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Cardiology Flashcards

1
Q

Pathology of AF

A

Left atrium loses its refractoriness before end of atrial systole
Gives recurrent uncoordinated contraction 300bpm
atrial contraction is responsible for around 25% CO thus it often triggers HF.

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2
Q

Causes of AF

A 
Common
 IHD
 Rheumatic heart disease
 Thyrotoxicosis
 Hypertension
Other
 Alcohol
 Pneumonia
 PE
 Post-op
 Hypokalaemia
 RA
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3
Q

Symptoms AF

A 
Symptoms
 Asympto
 Chest pain
 Palpitations
 Dyspnoea
 Faintnes
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4
Q

Signs AF

A

Signs

 Irregularly irregular pulse
 Pulse deficit: difference between pulse and HS
 Fast AF → loss of diastolic filling → no palpable pulse
 Signs of LVF

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5
Q

Investigations AF

A
  • ECG
     FBC, U+E, TFTs, Trop
     Consider TTE: structural abnormalities
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6
Q

Management acute AF

A

haemodynamically unstable –
1st line – emergency cardioversion
2nd line – IV amiodarone

control ventricular rate:
1st line – diltiazem/verapamil/metoprolol
2nd line – digoxin or amiodarone

start LMWH

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7
Q

Cardioversion in AF

A

only done in acute causes <48 hours

electrical or pharmacological
Pharm:
1st line – flecainide if no structural heart disease
2nd line – amiodarone IV

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8
Q

Flecainide MOA

A

sodium channel blocker

slows upstroke of cardiac action potential

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9
Q

Paroxysmal AF

A

a self limiting flare up of AF lasting less than 7 days with recurrence tendency

use CHADSVASC to decide to anticoagulate

Treatment with pill in pocket
(flecainide) to manage flare up

Prevention

  • B blocker
  • Sotalol
  • amiodarone
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10
Q

What is persistent AF

A

AF lasting > 7 days

may recur even after cardioversion

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11
Q

How to treat persistent AF

A

Try rhythm control if:

  • symptomatic
  • age< 65
  • first incidence
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12
Q

What is rhythm control treatment AF

A

Rhythm Control (cardioversion) need to follow these steps as it is a risky treatment
 TTE first: look for structural abnormalities
 Anticoagulate ̄c warfarin for ≥3wks
 or use TOE to exclude intracardiac thrombus.
 Pre-Rx ≥4wks ̄c sotalol or amiodarone if ↑ risk of failure
 Electrical or pharmacological cardioversion eg flecainide (this is the treatment step)
 ≥ 4 wks anticoagulation afterwards (target INR 2.5)

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13
Q

AF maintenance antiarrhythmic

A

Not needed if successfully treated precipitant
1st line — B blocker
2nd line – amiodarone

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14
Q

Final options for AF treatment

A

radiofrequency ablation of AV node
Maze procedure create scar tissue
Pacing

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15
Q

Rate control for AF

A

This is used when can’t do rhythm control
Target HR <90

1st line – B blocker or rate limiting CCB (not together)
2nd line – add digoxin
3rd line – Consider amiodarone

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16
Q

When to use rate control in AF

A

failed cardioversion
patient doesn’t want cardioversion
AF>1 year/ valve disease/ poor LV function

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17
Q

Management of atrial flutter

A

manage as for AF
drugs may not work

amiodarone to restore sinus
amiodarone to maintain sinus

cavotricuspid isthmus ablation right atrium is treatment of choice.

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18
Q

CHA2DS2VAS score

A

determines necessity of anticoagulation in AF

CCF
HTN
AGE >75 (2 points)
Diabetes
Stroke or TIA (2 points)
Vascular disease
Age 65-74 
Sex female

Score
1- aspirin 300mg
2+ - warfarin

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19
Q

Acute coronary syndrome definition

A

unstable angina + evolving MI

ST elevation or new onset LBB
NSTEMI

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20
Q

Pathophysiology of ACS

A

plaque rupture
thrombosis
inflammation

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21
Q

Symptoms ACS

A 
acute central chest pain < 20mins
radiates to left arm/jaw
nausea
sweating
dyspnoea
palpitations
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22
Q

Signs of ACS

A 
anxiety
pallor sweating
pulse up then down
BP up then down
4th heart sound
signs of LVF 
- basal crepitations, raised JVP, 3rd HS
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23
Q

DDX of ACS

A 
angina
peri/endo/myo carditits
dissection
PE, pneumothorax, pneumonia
costochondritis
GORD
anxiety
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24
Q

Investigations ACS

A 
ECG
Bloods
- troponin
- FBC
-U&amp;E
- glucose
-lipids
-INR
CXR
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25
Q

STEMI ECG

A 
STEMI Sequence
 Normal
 ST elevation + hyperacute (tall) T waves 
 Q waves: full-thickness infarct
 Normalisation of ST segments
 T wave inversion
 (New onset LBBB also = STEMI)
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26
Q

NSTEMI ECG

A

ST depression

T wave inversion

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27
Q

Subendocardial infarct ECG

A

No Q waves

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28
Q

Inferior MI ECG

A

2
3
avf

vessel RCA

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29
Q

anterolateral MI ECG

A

1
avl
V4-V6

vessel LCx

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30
Q

Anteroseptal MI ECG

A

V2-V4

vessel LAD

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31
Q

Anterior MI ECG

A

V2-V6

vessel LMCA

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32
Q

Posterior MI ECG

A

V1-V3 reciprocal changes

vessel RCA

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33
Q

ACS blood results

A

Troponin T and I
look at 3 and 12 hours
peak 24 hours returns to baseline 5-14 days

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34
Q

CXR ACS

A

cardiomegaly
pulmonary oedema
widened mediastinum - aortic rupture

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35
Q

ACS diagnosis

A

STEMI/LBB
- typical symptoms + ST elevation / LBB

NSTEMI
- typical symptoms + no ST elevation + +ve troponin

UA
- typical symptoms + no ST elevation + -ve troponin

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36
Q

STEMI treatment brief

A

PCI or thrombolysis

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37
Q

NSTEMI/UA treatment brief

A

medical + elective angioplasty +- PCI/CABG

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38
Q

MI complications

A

Death Passing PRAED st.

