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CRD Flashcards

1
Q

Epidemiology and risk factors for ACS

A 
Most common cause of death in the UK (1/5 men, 1/6 women)
More common in men
Mortality equal in both sexes
Increases with age
Increased in South Asians

RF
Modifiable - smoking, diabetes, metabolic syndrome, hypertension, obesity, hyperlipidaemia, physical inactivity

Non-modifiable - male, increased age, FHx of premature CHD, premature menopause, south Asian

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2
Q

Definition of ACS

A

STEMI, NSTEMI and unstable angina

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3
Q

Symptoms of ACS

A 
Chest pain (central or epigastric) lasting longer than 15 minutes
Radiates to arms, shoulders, neck or jaw
Sweating
Nausea and vomiting
Collapse/syncope
Dyspnoea
Fatigue
Palpitations

Atypical presentation is seen in women, older men, diabetics and ethnic minorities.
- abdominal discomfort, jaw pain, altered mental state

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4
Q

Signs of ACS

A 
Tachycardia (sympathetic)
Hypotension
Pallor
Sweating
Vomiting, bradycardia (vagal)
Pale, cool, clammy
Cold peripheries
3rd heart sound
Oliguria
Narrow pulse pressure
Raised JVP
Lung crepitations
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5
Q

Diagnostic criteria for MI

A

Detection of rise and/or fall of troponin and at least one of:

  • symptoms of ischaemia
  • ECG changes
  • Imaging evidence of new loss of myocardium or wall motion abnormality
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6
Q

Causes of MI

A 
Atherosclerosis
Infected cardiac valve
coronary occlusion secondary to vasculitis
coronary artery spasm
cocaine use
congenital coronary abnormality
coronary trauma
raised O2 requirement (hyperthyroid)
decreased oxygen delivery (severe anaemia)
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7
Q

Investigations for ACS

A

Observations - stabilise

FBC - anaemia, CRP, ESR
U&Es - potassium and electrolytes
Lipid profile

Troponin
(can use CK-MB or myoglobin)

ECG (ST elevation, Q waves, T wave inversion)

ABG - high lactate and hypoxia

Echo for extent of infarction

Angiography

Myocardial perfusion scintigraphy (SPECT)

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8
Q

Cardiac enzymes

A

Troponin

  • increases within 3-12 hours from pain onset, peak at 48 hours, returns to baseline in 5-14 days
  • measure at presentation and 10-12 hours after onset
  • T binds to tropomysin, I binds to actin, C bind to calcium

Myocardial muscle creatinine kinase (MB-CK) - increase within 3-12 hours, peak at 24 hours, baseline within 3 days. Not as sensitive or specific

Myoglobin - most sensitive early marker

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9
Q

Causes of raised troponin

A 
ACS
Congestive heart failure
Sepsis
PE
CKD
Myocarditis
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10
Q

ECG changes in anterior STEMI

Which artery is occluded?

A

LAD

V3-V4 (septal may be involved V1-V2)
Reciprocal ST depression in III and AVF

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11
Q

ECG changes in inferior STEMI

Which artery is occluded?

A

80% R coronary, 20% L circumflex

ST elevation, ST depression, T wave inversion, Q waves
II, III, aVF

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12
Q

ECG changes in lateral STEMI

Which artery is occluded?

A

V5-V6

1st diagonal branch of LAD or obtuse branch of L circumflex

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13
Q

Management for STEMI

A

Stabilise

Troponin, ECG

Pain relief (GTN, opioids)
300mg aspirin
Supplemental O2 if hypoxic

PCI if able within 12 hours of onset
Fibrinolysis if not - alteplase, reteplase or streptokinase

Secondary prevention - ACEi, aspirin, 2nd anticoagulant (usually NOAC), beta blocker, statin

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14
Q

Management of NSTEMI

A

Stabilise

Troponin, ECH

Pain relief (GTN, opioids)
300mg aspirin
Supplemental O2 if hypoxic
Fondaparinux or unfractionated heparin within 24 hours

GRACE risk assessment

Lowest risk - aspirin only (no angio)
Low risk - aspirin + clopidogrel + consider angio
High risk - aspirin + clopidogrel + urgent coronary angiography

Secondary prevention - ACEi, aspirin, 2nd anticoagulant (usually ticagrelor), beta blocker, statin

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15
Q

When is a CABG required?

