA - ischaemic or haemorrhage
Tumour
Demyelination
Abscess
Post-Octal (Todds)
Functional
202
Q

Why should pain/temp and JPS/vibration be tested?

A

If there is dissociation between two it suggests c-spine lesion not cerebral (Brown-Sequard)

203
Q

Clinical Features of Chorea

A

Brief, irregular, non repetitive movements with flow and dancing quality
Accentuated by activity
Motor impersistence - unable to sustain posture, tongue protrusion or eyelid closure
Milkmaids grip

Look for features of underlying cause:

  • Huntingtons: mental status/dementia
  • Wilsons: K-F rings, stigmata of CLD
  • SLE: rash, purpura
  • Drugs
204
Q

Causes of Chorea

A

Inherited

  • Huntingtons
  • Wilsons
  • Benign familial chorea
  • Spinocerebellar ataxia

Acquired

  • Sydenhams chorea
  • SLE
  • Thyrotoxicosis
  • Pregnancy
  • OCP
  • CVA
205
Q

Tardive dyskinesia

A

Long term dopamine antagonists leads to up regulation and supersensitive to dopamine leading to exaggerated response

Drugs implicated include phenothiazines, metoclopramide

206
Q

Features of Bulbar Palsy (flaccid dysarthria)

A

Speech nasal quality and lacks modulation
Weak voice, low volume
Slurring of consonants
Bilateral palatal weakness
Flaccid paralysis of tongue with fasciculations
Absent jaw jerk

207
Q

Features of pseuobulbar palsy (spastic dysarthria)

A 
High pitch slow speech which lacks modulation
Harsh vocal quality
Strained voice
Bilateral palatal weakness
Small, immobile, spastic tongue
Brisk jaw jerk
Emotional lability
208
Q

What are causes of bulbar palsy

A

Higher Cranial nerve lesion

True bulbar palsy is LMN
-MND
-Brainstem ischaemia
Brainstem tumour
-Poliomyelitis
-GBS

Pseudo bulbar is UMN

  • MND
  • MS
  • Brainstem tumour
209
Q

Clinical Features of Old Poliomyelitis

A 
Hypoplastic limb with distal wasting, weakness and hypotonia
Hyporeflexia
Absent plantar responses
Normal sensation
Pes Casus

LMN but may have contractures from immobility
look for walking aids, orthoses

No sensory involvement, otherwise consider HSMN

210
Q

Poliovirus

A

Enterovirus
Single strand RNA virus surrounded by protein capsid
3 different strains

211
Q

Pathophysiology of poliomyelitis

A

Faecal oral transmission or ingestion of contaminated water
1-3 week incubation period
only 5% get nervous system involvement

5 clinical syndromes:

  1. Abortive poliomyeletis - mild pharyngitis
  2. Non-paralytic poliomyelitis - features of meningism
  3. Paralytic - flaccid limb paresis followed by atrophy, may be partial/complete recovery
  4. Paralytic with bulbar involvement
  5. Encephalitis - very rare, very high mortality
212
Q

Differential for Acute Limb Paralysis

A

Virus: polio, enterovirus 71, tick paralysis
Bacteria: botulism, diphtheria, lyme
Neuropathy: GBS, acute intermittent porphyria
Spinal disease: acute transverse myelitis, spinal cord compression

213
Q

Clinical Features of Facial Nerve Palsy

A 
Facial weakness with no forehead sparing
No ophthalmoplegia
Normal sensation
Check no parotid enlargement (cause of peripheral palsy
Check for hearing defect
214
Q

Causes of Bells LMN palsy

A 
Idiopathic
Structural:
-brainstem demyelination/tumour
-cerebellopontine angle acoustic neuroma
-middle ear infection
-parotid infection/tumour
Mononeuritis multiplex
215
Q

Investigations for Bells Palsy

A

Bloods: glucose, CRP, ESR, ACE, lyme serology etc if atypical presentation
Nerve conduction studies if concerned about GBS
LP if multiple cranial nerves etc

216
Q

Treatment of Bells Palsy

A

High dose oral red for 5 days
Oral acyclovir sometimes given in first week if suggestion of ramsay-hunt
Corneal protection - check eye before steroids then lubrication/tape eye shut at night

217
Q

Complications of Bells Palsy

A

Persistence
Corneal abrasion
Pain in distribution of nerve
Hemifacial spasm

218
Q

Clinical Features of DMD

A 
Young patient
Wheelchair bound
Generalised wasting and weakness predominantly affecting neck and proximal muscles
Contractures on lower limbs
Reduces reflexes
Pseudo hypertrophy of calves
Kyphoscoliosis
Inability to generate forceful cough
219
Q

Genetics of DMD and Beckers Muscular Dystrophy

A

Both X linked recessive mutation in dystrophin gene

220
Q

Riluzole

A

used to treat ALS

Delays ventilator dependence & increase survival by 2-3 months

PACES (3 decks)

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