Death- VF, LVF, CVA
Pump failure
Pericarditis - mild fever pericardial friction rub relieved by sitting forward, ECG saddle shaped ST elevation, give ibuprofen
Rupture - myomalacia cordis, cardiac tamponade giving beck’s triad (drop BP, rise JVP, muffled heart sounds) and pulsus paradoxus. Papillary muscle = Mitral regurg. septum = heart failure
Arrhythmias
Aneurysm- ventricular
Embolism from LV mural thrombus
Dressler’s syndrome - autoantibodies against myocyte sarcolemma

read through notes following this flashcard more info

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39
Q

Pulsus paradoxus

A

drop in systolic BP >10mmHg on inspiration

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40
Q

STEMI management

A 
MONAC
Morphine- 5-10mg IV
Metoclopramide - 10mg IV
Oxygen - 2-4L sats 94-98%
Nitroglycerin - 2 puffs
Aspirin 300mg PO then 75mg/day
Clopidogrel - 300mg po then 75mg/day

12 lead ECG
LMWH eg enoxaparin IV then subcut
Admit to CCU
Primary PCI or thrombolysis

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41
Q

Choosing PCI or thrombolysis

A

PCI if <12 hours
Thrombolysis if >24 hours from pain onset

If not suitable for either then give fondaparinux

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42
Q

What does PCI involve

A

angioplasty and stenting

+ GP IIA/IIIA antagonist eg clopidogrel, tirofiban
- give this if patient is delayed PCI, diabetes, complex

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43
Q

Complications of PCI

A

bleeding
emboli
arrhythmia

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44
Q

ECG criteria for thrombolysis

A

ST elevation >1mm in 2+ limb leads or >2mm in 2+ chest leads
New LBBB
Posterior MI - DEEP ST depression in V1-V3 and tall R waves

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45
Q

Contraindications for thrombolysis

A

AGAINST

Aortic dissection
GI bleeding
Allergic reaction previously
Iatrogenic- recent surgery
Neuro- cerebral neoplasm
Severe HTN
Trauma - including CPR
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46
Q

Thrombolysis drugs

A

Alteplase (tissue plasminogen activator )
streptokinase
tenecteplase

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47
Q

Complications thrombolysis

A

bleeding
stroke
arrhythmia
allergic reaction

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48
Q

Continuing therapy post MI

A

ACEi- start within 24 hours
B blocker
Aspirin (+- clopidogrel)
statin

and cardiac rehabilitation programme
lifestyle advice

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49
Q

lifestyle advice post MI

A 
stop smoking
diet- oily fish, decrease sat fats
exercise 30min/day
work== return in 2 months
sex == avoid 1 month
driving== avoid 1 month
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50
Q

NSTEMI and UA management

A

MONAC
fondaparinux
12 lead ECG

GRACE score
High risk - persistent recurrent ischaemia, ST depression, DM, positive troponin

Low risk- No pain , flat or inverted T waves, normal ECG, negative troponin

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51
Q

GRACE score

A

used to assess ACS risk

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52
Q

Managing high risk GRACE UA NSTEMI

A

GP2a/3a antagonist- tirofiban
angiography +- PCI within 96 hours
clopidogrel 75mg/day for one year

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53
Q

Managing low risk GRACE UA NSTEMI

A

may discharge after 12 hours if troponin negative

follow up outpatient tests

  • angiography
  • perfusion scan
  • stress echo
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54
Q

Angina pectoris pathophysiology

A

atherosclerosis leading to ischaemia

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55
Q

Causes of angina

A 
mostly atheroma 
anaemia 
aortic stenosis
tachyarrhythmias
arteritits
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56
Q

Symptoms angina pectoris

A

central chest tightness
brought on by exertion and relieved by rest
may radiate to arms/jaw
precipitants - emotion, cold weather, heavy meals

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57
Q

Classification of Angina

A

Stable - induced by effort
Unstable - occurs at rest, minimal exertion
Decubitus - induced by lying down
Variant - at rest due to coronary spasm, gives ST elevation during attack, treat with CCB and long acting nitrate
Syndrome X - angina pain and ST elevation on exercise test no evidence of coronary atherosclerosis

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58
Q

DDX angina

A

Aortic stenosis
Aortic aneurysm
GORD
chostrochondritis

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59
Q

Investigations angina

A 
Angiography (gold standard)
Bloods - FBC UE lipids glucose ESR TFTs
ECG - usually normal
Exercise ECG
Stress echo
Perfusion scan
CT coronary calcium score
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60
Q

Management of angina pectoris overview

A

Lifestyle
Medical
Interventional
Surgical

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61
Q

Medical management angina

A

secondary prevention

  • aspirin
  • ACEi
  • Statin
  • Antihypertensive
Anti anginals
- GTN spray/sublingual 
\+ B blocker
\+ CCB 
\+ Both (Amlodipine)

+ ivabradine
+nicorandil

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62
Q

Interventional management of angina pectoris

A

What
-PCI

When

  • poor response to medical treatment
  • not suitable for CABG

Complications

  • restenosis
  • MI
  • Death

clopidogrel reduces risk of restenosis best to use drug eluting stent as well

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63
Q

Surgical management of Angina

A

What
- CABG

When

  • LMCA disease
  • Triple vessel disease
  • Refractory angina
  • Unsuccessful PCI

Complications

  • stroke
  • MI
  • Pericardial tamponade
  • Post perfusion syndrome
  • Post op AF
  • Graft stenosis
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64
Q

Heart failure definition

A

CO is inadequate for the body’s requirements despite adequate filling pressures

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65
Q

Pathophysiology of Heart failure

A 
Initial reduction in CO== compensation
starling effect dilates heart to enhance contractility 
remodelling == hypertrophy
RAAS activation 
ANP/BNP release 
Sympathetic activation

Progressive decline in CO == decompensation
progressive dilation gives impaired contractility and valve regurgitation
hypertrophy leads to relative myocardial ischaemia
RAAS activation leads to Na+ retention and fluid retention == increased venous pressure and oedema
sympathetic excess - increased afterload and decreased CO

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66
Q

Causes of low output cardiac failure

A

Low output cardiac failure is when CO drops and it can’t increase with exertion

1. Pump failure:
Systolic failure → impaired contraction
 Ischaemia/MI (commonest cause) 
 Dilated cardiomyopathy
 Hypertension
 Myocarditis

Diastolic failure → impaired filling
 Pericardial effusion / tamponade / constriction
 Cardiomyopathy: restrictive, hypertrophic

Arrhythmias
 Bradycardia, heart block
 Tachycardias
 Anti-arrhythmics (e.g. beta-blocker, verapamil)

2. Excessive pre-load
 AR,MR
 Fluid overload
 t
3. Excessive afterload
 AS
 HTN
 HOCM hypertrophic cardiomyopathy
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67
Q

Causes of high output cardiac failure

A

This is when body has increased needs which the heart can’t meet, initially gives RVF then LVF.