A

Failed PCI (occlusion not amendable or refractory symptoms)
Cardiogenic shock
Mechanical complications (rupture, mitral regurgitation)
Multivessel disease

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16
Q

What is the secondary prevention post ACS?

A

Aspirin +/- clopidogrel
Beta blocker
Ace inhibitor - check GFR and BP prior
Statin

Stop smoking, lower cholesterol, lower weight, increase exercise

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17
Q

Prognosis of MI

A

50% die in 30 days with 1/3 dying in first hour

Earlier perfusion = decreased mortality

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18
Q

What are the risk scores used in ACS?

A

GRACE - risk stratification in ACS - probability of in-hospital death. Uses Kilip class, SBP, HR, age, creatinine, ST deviation, Cardiac arrest, trop levels

Kilip’s classification - severity of cardiac failure after MI
1-4 from 1 no crackles, no added heart sounds to 4 - cardiogenic shock

TIMI score - risk of death post NSTEMI/UA

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19
Q

Complications post-MI

A 
angina, re-infarct,
heart failure
cardiogenic shock
valve dysfunction 
cardiac rupture
arrhythmia 
PE
Pericarditis
Depression
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20
Q

Epidemiology and RF for angina

A

8% men, 3% women aged 55-64, 14% men, 8% women over 65
Increased in South Asian and Afro-Caribbean
Increasing age

RFs
FHx
Metabolic syndrome
Smoking
Diabetes
Obesity
Decreased exercise
Hypertension
Hyperlipidaemia
Past CHD
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21
Q

Symptoms of angina

A

Constricting discomfort in the chest
Precipitated by physical exertion
Relieved by GTN or rest in minutes
Precipitating factors: physical exertion, heavy meals, cold exposure, intense emotion

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22
Q

What are the different types of angina?

A

Stable - precipitated by predictable factors
Unstable - symptoms occur at rest and occur at any time
Refractory - symptoms cannot be controlled by medication
Prinzmetal - occurs at rest and exhibits a circadian pattern - most episodes in the early hours of the morning

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23
Q

Causes of angina

A 
Atherosclerosis
Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Hypertensive heart disease 
Arrhythmias
Anaemia
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24
Q

Investigations for angina

A

12 lead ECG - LBBB, ST or T wave abnormalities (not NICE recommended)

FBC - rule out anaemia
U&E for renal function
Fasting blood glucose
LFTs
Check TFTs
Troponin

Echo

Exercise tolerance test

Estimate likelihood of coronary artery disease

  • 90%+ treat as angina
  • 61-90% - invasive coronary angiography
  • 30-60% - non invasive functional testing for myocardial ischaemia
  • 10-29% - CT calcium testing
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25
Q

Management of angina

A

Modify CV risk factors
Treatment should start before results

Advice - during attack - rest, use GTN (wait 5 mins), use up to 3 times, call 999

Beta blocker or calcium channel blocker
Add long acting nitrate e.g. nicorandil
Start aspirin
If diabetes + angina - ACEi

If symptomatic on 2 anti-angina meds then PCI or CABG

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26
Q

Differentials for chest pain

A 
MI - NSTEMI or STEMI
Angina - stable or unstable
Prinzmetal angina
Acute pericarditis (constant pain, worse on inspiration, lying flat and movement)
PE
Pneumonia
MSK e.g. costochondritis
Aortic dissection
Gallstones
GORD
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27
Q

Prognosis of angina

A

1 in 10 will have MI within 1 year

Benign

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28
Q

Classification of angina

A

Canadian CV society functional classification

  1. No angina with ordinary activity, only strenuous
  2. angina during ordinary activity e.g. walking up hill with mild limitations
  3. angina with low level activity e.g. walking on flat, marked limitation
  4. angina at rest or with any exercise
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29
Q

Identifying high risk ACS patients

A

QRISK2

  • Age, BP, smoking, diabetes, cholesterol, BMI, ethnicity, deprivation, FHx, CKD, RA, AF, diabetes, HTN
  • If >10 start statin
  • Number = % who will have CV event in 10 years

GRACE score
Estimates 6 month mortality for those with ACE

TIMI score
Likelihood of ischaemic event or mortality in UA or NSTEMI

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30
Q

Describe cardiac rehabilitation

A

Education, psychological support, exercise training and behavioural change

  • Decreases morbidity and mortality
  • NICE recommended
  • Offer to all MI patients
  • Only 40% uptake
  1. assess. reassure. educate. mobilise. discharge
  2. screen for anxiety/depression
  3. structured exercise and rehabilitation. graded exercise. aerobic low intensity.
  4. regular review of patients in primary care long term
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31
Q

What does a loud first heart sound suggest

A

Hyperdynamic circulation

  • Anaemia
  • pregnancy
  • hyperthyroidism
  • mitral stenosis
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32
Q

When would you hear a systolic click?

A

Early or mid-systole
aortic stenosis
pulmonary stenosis
prosthetic heart valve

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33
Q

When would you hear an ejection systolic murmur?

A

Aortic stenosis
Pulmonary stenosis

Crescendo - decrescendo pattern

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34
Q

When would you hear a pansystolic murmur?

A

Mitral regurgitation

Tricuspid regurgitation

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35
Q

When would you hear an early diastolic murmur?

A

Aortic regurgitation
Pulmonary regurgitation

Soft blowing decrescendo pattern
Best hear when sitting forward in expiration

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36
Q

When would you hear a late diastolic murmur?

A

Mitral stenosis
Tricuspid stenosis

Associated with opening snap

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37
Q

Describe murmur associated with aortic stenosis?

A

Ejection systolic
Crescendo-descrescendo
Radiates into neck
Best heart at left sternal edge

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38
Q

Murmur of mitral regurgitation

A 
Pansystolic 
Blowing
Best heard at the apex 
Radiates to axilla
best heard in left lateral position
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39
Q

Causes of mitral regurgitation

A 
Rheumatic fever
Degenerative calcification in elderly
Congenital
SLE
RA
Infective endocarditits
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40
Q

What happens to the heart with mitral stenosis?

A

Flow from LA to LV is restricted
Left atrial pressure rises
Pulmonary venous congestion (breathlessness) leading to pulmonary hypertension
Dilation and hypertrophy of LA
Can develop AF
Exercise and pregnancy poorly tolerated as increase HR, shortens diastolic period with mitral valve open

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41
Q

Presentation of mitral stenosis

A 
Progressive breathlessness
Orthopnoea, PND, pulmonary oedema
Cough (pulmonary congestion)
Chest pain (pulmonary hypertension)
Oedema (right heart failure)
Fatigue (low cardiac output)
AF / Palpitations
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42
Q

Signs of mitral stenosis

A 
Malar flush
Raised JVP
Right ventricular heave
Laterally displaced apex beat
Mid-late diastolic murmur best heard in left lateral position 
AF
Signs of R heart failure - ascites, peripheral oedema
Pulmonary oedema
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43
Q

Investigations and findings in mitral stenosis

A

CXR - LA enlarged, Kerley B lines (interstitial oedema)

ECG - AF, tall R waves in V1-3, may have bifid p waves

Echo - thickens immobile cusps
Doppler - increases pressure gradient across valve

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44
Q

Management of mitral stenosis

A

If asymptomatic - no intervention - yearly echos

Diuretics or long acting nitrates (for dyspnoea)
Beta blocker or calcium channel blocker
Anticoagulation if AF
If tachy, consider heart rate control

PMC - percutaneous mitral commissurotomy (valvotomy)

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45
Q

Epidemiology of heart failure

A

1-2% of adults
Increased in men
Increases with age
Increasing prevalence with increasing survival post MI and secondary prevention

RFs
HTN
IHD
Valvular disease
Cardiomyopathy
Diabetes
FHx
Smoking
Endocarditis
Glitazones
Sleep apnoea
Alcohol
Congenital defects
Arrrhythmia
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46
Q