Anaemia, Arteriovenous malformation
Thyrotoxicosis, Thiamine deficiency (beri Beri)
Pregnancy, Pagets

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68
Q

What are the causes, symptoms and signs of RVF

A

Causes:

  • LVF
  • Cor pulmonale
  • Tricuspid and pulmonary valve disease

Symptoms:

  • Anorexia
  • Nausea
Signs:
 ↑JVP + jugular venous distension
 Tender smooth hepatomegaly (may be pulsatile) 
  Pitting oedema
 Ascites
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69
Q

LVF causes symptoms and signs

A 
Causes
 1st: IHD
 2nd: idiopathic dilated cardiomyopathy 
 3rd: Systemic HTN
 4th: Mitral and aortic valve disease
 Specific cardiomyopathies

Symptoms
 Fatigue
 Exertional dyspnoea
 Orthopnoea + PND paroxysmal nocturnal dyspnoea
 Nocturnal cough (± pink, frothy sputum)
 Wt. loss and muscle wasting

Signs
 Cold peripheries ± cyanosis
 Often in AF
 Cardiomegaly  ̄c displaced apex 
 S3 + tachycardia = gallop rhythm 
 Wheeze (cardiac asthma)
 Bibasal creps
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70
Q

Chronic HF FRAMINGHAM Criteria

A

For CCF diagnosis need 2 major

or 1 major + 2 minor

Major:

  • Paroxysmal nocturnal dyspnoea
  • Neck vein distension
  • Cardiomegaly
  • Acute pulmonary oedema
  • Increase CVP
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71
Q

CCF Investigations

A

Bloods- FBC UE BNP TFTs glucose lipids

CXR - ABCDE (Alveolar shadowing bats wings, B kerley lines, Cardiomegaly, Dilated upper veins, Effusions)

ECG- Ischaemia, hypertrophy, AF

Echocardiogram - Hypertrophy, valve lesions, Intracardiac shunts, Reduced ejection fraction, hypokinesia

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72
Q

BNP actions and use as a marker

A

Actions:
 ↑ GFR and ↓ renal Na reabsorption
 ↓ preload by relaxing smooth muscle

Marker:
 ↑ BNP (>100) better than any other variable and
clinical judgement in diagnosing heart failure
 BNP correlates ̄c LV dysfunction
 i.e. ↑ most in decompensated heart failure
 ↑ BNP = ↑ mortality
 BNP <100 excludes heart failure (96% NPV)
 BNP also ↑ in RHF: cor pulmonale, PE

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73
Q

New York Heart Association Classification

A
  1. No limitation of activity
  2. Comfortable @ rest, dyspnoea on ordinary activity
  3. Marked limitation of ordinary activity
  4. Dyspnoea @ rest, all activity → discomfort
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74
Q

CCF specific management

A

1st line:
ACEi/ARB + B Blocker + Loop Diuretic

with B blockers start low and go slow

2nd line:
K+ saving diuretic - spironolactone
(watch for hyperkalaemia especially if on ACEi as well)

ACEi + ARB

Vasodilators (hydralazine + ISDN)

3rd line:
Digoxin
ICD

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75
Q

Things to monitor in chronic CCF

A

BP may be very low
Renal function
Plasma K if on spironolactone and ACEi
Daily weight

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76
Q

Management severe pulmonary oedema

A
  1. Sit patient up
  2. Oxygen 15L non rebreath mask target 94-98%
  3. IV access and monitor ECG (bloods and treat any arrhythmias
  4. Diamorphine 2.5-5mg IV (pain and is pulmonary venodilator) + metoclopramide 10mg IV
  5. Furosemide 40-80mg IV
  6. GTN 2 puffs or 2 buccal tablets (unless SBP<90)
  7. If SBP>100 start nitrate infusion
  8. if worsening consider CPAP dialysis

If SBP drops below 100 treat as cardiogenic shock and give inotropes

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77
Q

Causes severe pulmonary oedema cardiac and non cardiac

A

Cardiogenic
 MI
 Arrhythmia
 Fluid overload: renal, iatrogenic

Non-cardiogenic
 ARDS: sepsis, post-op, trauma
 Upper airway obstruction
 Neurogenic: head injury

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78
Q

Pulmonary oedema symptoms

A

Dyspnoea
Orthopnoea
pink frothy sputum

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79
Q

Pulmonary oedema signs

A 
Distressed, sweaty, cyanosed
Tachycardia
Tachypnoea
Raised JVP
S3 gallop rhythm 
Bibasal crepitations
Pleural effusions
Wheeze
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80
Q

Pulmonary oedema DDx

A

Asthma
COPD
Pneumonia
PE

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81
Q

Cardiogenic shock definition

A

decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.

the failure of CO is due to pump failure

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82
Q

Management cardiogenic shock

A
  1. Oxygen 15L nonrebreath mask 94-98%
  2. IV access and monitor ECG
  3. Diamorphine 2.5-5mg IV + metoclopramide
  4. Correct any arrhythmias, electrolyte disturbances, acid-base abnormalities
  5. CXR, Echo, CT thorax
  6. Monitor CVP, BP, ABG, ECG, Urine
  7. Consider need for inotropes dobutamine
  8. Treat underlying cause
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83
Q

Causes of cardiogenic shock

A

MI HEART

 MI
 Hyperkalaemia (inc. electrolytes)
 Endocarditis (valve destruction)
 Aortic Dissection
 Rhythm disturbance
 Tamponade

+ obstructive causes

  • Tension pneumothorax
  • Massive PE
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84
Q

Presentation of cardiogenic shock

A

Unwell, pale, sweaty, cyanosed, distressed
cold clammy peripheries,
↑RR ± ↑HR
Pulmonary oedema

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85
Q

Cardiac tamponade causes

A 
 Trauma
 Lung/breast Ca
 Pericarditis
 MI
 Bacteria (e.g. TB)
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86
Q

Cardiac tamponade signs

A

 Beck’s triad: ↓BP, ↑JVP, muffled heart sounds
 Kussmaul’s sign: ↑JVP on inspiration
 Pulsus paradoxus (pulse fades on inspiration)

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87
Q

Cardiac tamponade investigations

A

Echo - diagnostic

CXR - globular heart

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88
Q

Cardiac tamponade Management

A

ABCDE

Pericardiocentesis using echo guidance is best

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89
Q

Hypertension definitions stages

A 
 Stage 1: Clinic BP > 140/90
 Stage 2: Clinic BP > 160/100
 Severe: Clinic BP > 180/110
 Malignant: BP > 180/110 + papilloedema and/or retinal
haemorrhage
 Isolated SHT: SBP ≥140, DBP <90
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90
Q

Causes of Hypertension

A

PREDICTION

Primary/Essential 95%
Renal - RAS, glomerulonephritis, PKD
Endocrine - Hyperthyroid, cushing's, phaeochromocytoma, acromegaly, conn's
Drugs- cocaine, cocp, NSAIDS
ICP raised
Coarctation of aorta
Toxaemia of pregnancy 
Increased viscocity
Overload with fluid
Neurogenic
91
Q

Clues for hypertension cause

A 
Increased HR thyrotoxicosis
Radio-femoral delay = Coarctation of aorta
Renal bruits = Renal artery stenosis 
Palpable kidneys = PKD
Paroxysmal symptoms = phaeochromocytoma
92
Q

Hypertension end organ damage

A

CANER

Cardiac
 IHD
 LVH → CCF
 AR,MR

Aortic
 Aneurysm
 Dissection

Neuro
 CVA: ischaemic, haemorrhagic
 Encephalopathy (malignant HTN)

Eyes - hypertensive retinopathy
Keith-Wagener Classification:
1. Tortuosity and silver wiring
2. AV nipping
3. Flame haemorrhages and cotton wool spots
4. Papilloedema
grades 3 and 4 signify malignant hypertension

Renal

  • proteinuria
  • CKD
93
Q

Hypertension investigations

A

24 HR ABPM
Urine - haematuria Albumin:creatinine ratio
Bloods - FBC, UE eGFR glucose fasting lipids
12 lead ECG - LVH, old infarct
Calculate 10 year CV risk Q score

important to do ABPM first before starting treatment so you can confirm diagnosis

94
Q

What are the indications for pharmacological management in hypertension

A

<80yrs, stage 1 HTN (>140/90) and one of:
 Target organ damage (e.g. LVH, retinopathy)
 10yr CV risk ≥20%
 Established CVD
 DM
 Renal disease

 Anyone with stage 2 HTN (>160/100)

 Severe / malignant HTN (specialist referral)

 Consider specialist opinion if <40yrs with stage 1 HTN
and no end organ damage.

95
Q

Hypertension BP targets

A

 Under 80yrs: <140/90 (<130/80 in DM)

 Over 80yrs: <150/90

96
Q

Antihypertensive treatment

A
  1. <55 = A
    > 55 or black = C
  2. A+C
  3. A+C+D
  4. A+C+D
    + consider further diuretic eg spironolactone
    + consider a blocker or B blocker
    + seek expert opinion

A: ACEi or ARB
 e.g. lisinopril 10mg OD (↑ to 30-40mg)
 e.g. candesartan 8mg OD (max 32mg OD)
C: CCB: e.g. nifedipine MR30-60mg OD
D: Thiazide-like diuretic: e.g. chlortalidone 25-50mg OD
In step 2, use ARB over ACEi in blacks.
Avoid thiazides + β-B if possible (↑ risk of DM).
Only consider β-B if young and ACEi/ARB not tolerated.

97
Q

How to manage malignant HTN

A

 Controlled ↓ in BP over days to avoid stroke
 Atenolol or long-acting CCB PO
 Encephalopathy/CCF: fruse + nitroprusside / labetalol IV
 Aim to ↓ BP to 110 diastolic over ~4h
 Nitroprusside requires intra-arterial BP monitoring

98
Q

Aortic stenosis causes

A

 Senile calcification (60yrs +): commonest
 Congenital: Bicuspid valve (40-60yrs), William’s syn.
 Rheumatic fever

99
Q

Aortic stenosis symptoms

A 
 Triad: angina, dyspnoea, syncope (esp.  ̄c exercise)
 LVF: PND, orthopnoea, frothy sputum
 Arrhythmias
 Systemic emboli if endocarditis
 Sudden death
100
Q

Aortic stenosis signs

A

 Slow rising pulse ̄c narrow PP
 Aortic thrill
 Apex: Forceful, non-displaced (pressure overload)

Heart Sounds
 Quiet A2
 Early syst. ejection click if pliable (young) valve
 S4 (forceful A contraction vs. hypertrophied V)

Murmur
 ESM
 Right 2nd ICS
 Sitting forward in end-expiration 
 Radiates to carotids
101
Q

Aortic stenosis DDX

A 
 Coronary artery disease
 MR
 Aortic sclerosis
 Valve thickening: no pressure gradient  Turbulence → murmur
 ESM  ̄c no radiation and normal pulse

HOCM
 ESM murmur which ↑ in intensity ̄c valsalva (AS↓)

102
Q

Aortic stenosis investigations

A

Bloods:
ECG:
 LVH
 LV strain: tall R, ST depression, T inversion in V4-V6
 LBBB or complete AV block (septal calcification)
 May need pacing

CXR
 Calcified AV (esp. on lateral films)
 LVH
 Evidence of failure
 Post-stenotic aortic dilatation

Echo + Doppler: diagnostic
 Thickened, calcified, immobile valve cusps

Cardiac Catheterisation + Angiography
 Can assess valve gradient and LV function
 Assess coronaries in all pts. planned for surgery

Exercise Stress Test
 Contraindicated if symptomatic AS
 May be useful to assess ex capacity in asympto pts.

103
Q

Medical management aortic stenosis

A

 Optimise RFs: statins, anti-hypertensives, DM
 Monitor: regular f/up ̄c echo
 Angina: β-B
 Heart failure: ACEi and diuretics

104
Q

Surgical management aortic stenosis

A 
Poor prog. if symptomatic
 Angina/syncope: 2-3yrs 
 LVF: 1-2yrs
Indications for valve replacement
 Severe symptomatic AS
 Severe asymptomatic AS  ̄c ↓ EF (<50%)
 Severe AS undergoing CABG or other valve op
Valve types
 Mechanical valves last longer but need
anticoagulation: young pts.
 Bioprosthetic don’t require anticoagulation but
fail sooner (10-15yrs)
105
Q

Aortic regurgitation causes

A

Acute:
Infective endocarditis
Type A aortic dissection

Chronic:
Congenital - bicuspid aortic valve
Rheumatic heart disease
Connective tissue disease: Marfan's , Ehler's danlos 
Autoimmune: ankylosing spondylitis RA
106
Q

Aortic regurgitation symptoms

A

 LVF: Exertional dyspnoea, PND, orthopnoea
 Arrhythmias (esp. AF) → palpitations
 Forceful heart beats
 Angina

107
Q

Aortic regurgitation signs

A

 Collapsing pulse (Corrigan’s pulse)
 Wide PP
 Apex: displaced (volume overload)