Symptoms of heart failure

A 
Dyspnoea
Fatigue
Peripheral oedema
Orthopnoea
Paroxysmal nocturnal dyspnoea (PND)
Noctural cough
Pink frothy sputum
Wheeze
Nocturia
Cold peripheries
Weight loss
Muscle wasing
Nausea 
Anorexia
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47
Q

Signs of heart failure

A 
Peripheral oedema
Dyspnoea
Raised JVP
Cardiomegaly
Murmur
Crackles on lung auscultation
Displaced apex
R ventricular heave
Hypotension
Narrow pulse pressure
Tachycardia
Tachypnoea
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48
Q

Aetiology of heart failure

A

HYPERTENSION
Valvular disease (10%)
2y to myocardial disease - CHD, HTN, cardiomyopathy
Drugs - beta blockers, calcium channel blockers, anti-arrhythmics, cytotoxic drugs
Toxins: alcohol, cocaine
Endocrine: diabetes, hypothyroid, hyperthyroid, Cushings, adrenal insufficiency
Nutritional deficiency - thalamine, selenium
Infiltrative: amyloidosis, sarcoidosis
High output failure - anaemia, pregnancy, hyperthyroid, Paget’s
AF

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49
Q

Pathophysiology of heart failure

A

Heart failure with reduced ejection fraction

  • Heart unable to pump blood which prevents filling with new blood
  • SYSTOLIC FAILURE
  • Long term cardiac remodelling leads to ventricular dilation
  • Increases preload and end diastolic volume
  • Dilation is a compensatory mechanism to decrease preload
  • Severe dilation is maladaptive

Heart Failure with Normal Ejection Fraction

  • heart unable to relax fully preventing blood from entering or exiting the heart
  • DIASTOLIC FAILURE
  • Increased afterload, usually due to increased BP
  • Ventricular wall hypertrophy to try to decrease adterload
  • decrease ventricular size, decrease compliance, decrease cardiac output
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50
Q

Investigations for heart failure

A

If no MI

  • Measure serum BNP and pro-BNP (they are released when myocardium stressed)
  • NT-proBNP commonly used
  • If over 400 then refer to specialist and Doppler echo

If previous MI
- Refer to specialist and Doppler echo

  • CXR for cardiomegaly, prominent upper lobe vessels, bat winging, kerley B lines, pleural effusions
  • Blood tests: FBC, U&Es, creatinine, LFTs, glucose, fasting lipids, troponin
  • ECG: for heart block, AF, IHD
  • ABGs: acidosis or hypoxia
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51
Q

Signs of heart failure on CXR

A 
Cardiomegaly
Prominent upper lobe vessels 
Bat winging (alveolar oedema)
Kerley B lines (interstitial oedema)
Pleural effusions
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52
Q

Management of heart failure

A

Lifestyle changes: smoking cessation, dietary changes, regular exercise, reduce alcohol

First line: diuretic + ACEi + beta blocker

Second line: ADD aldosterone antagonist OR ARB or hydralazine + nitrate

3rd line: digoxin or cardiac resynchronisation therapy

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53
Q

Classification of heart failure

A

New York Heart Association

Class 1: no symptoms on ordinary physical activity

Class 2: slight limitation of physical by symptoms

Class 3: less than ordinary activity leads to symptoms

Class 4: inability to carry out any activity without symptoms

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54
Q

Management of acute heart failure

A
  • Bloods, ECG, CXR
  • BNP or NT-proBNP, if raised Doppler echo with 48 hours
  • IV diuretics bolus or infusion
  • IV nitrates of myocardial ischaemia
  • Start beta blockers
  • Offer ACEi
  • Monitor renal function and electrolytes
  • ionatropes for short term acute decompensation
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55
Q

Epidemiology of asthma

A 
Very common
1 in 11 children, 1 in 12 adults
Commonly starts at 3-5 years
More common in boys, but more common in women
FHx of atopy
Increased in developed countries

RFs
Personal history of atopy
Inner city environment
Obesity
Prematurity and low birth weight
Viral infections in early childhood
Smoking
Maternal smoking 
Early exposure to broad spec antibiotics

PROTECTIVE factors: breast feeding, vaginal birth, farming environment

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56
Q

Symptoms of asthma

A

Breathlessness
Wheeze
Chest tightness
Cough
Symptoms worse at night or early morning
Symptoms in response to exercise, allergen exposure or cold air
Symptoms present after taking aspirin or beta blockers.