Heart Sounds
 Soft / absent S2
 ± S3

Murmur
 Early DM decrescendo 
 UR Sternal Edge + 3rd left IC parasternal
 Sitting forward in end-expiration 
 ± ejection systolic flow murmur 
 ± Austin-Flint murmur

Underlying cause
 High-arched palate
 Spondyloarthropathy
 Embolic phenomena

108
Q

Investigations aortic regurgitation

A

Bloods: FBC, U+E, lipids, glucose ECG: LVH (R6+S1 > 35mm)

CXR
 Cardiomegaly
 Dilated ascending aorta
 Pulmonary oedema

Echo
 Aortic valve structure and morphology (e.g. bicuspid)
 Evidence of infective endocarditis (e.g. vegetations)

Cardiac Catheterisation
 Coronary artery disease
 Assess severity, LV function, root size

109
Q

Management of aortic regurgitation

A

Medical
basically just manage the risk factors
HTN, DM etc and have regular follow up

Surgical
Aortic valve replacement
reserved for severe cases with HF symptoms

110
Q

Mitral Stenosis causes

A

Rheumatic fever
Prosthetic valve
Congenital

111
Q

Mitral stenosis pathophysiology consequences

A

 Valve narrowing → ↑ left atrial pressure → loud S1 and atrial hypertrophy → AF
 → pulmonary oedema and PHT → loud P2, PR
 → RVH → left parasternal heave
 →TR→largevwaves
 → RHF → ↑JVP , oedema, ascites

112
Q

Mitral stenosis symptoms

A 
Dyspnoea
Fatigue
Chest pains
AF == palpitations and emboli
haemoptysis == rupture of bronchial veins due to dilated rleft atrium
113
Q

Mitral stenosis signs

A

Symptoms manifest when orifice <2cm2 (norm 4-6)
 AF, low volume pulse
 Malar flush (↓CO → backpressure + vasoconstriction)

JVP may be raised late on
 Prominent a waves: PTH
 Large v waves: TR
 Absent a waves: AF

 Left parasternal heave (RVH secondary to PHT)
 Apex: Tapping (palpable S1), non-displaced

Heart sounds
 Loud S1
 Loud P2 (if PHT)
 Early diastolic opening snap

Murmur
 Rumbling MDM
 Apex
 Left lateral position in end expiration
 Radiates to the axilla
 ± Graham Steell murmur (EDM 2O to PR)
114
Q

What are heaves a sign of

A

Hypertrophy

115
Q

What are thrills a sign of

A

Palpable murmur

116
Q

Complications of Mitral stenosis

A

 Pulmonary HTN
 Emboli: TIA, CVA, PVD, ischaemic colitis
 Hoarseness: rec laryngeal N. palsy = Ortner’s Syn
 Dysphagia (oesophageal compression)
 Bronchial obstruction

117
Q

Mitral stenosis investigations

A

Bloods: FBC, U+E, LFTs, glucose, lipids

ECG
 AF
 P mitrale (if in sinus)
 RVH ̄c strain: ST depression and T wave inversion in V1-V2

CXR
 LA enlargement
 Pulmonary oedema: ABCDE
 Mitral valve calcification

Echo and doppler
Severe MS (AHA 2006 Criteria)
 Valve orifice <1cm2
 Pressure gradient >10mmHg
 Pulmonary artery systolic pressure >50mmHg
Use TOE to look for left atrial thrombus if intervention considered.

Cardiac Catheterisation
 Assess coronary arteries

118
Q

Management of mitral stenosis

A

Medical monitor risk factors and treat them
prophylaxis for rheumatic fever
Treat AF

Surgical
 Indicated in mod–severe MS (asympto and symptomatic)

Percutaneous balloon valvuloplasty
 Rx of choice
 Suitability depends on valve characteristics
 Pliable, minimally calcified
 CI if left atrial mural thrombus

 Surgical valvotomy / commissurotomy: valve repair
 Valve replacement if repair not possible

119
Q

Mitral regurgitation causes

A

 Mitral valve prolapse
 LV dilatation: AR, AS, HTN
 Annular calcification → contraction (elderly)
 Post-MI: papillary muscle dysfunction/rupture
 Rheumatic fever
 Connective tissue: Marfan’s, Ehlers-Danlos

120
Q

Mitral regurgitation symptoms

A

Dyspnoea fatigue
AF == palpitations and emboli
Pulmonary congestion == Hypertenison and oedema

121
Q

Mitral regurgitation signs

A

 AF
 Left parasternal heave (LVH)

Apex: displaced
 Volume overload as ventricle has to pump forward SV and regurgitant volume
 → eccentric hypertrophy

Heart Sounds
 Soft S1
 S2 not heard separately from murmur
 Loud P2 (if PTH)

Murmur
 Blowing PanSystolicMurmur  
 Apex 
 Left lateral position in end expiration
 Radiates to the axilla
122
Q

Mitral regurgitation investigations

A

Bloods: FBC, U+E, glucose, lipids

ECG
 AF
 P mitrale (unless in AF)
 LVH

CXR
 LA and LV hypertrophy
 Mitral valve calcification
 Pulmonary oedema

Echo

  • Doppler echo to assess severity
  • TOE to assess severity and suitability of repair

Cardiac Catheterisation
 Confirm Dx
 Assess CAD

123
Q

Management of mitral regurgitation

A

Medical
Control risk factors
Control AF
Drugs to reduce afterload

Surgical
 Valve replacement or repair
Indications
 Severe symptomatic MR
 Severe asympto MR  ̄c diastolic dysfunction: ↓EF
124
Q

Mitral valve prolapse (barlow syndrome)

A

Most common valve problem

Gives mitral regurgitation

125
Q

Barlow syndrome causes

A 
 Primary: myxomatous degeneration 
 Often young women
 MI
 Marfan’s, ED
 Turner’s
126
Q

Barlow syndrome symptoms and signs

A 
Symptoms
 Usually asymptomatic
 Autonomic dysfunction: Atypical chest pain,
palpitations, anxiety, panic attack
 MR: SOB, fatigue

Signs:
 Mid-systolic click ± late-systolic murmur

127
Q

Tricuspid regurgitation causes

A

Functional RV dilation
Rheumatic fever
Infective endocarditis especially IVDU
Carcinoid syndrome

128
Q

Tricuspid regurgitation symptoms

A

Fatigue
hepatic pain on exertion
Ascites
Oedema

129
Q

Tricuspid regurgitation signs

A

 ↑JVP ̄c giant V waves
 RV heave

Murmur:
 PanSystolicMurmur
 LowerLeftSternalEdge in inspiration (Carvallo’s sign)