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57
Q

Signs of asthma

A

Widespread wheeze on auscultation
Low FEV1 or PEFR
Peripheral blood eosinophilia

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58
Q

Pathophysiology of asthma

A

Airflow limitations, airway hyper-responsiveness and bronchial inflammation

Type 1 hypersensitivity reaction

Triggers cause inflammatory cascade.
2 phase Broncho constrictor response

Early: type 1. Preformed mediator release 0-90 minutes
Late: types 2. Inflammatory cell recruitment and activation. Mast cells, eosinophils, oedema, smooth muscle hypertrophy, mucus plugging and epithelial damage.

Raised IgE

  • Antigen detected by dendritic cell which presents it to TH1 and TH2 cells via IL12
  • TH2 cells recruit mast cells, basophils and eosinophils
  • Release of inflammation mediators e.g. histamine, prostaglandins, leukotrienes
  • bronchial hyper responsiveness and airway obstruction
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59
Q

Triggers for asthma

A 
Allergens: grass pollen, dander
Occupational sensitizers
Viral infections
Cold air
Emotion
Irritants: dust, vapour, fumes, smoker
Genetic factors
Drugs: NSAIDs, beta blockers
Atmospheric pollution
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60
Q

Aspirin sensitive asthma

A

Symptoms triggered by aspiring
These inhibit cyclo-oxygenase which leads to shunting or arachidonic acid metabolism through lipo oxygenase pathway producing cysteinyl leukotrienes

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61
Q

Extrinsic vs intrinsic asthma

A

Extrinsic - atopic individuals. Often starts in childhood

Intrinsic - middle age, non-atopic. More severe

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62
Q

Causative agents for occupational asthma

A 
Isocyanates - paint sprayers
Flour - bakers
Colophony and fluxes - soldering and printers
latex - medical
Animal - vets
Aldehydes
Wood dust - carpentry
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63
Q

Investigations in asthma

A

SPIROMETRY for diagnosis
FEV1>15% increase following bronchodilator or steroid trial or >20% diurnal variation on 3+ days/week for 2 weeks

Peak flow - unreliable in under 5s
Nocturnal dips or work related
Should be measured every 15-30 minutes in acute attack

Histamine or methacholine provocation or exercise or inhaled mannitol challenge

Measure allergic status using skin prick test for attopy

FBC: may have eosinophilia

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64
Q

Brittle asthma

A

Exacerbations occur with little or no warning

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65
Q

Classification of asthma severity

A

Mild: PEFR 75-100%

Moderate: PEFR 50-75%

Acute Severe: PEFR 33-50%, RR>25, HR >110, inability to complete sentence

Life threatening: PEFR <33%, Sats <92%
Normal or raised PaCo2
Silent chest
Cyanosis
Bradycardia/arrhythmias
Hypotension. Exhaustion. Confusion

Near fatal.
Raised pCO2 requiring mechanical ventilation with raised inflation pressure

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66
Q

Treatment of acute asthma

A

Mild - use inhaler, wait 60 minutes, home

Moderate - ABG, nebulise 5mg salbutamol. high flow o2. Prednisolone 40mg PO.
Wait 30 minutes, if PEFR<60% see below, if higher home

Acute severe: ABG, nebulise 5mg salbutamol 2-4 hourly
High flow o2
prednisolone 40mg PO or 200mg IV
IV access, K+ levels, ADMIT
Consider continuous nebuliser
Consider IV mag sulphate
Correct fluids and electrolytes - watch K+, often hypokalaemic

On discharge (for all): oral prednisolone 40mg PO for 5/7
Start or double inhaled corticosteroids
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67
Q

Treatment of chronic asthma

A
  1. Salbutamol inhaler
  2. Inhaled corticosteroid - If need to use >3 per week or waking due to asthma then start
  3. Long acting B2 agonist. Should never be used without steroid
  4. Increased inhaled steroid to 2000mcg/day
    - Leukotriene receptor antagonist
    - Theophylline
    - Oral B2 agonist
  5. Oral steroid while maintaining inhaled steroids

Once controlled, steroids should be lowered to the lowest possible dose to maintain symptom control.

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68
Q

Asthma in pregnancy

A

1/3 worsen
1/3 stable
1/3 improve

Uncontrolled asthma is biggest risk to foetus

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69
Q

ABG finding in asthma

A

Respiratory alkalosis

Hypoxaemia or hypercapnia secondary to hyperventilation

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70
Q

Risk factors for cardiovascular disease

A 
Smoking
Increasing age
Family history (1st degree male under 55, or female under 65)
Obesity
Hypertension
High cholesterol
Ethnicity - South Asian or African
T2DM
Alcohol
Low socioeconomic background
Male
Stress
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71
Q

Stages of hypertension

A

1 - Clinic BP >140/90 and ambulatory blood pressure (ABPM) >135/90
2 - Clinic BP > 160/110 |AND ABPM >150/95
3 - Clinic BP > 180 systolic or >110 diastolic

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72
Q

Relevance of FHx to CV disease

A

1st degree male under 55,

or female under 65

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73
Q

Diagnosing hypertension

A

BP in both arms, if difference >20mmHg then repeat

If BP >140/90 measure twice, if different then take 3rd. Record LOWEST of last 2 BPs

If over 140/90 offer ABPM

If stage 3 - >180 or >110 then treat without ABPM

Test for organ damage - LV hypertrophy, CKD, hypertensive retinopathy and CV risk

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74
Q

Phaeochromocytoma

A 
Labile or severe hypertension
headache
Palpitations
Pallor
Diaphoresis
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75
Q

When should secondary hypertension be considered?

A

Under 40s
Low potassium and high sodium (adrenal disease)
Raised creatinine or low GFR (renal disease)
Proteinuria or haematuria
With labile or worsening HTN

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76
Q

Long term complications of hypertension

A 
LV hypertrophy
CCF
CAD
Arrhythmias - AF
Microvascular disease

Increased risk of stroke and dementia

Hypertensive retinopathy

Hypertensive nephropathy
End stage renal disease
Glomerular injury

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77
Q

Causes of secondary hypertension

A

RENAL

  • chronic pyelonephritis
  • diabetic nephropathy
  • glomerulonephritis
  • PKD
  • Obstructive nephropathy
  • Renal cell carcinoma

VASCULAR

  • Renal artery stenosis
  • Coarctation of aorta

ENDOCRINE

  • Primary hyperaldosteronism (low potassium, high bicarbonate, high sodium)
  • Phaeochromocytoma
  • Cushing’s syndrome
  • Acromegaly
  • Hypothyroidism
  • Hyperthyroidism

DRUGS

  • Alcohol misuse
  • Cocaine
  • ciclosporin, COCP, corticosteroids, EPO, leflunomide, NSAIDs, liquorice, sympathomimetics (cough and cold meds), venlafaxine
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78
Q

Coarctation of aorta

A 
Upper limb hypertension
Large difference between arms
Absent or weak femoral
Radio-femoral delay
Suprasternal murmur, radiating to back
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79
Q

Management of hypertension

A

Aim for under 140/90 in under 80s, or 150/90 in over 80s

Lifestyle: smoking cessation, weight loss, low salt diet, reduce alcohol.