 Pulsatile hepatomegaly
 Jaundice

130
Q

Tricuspid stenosis causes

A

Rheumatic fever with comorbid mitral valve and aortic valve disease

131
Q

Tricuspid stenosis symptoms

A

Fatigue
Ascites
oedema

132
Q

Tricuspid stenosis signs

A 
Increased JVP
Opening snap
Murmur:
- End diastolic murmur 
- Lower left sternal edge in inspiration
133
Q

Pulmonary regurgitation causes

A

Any cause of pulmonary hypertension

If PR is secondary to Mitral stenosis = Graham Steel murmur

134
Q

Pulmonary regurgitation signs

A

Murmur
Decrescendo early diastolic murmur
heard at left upper sternal edge

135
Q

Pulmonary stenosis causes

A 
Usually congenital 
Turner's syndrome 
Tetralogy of fallot 
rheumatic fever
carcinoid syndrome
136
Q

Pulmonary stenosis symptoms

A

Dyspnoea
fatigue
ascites
oedema

137
Q

Pulmonary stenosis signs

A 
JVP changes
RV heave
Murmur
- crescendo decrescendo systolic murmur 
- ULSE radiates to left shoulder
138
Q

Infective endocarditis definition

A

Cardiac valves develop vegetations composed of bacteria and platelet-fibrin thrombus

139
Q

infective endocarditis risk factors

A 
Prosthetic valves
Degenerating valvulopathy
Congenital abnormality
Rheumatic fever
Post-op wounds
IVDU== especially tricuspid valve  
Immunocompromised including DM
140
Q

Cause of infective endocarditis

A

Bacterial infection
+ve S.aureus
-ve Haemophilus

Non-infective
SLE

141
Q

Infective endocarditis clinical features

A

Sepsis

  • fever
  • rigors
  • Anaemia
  • Clubbing

Embolic phenomena

  • Janeway lesions
  • abscesses in brain, heart, kidney, spleen

Cardiac

  • New murmur MR most common
  • atrio-ventricular block
  • LV failure

Immune complex deposition

  • Haematuria due to glomerulonephritis
  • Vasculitis
  • Roth spots
  • Splinter haemorrhages
  • Osler’s nodes

Roth spots are boat shaped retinal haemorrhages with pale centre

142
Q

How to diagnose infective endocarditis

A

Use Duke criteria
Diagnose if 2 major, 1 Maj + 3 min , all 5 minor
Major
1. +ve blood culture
 Typical organism in 2 separate cultures, or
 Persistently +ve cultures, e.g. 3, >12h apart

  1. Endocardium involved
     +ve echo (vegetation, abscess, valve dehiscence) or
     New valvular regurgitation

Minor

  1. Predisposition: cardiac lesion, IVDU
  2. Fever >38
  3. Emboli: septic infarcts, splinters, Janeway lesions
  4. Immune phenomenon: GN, Osler nodes, Roth spots, RF 5. +ve blood culture not meeting major criteria
143
Q

Investigations

A 
Bloods
 N.chromic, N.cytic anaemia
 ↑ESR, ↑CRP
 +ve IgG RF (immune phenomenon)
 Cultures x 3, >12h apart
 Serology for unusual organisms

Urine: Micro haematuria

ECG: AV block

Echo
 TTE detects vegetations > 2mm
 TOE is more sensitive (90-100% vs. 50-60%)

144
Q

Treatment infective endocarditis

A

Empiric
= Acute sever – flucloxacillin and gentamicin IV
= Subacute – Benzylpenicillin + gentamicin IV

Then once bacteria is elucidated treatment is accordingly

145
Q

different antibiotics for different agents in infective endocarditis

A

 Streps: benpen + gent IV
 Enterococci: amoxicillin + gent IV
 Staphs: fluclox ± rifampicin IV
 Fungi: flucytosine IV + fluconazole PO.
 Amphotericin if flucytosine resistance or Aspergillus.

146
Q

Mortality for infective endocarditis

A

30% with staphs

147
Q

Rheumatic fever Cause

A

Group A beta haemolytic strep. pyogenes

148
Q

Epidemiology of rheumatic fever

A

5-15 years
rare in west
common in developing world
Only 2% of population susceptible

149
Q

Pathophysiology of rheumatic fever

A

Antibody cross reactivity following strep pyogenes infection gives T2 hypersensitivity reaction due to molecular mimicry
Abs attack Myosin protein in cell wall
Cross react and creates damage

Pathology gives Aschoff bodies and Anitschkow myocytes

150
Q

How to diagnose rheumatic fever

A

use the revised Jones criteria
evidence of Group A strep infection + 2 major criteria
or evidence of GAS infection + 1 major + 2 minor

Evidence of GAS infection
 +ve throat culture
 Rapid strep Ag test
 ↑ ASOT or DNase B titre
 Recent scarlet fever
Major Criteria
 Pancarditis
 Arthritis
 Subcutaneous nodules
 Erythema marginatum
 Sydenham’s chorea
Minor criteria
 Fever
 ↑ESR or ↑CRP
 Arthralgia (not if arthritis is major)
 Prolonged PR interval (not if carditis is a major)
 Prev rheumatic fever
151
Q

What are the symptoms of rheumatic fever

A 
Pancarditis (60%)
 Pericarditis: chest pain, friction rub
 Myocarditis: sinus tachy, AV block, HF, ↑CK, T
inversion
 Endocarditis: murmurs
 MR, AR, Carey Coombs’ (MDM)

Arthritis (75%)
 Migratory polyarthritis of large joints (esp. knees)

Subcutaneous nodules (2-20%)
 Small mobile, painless nodules on extensor surfaces (esp. elbows)
Erythema marginatum (2-10%)
 Red, raised edges  ̄c central clearing.
 Trunk, thighs and arms.