  1. ACE inhibitor, unless over 55 or Black then calcium channel blocker
  2. ACEi or ARB + CCB
  3. Add thiazide like diuretic
    (Monitor U&Es)
  4. Add spironolactone

No ACEi in pregnancy or renovascular disease
ACEi best for heart failure and Type 1 diabetes

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80
Q

Assessing CV risk

A

QRISK2
Used up to 84 year olds
Age, sex, ethnicity, postcode, smoking, diabetes, FHx, CKD, AF, RA, cholesterol, BMI, BP

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81
Q

Diagnostic criteria for metabolic syndrome

A

Clustering of CV risk factors relating to insulin resistance
1 in 5 adults

Any 3 or more of the following:

  • Increased weight, BMI or waist circumference
  • Raised triglycerides
  • Low HDL
  • Hypertension
  • Raised fasting plasma glucose
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82
Q

Define COPD

A

Chronic obstructive pulmonary disease
Airflow obstruction, not reversible.
Airflow limitation if progressive and encompasses bronchitis and emphysema

FEV1

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83
Q

Epidemiology of COPD

A

Affects men and women equally
Increases with age

RF
Smoking
Occupational exposure to dust/chemicals
Air pollution
alpha 1 antitrypsin deficiency
Low birth weight
Childhood infections
Maternal smoking
Recurrent infections
Low socioeconomic status
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84
Q

Symptoms of COPD

A 
Exertional breathlessness
Chronic cough
Regular sputum production
Frequent winter bronchitis
Wheeze
Weight loss
Ankle swelling
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85
Q

Signs of COPD

A 
Tachypnoea
Dyspnoea
Increased use of accessory muscles
Asterixis
Confusion
Pursed lip breathing
Peripheral oedema
Cyanosis
Wheeze
Hyperinflation of chest
Quiet vesicular breath sounds
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86
Q

Pathophysiology of COPD

A

Loss of elastic recoil and collapse of small airways on expiration
Abnormal enlargement of air spaces distal to terminal wall
Enlargement of goblet cells and increased numbers
Pulmonary vascular remodelling
Unopposed action of proteases and oxidants leading to destruction of alveoli
Infiltration of walls with inflammatory cells - CD8+

Expiratory airlflow limitation and decreased recoil = VQ mismatch

Patients rely on hypoxic drive due to persistent raised pCO2
If rely on hypoxic drive = renal hypoxia = fluid retension & polycythaemia

Alpha1 antitrypsin is an antiprotease deactivated by smoking

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87
Q

Investigations for COPD

A

Spirometry

  • FEV1/FVC <70%
  • FEV1 <80%

Chest x-ray can be normal

  • low flattened diaphragms
  • large bullae
  • vessels may be large proximally

Bloods
- Hb may be raised with raised PCV (polycythaemia)

ABGs
- Hypoxia and hypercapnia if severe

Sputum culture if ? infection

  • Can test alpha 1 antitrypsin
  • CT
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88
Q

Management of COPD

A
  • Pneumococcal and influenza vaccinations
  • Smoking cessation
  • Regular assessment of lung function
  1. Short acting B2 (salbutamol)
  2. Long acting B2 (salmetrol)
  3. Antimuscarinic (ipratropium)
  4. Add theophylline/phosphodiesterase inhibitor (moneleukast)
  5. Inhaled corticosteroid (never without long acting B2)
  6. Pulmonary rehab
  7. Home oxygen

Can add carbocysteine (antimucolytic)

If acute

  • O2 where tolerated
  • Removal of secretions
  • Respiratory support
  • Corticosteroids
  • Antibiotics
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89
Q

Complications of COPD

A 
Chronic hypoxia
Cor pulmonale from pulmonary hypertension
Pneumothorax
Respiratory failure
Arrhythmias - AF
Infection
Secondary polycythaemia
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90
Q

MRC dyspnoea grading

A

0 - only breathless on regular exercise
1 - SOB on slight incline or hurried on flat
2 - walks slower than others or has to stop
3 - stops after 100m or few minutes on level
4 - too breathless to leave the house of on dressing

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91
Q

Classifying severity of COPD

A

GOLD or BODE index

BODE uses FEV1, GOLD FEV1/FVC

GOLD
1 - mild FEV1/FVC <70% but FEV1>80%
2 - moderate FEV1/FVC 50-79%
3 - severe FEV1/FVC 30-50%
4 - very severe FEV1<30% or respiratory failure
BODE 
1 - mild FEV1>80% but symptomatic
2 - moderate FEV1 50-79%
3 - severe 30-49%
4 - <30% or respiratory failure
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92
Q