Sydenham’s Chorea (10%)
 Occurs late
 Grimacing, clumsy, hypotonia (stops in sleep)

152
Q

Investigations rheumatic fever

A

Bloods
 Strep Ag test or ASOT
 FBC, ESR/CRP

ECG

Echo

153
Q

Treatment of rheumatic fever

A 
Bed rest until CRP normalises
BENPEN IM 10 days
Analgesia ASPIRIN
add oral prednisolone if CCF
of chorea symptoms give HALDOL or DIAZEPAM
154
Q

Prognosis of rheumatic fever

A

Attacks last around 3 months
60% with carditis will develop chronic rheumatic heart disease
Mitral valve disease is very common complication

Secondary prophylaxis
helps prevent recurrence
take peniciliin po for a while depending on initial severity

155
Q

Acute pericarditis causes

A

Causes
 Viral: coxsackie, flu, EBV, HIV
 Bacterial: pneumonia, rheumatic fever, TB, staphs
 Fungi
 MI, Dressler’s
 Drugs: penicillin, isoniazid, procainamide, hydralazine
 Other: uraemia, RA, SLE, sarcoid, radiotherapy

156
Q

acute pericarditis clinical features

A

Clinical Features

Central / retrosternal chest pain 
 Sharp
 Pleuritic
 Worse lying down
 Relieved by sitting forward 
 Radiates to left shoulder

 Pericardial friction rub.
 Fever
 Signs of effusion / tamponade

157
Q

acute pericarditis investigations

A

ECG

  • saddle shaped ST elevation
  • PR depression

Bloods

  • FBC
  • troponin may be raised
  • cultures
  • virology
158
Q

Management of acute pericarditis

A

Analgesia ibuprofen
Treat cause
Consider steroids and immunosuppression

159
Q

Constrictive pericarditis cause

A

Heart becomes encased in rigid pericardium

often unknown cause
often follows acute pericarditis

160
Q

Clinical features of constrictive pericarditis

A 
Clinical features
 RHF  ̄c ↑JVP (prominent x and y descents)
 Kussmaul’s sign: ↑JVP  ̄c inspiration
 Quiet heart sounds
 S3
 Hepatosplenomegaly
 Ascites, oedema
161
Q

Investigations of constrictive pericarditis

A

CXR - small heart and pericardial calcification

Echo

Cardiac catheterisation

162
Q

cause if 3rd heart sound

A

A third heart sound occurs early in diastole.

In young people and athletes it is a normal phenomenon.

In older individuals it indicates the presence of congestive heart failure.

The third heart sound is caused by a sudden deceleration of blood flow into the left ventricle from the left atrium

163
Q

Cause of 4th heart sound

A

Forceful atria contraction in late diastole to force blood into ventricle which wont expand any further

164
Q

Management of constrictive pericarditis

A

surgical excision of the heart from it’s restricting chamber

165
Q

Pericardial effusion cause

A

Any cause of pericarditis

166
Q

Pericardial effusion clinical features

A

 Dyspnoea
 ↑JVP (prominent x descent)
 Bronchial breathing @ left base
 Ewart’s sign: large effusion compressing left lower lobe
 Signs of cardiac tamponade may be present.

167
Q

Investigations of pericardial effusion

A

 CXR: enlarged, globular heart

ECG
 Low-voltage QRS complexes
 Alternating QRS amplitude (electrical alterans)

Echo: echo-free zone around heart

168
Q

Management of pericardial effusion

A

Treat cause

Pericardiocentesis may be diagnostic and therapeutic use it for culture and cytology

169
Q

Cardiac tamponade definition

A

 Accumulation of pericardial fluid → ↑ intra-pericardial pressure → poor ventricular filling → ↓ CO

170
Q

Tamponade causes

A 
any cause of pericarditis 
aortic dissection 
bacterial endocarditis
warfarin
trauma
171
Q

Signs of tamponade

A

 Beck’s Triad: ↓ BP, ↑ JVP, quiet heart sounds
 Pulsus paradoxus: pulse fades on inspiration
 Kussmaul’s sign = JVP rise on inspiration

172
Q

Investigations of tamponade

A

ECG

  • low voltage QRS
  • electrical alterans

CXR
- Large globular heart

Echo

  • diagnostic
  • echo free zone around the heart
173
Q

Management of tamponade

A

 Urgent pericardiocentesis
 20ml syringe + long 18G cannula
 45degrees, just left of xiphisternum, aiming for tip of left
scapula.
 Aspirate continuously and watch ECG.
 Treat cause
 Send fluid for cytology, ZN stain and culture

174
Q

Acute myocarditis causes

A

Idiopathic - 50%
Viral - cocksackie flu HIV
Bacterial - staph aureus syphilis
Drugs - Herceptin Phenytoin

175
Q

Acute myocarditis symptoms

A

Flu like prodrome– sore throat myalgia

dyspnoea
fatigue
chest pain

Arrhythmias == palpitations

176
Q

Signs of acute myocarditis

A

Soft S1

S4 gallop as atria contract to hard ventricles

177
Q

Investigations for acute myocarditis

A

ECG
 ST-elevation or depression
 T wave inversion
 Transient AV block

Bloods: +ve trop, ↑CK

178
Q

Hypertrophic obstructive cardiomyopathy causes

A

Left ventricular outflow tract obstruction due to asymmetrical septal hypertrophy
Autosomal dominant inheritance
B - myosin heavy chain mutation commonest
Ask questions about family history of sudden death

179
Q

Symptoms of HOCM

A

Angina
Dyspnoea
Palpitations: AF, WPW, VT
Exertional syncope or sudden death

180
Q

Signs of HOCM

A

Jerky pulse
Double apex beat
S4 sound
Harsh early systolic murmur

181
Q

Investigations HOCM

A

ECG

-LVH

182
Q

Management of HOCM

A

Medical
 -ve inotropes: 1st – β-B, 2nd –verapamil
 Amiodarone: arrhythmias
 Anticoagulate if AF or emboli

Non-medical
 Septal myomectomy (surgical or chemical) if severe symptoms
Consider ICD

183
Q

Cardiac myxoma definition and cause

A

Rare benign cardiac tumour

May be familial eg due to part of Carney Complex

  • cardiac myxoma
  • skin pigmentation
  • cushing’s

90% found in Left atrium

184
Q

Features of cardiac myxoma

A 
Clubbing
fever
weight loss
signs similar to MS (MDM, systemic emboli and AF)
but vary with posture

Diagnosed with echo

Treatment with excision

185
Q

Restrictive cardiomyopathy causes

A 
miSSHAPEN
Sarcoid
Systemic sclerosis
Haemochromatosis 
Amyloidosis 
Primary - endoymyocardial fibrosis 
Eosinophilia 
Neoplasia == carcinoid ==> TR + PS
186
Q

Clinical features restrictive cardiomyopathy

A 
Clinical features
 RHF  ̄c ↑JVP (prominent x and y descents)
 Kussmaul’s sign: ↑JVP  ̄c inspiration
 Quiet heart sounds
 S3
 Hepatosplenomegaly
 Ascites, oedema

this is the same as restrictive pericarditis

187
Q

Dilated cardiomyopathy causes

A 
DILATE
Dystrophy
Infection
Late pregnancy -- peri/post partum
Autoimmune -- SLE
Toxins - alcohol , doxorubicin 
Endocrine -- thryotoxicosis
188
Q

Presentation of dilated cardiomyopathy

A

LVF
RVF
Arrhythmias

189
Q

Signs of dilated cardiomyopathy

A 
 JVP ↑↑
 Displaced apex
 S3 gallop 
 ↓BP
 MR/TR
190
Q

Investigations dilated cardiomyopathy

A

 CXR: cardiomegaly, pulmonary oedema
 ECG: T inversion, poor progression
 Echo: globally dilated, hypokinetic heart + ↓EF
 Catheter + biopsy: myocardial fibre disarray

191
Q

Management dilated cardiomyopathy

A

 Bed rest
 Medical: diuretics, ACEi, digoxin, anticoagulation
 Non-medical: biventricular pacing, ICD
 Surgical: heart Tx

192
Q

Bicuspid aortic valve manifestations

A

No problems at birth
Most will eventually develop stenosis +- regurg
Predisposes to infective endocarditis

193
Q

Atria septal defect definition

A

Hole connects the atria
Secundum defects are commonest
Often asymptomatic until adulthood
LV compliance eventually gets worse so more blood in atria and gives L==> R shunt

194
Q

Signs and symptoms of Atrial septal defect

A

Symptoms:

  • dyspnoea
  • pulmonary HTN
  • arrhythmia
  • Chest pain
Signs:
 AF
 ↑JVP
 Pulmonary ESM
 PHT→TRorPR
195
Q

Complications of Atrial septal defect

A 
Paradoxical emboli (ie from venous origin)
Eisenmenger syndrome
196
Q

Investigations for Atrial septal defect

A

ECG:

CXR:
-pulmonary plethora, increased pulmonary perfusion due to the shunt

Echo:
-diagnostic

197
Q

Treatment for atrial septal defect

A

Transcatheter closure

this is recommended if there is a lot of blood flowing from pulmonary to systemic (eisenmenger) 1.5:1 ratio due to cyanosis problems it needs management.

198
Q

Coarctation of the aorta definition

A

Congenital narrowing of the aorta
usually just distal to the origin of the L subclavian artery

M>F

199
Q

Associations of coarctation of the aorta with other diseases

A

Bicuspid aortic valve

Turner’s syndrome

200
Q

Signs of coarctation of the aorta

A

Radio - femoral delay
Weak femoral pulse
Hypertension
Systolic murmur – bruit best heard over left shoulder

201
Q

Investigations for coarctation of aorta

A

CXR:
- inferior rib notching

ECG

CT angiogram

202
Q

Treatment coarctation of aorta

A

Balloon dilatation and stenting

203
Q

Ventricular septal defect definition

A

Hole connecting the ventricles

204
Q

Causes of ventricular septal defect

A

Congenital

Acquired post MI

205
Q

Presentation of ventricular septal defect

A

Either severe heart failure in childhood

Or incidental finding in adulthood depending on severity

206
Q

Signs of VSD

A

 Small holes which are haemodynamically less significant → louder murmurs
 Harsh, pansystolic murmur @ left sternal edge
 Systolic thrill
 Left parasternal heave

 Larger holes → PHT

207
Q

Complications of VSD

A

infective endocarditis
pulmonary hypertension
eisenmenger’s syndrome

208
Q

Investigations of VSD

A

ECG
 Small: normal
 Large: LVH + RVH

CXR
 Small: mild pulmonary plethora
 Large: cardiomegaly + marked pulmonary plethora

209
Q

Treatment VSD

A

surgical closure if symptomatic VSD from large hole

210
Q

Tetralogy of fallot definition

A

VSD
Pulmonary stenosis
Right ventricular hypertrophy
Overriding aorta

The commonest congenital cyanotic heart disease

occurs following abnormal separation of truncus arteriosus into aorta and pulmonary arteries

Associated with DiGeorge syndrome CATCH-22 gene

211
Q

Presentation of fallot

A

 Infants:
hypercyanotic episodes, squatting, clubbing

Adult
 Often asympto
 Unoperated: cyanosis, EarlySystolicMurmur of PS
 Repaired: dyspnoea, palpitations, RVF

212
Q

Fallot investigations

A

ECG: RVH + RBBB

CXR: Coeur en sabot

Echo: anatomy + degree of stenosis

213
Q

Treatment of fallot

A

surgically usually before age of 1

closure of VSD

correction of pulmonary stenosis

214
Q

Marfan’s syndrome epidemiology

A

Autosomal dominant
M=F
1/5000

215
Q

Pathophysiology of marfan’s syndrome

A

Mutation in FBN1 gene chromosome 5
- encodes fibrillin 1 glycoprotein

fibrillin 1 is an essential component of elastin

Histology gives cystic medial necrosis

216
Q

Presentation of Marfan’s syndrome

A

Cardiac
 Aortic aneurysm and dissection
 Aortic root dilatation → regurgitation
 MV prolapse ± regurgitation

Ocular
 Lens dislocation: superotemporal

MSK
 High-arched palate
 Arachnodactyly abnormal long and slender digits 
 Arm-span > height
 Pectus excavatum
 Scoliosis
 Pes planus
 Joint hypermobility
217
Q

Complications of marfan’s

A

Ruptured aneurysms
Spontaneous pneumothorax
Diaphragmatic hernias
Hernias

218
Q

Marfan’s DDX

A

MEN-2B
Homocystinuria
Ehlers-danlos

219
Q

Investigations of Marfan’s

A

 Slit-lamp examination: ectopia lentis

CXR
 Widened mediastinum
 Scoliosis
 Pneumothorax

ECG
 Arrhythmias: premature atrial and ventricular
ectopics

Echo
 Aortic root dilatation → AR
 MVP and MR

 MRI: dural ectasia (dilation of neural canal)

 Genetic testing: FBN-1 mutation

220
Q

Management of marfan’s syndrome

A

 Refer to ortho, cardio and ophtho
 Life-style alteration: ↓ cardiointensive sports
 Beta-blockers slow dilatation of the aortic root
 Regular cardiac echo
 Surgery when aortic root ≥5cm wide

221
Q

Ehlers-Danlos syndrome pathogenesis

A

Rare heterogeneous group of collagen disorders
6 subtypes
type 1&2 are commonest and autosomal dominant

222
Q

Presentation of ehlers danlos

A

 Hyperelastic skin
 Hypermobile joints
 Cardiac: MitralValveProlapse , AR, MR and aneurysms
 Fragile blood vessels → easy bruising, GI bleeds
 Poor healing

223
Q

Ehlers danlos syndrome DDX

A

Cutis laxa - loose skin and hypermobile joints

pseudoxanthoma elasticum - skin laxity

Marfan’s syndrome

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