Factors that can destabilise heart failure patient

A 
Ischaemia
Hypertension
Rapid AF
Medication initiation
Alcohol abuse
Non-adherence
Active infection
PE
Anaemia
Hyperthyroidism
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93
Q

Assessing end organ damage from HTN

A 
Urinalysis
FBC (Hb and Hct)
U&amp;Es 
Fasting glucose
Cholestrol work up
ECG
CXR
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94
Q

Signs of LV dysfunction

A 
Hypotension
Soft S1
S3 gallop
Decreased volume carotid pulse
LV apical enlargement
Pulmonary congestion (rales)
Mitral regurg
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95
Q

High risk patients with HTN

A 
Older age
Diabetes
Renal disease
LV hypertrophy
Vascular disease
CHD
Cerebrovascular disease

Aim for 130/80 vs 140/90

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96
Q

Define bronchiectasis

A

Permanent dilation and thickening of airways characterised by chronic cough, excessive sputum production, bacterial colonisation and recurrent acute infections.

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97
Q

Classification of bronchiectasis

A

More than 1 type can be present in the same patient.

  • Cylindrical: bronchi are enlarged and cylindrical (signet appearance of bronchi)
  • Varicose: bronchi are irregular with areas of dilation and constriction.
  • Saccular or cystic: dilated bronchi form clusters of cysts. Most severe form (often in CF patients). Degree of bronchial dilation increased from proximal to distal.
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98
Q

Epidemiology of bronchiectasis

A

More common in women
Increases in age
3 per 1000
Increase in pacific nationality

RFs
Cystic fibrosis
Immunodeficiency
PHx of infections
Alpha 1 antitrypsin deficiency
Connective tissue disorder
Primary ciliary dyskinesia
IBD
Aspiration or inhalation injury
Congenital disorder of bronchial airways
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99
Q

Aetiology of bronchiectasis

A

Caused by chronic inflammation
42% develop post-infection
No identifiable cause in up to 50%

Post infection - childhood viral infection (measles, pertussis, influenza), TB, bacterial pneumonia

Immunodeficiency e.g. HIV

Connective tissue disease - RA, Sjorgen’s, systemic sclerosis, SLE, Ehler’s Danlos syndrome, Marfan’s

Congenital defects - CF, primary ciliary dyskinesia, alpha 1 antitrypsin deficiency

Asthma
Allergic bronchopulmonary aspergillosis
Gastric aspirations
Bronchial obstruction by lymphadenopathy, tumour or inhaled foreign body
IBD
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100
Q

Pathophysiology of bronchiectasis

A
  1. Persistent airway inflammation
  2. Development of bronchial wall oedema and increased mucus production
  3. Recruitment of inflammatory cells
  4. Release of inflammatory cytokines, proteases and reactive oxygen mediators
  5. progressive destruction of airways

Vicious cycle - insult by primary infection, increased inflammation, bronchial damage, increase capacity for colonisation of airways

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101
Q

Symptoms of bronchiectasis

A 
Vary from intermittent episodes of expectoration to persistent daily expectoration of large volumes of purulent sputum.
Dyspnoea
Chest pain
Haemoptysis
Wheezing
Cough
Rhinosinusitis
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102
Q

Signs of bronchiectasis

A 
Coarse crackles - early in inspiration and in lower zones
Areas of crackles corresponds poorly with radiological findings
Large airway rhonchi 
Wheeze
High pitched inspiratory squeak
Dyspnoea
Haemoptysis
Fever
Clubbing
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103
Q

When should bronchiectasis be considered

A

Persistent productive cough AND ONE OF:

  • young age at presentation
  • Hx of symptoms spanning years
  • absence of smoking history
  • daily expectoration of large volumes of sputum
  • Haemoptysis
  • Colonisation of P. aeuroginosa
  • Unexplained haemoptysis
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104
Q

Investigations for bronchiectasis

A

CXR - baseline in all patients, 90% are abnormal. Ring or tubular opacities, tramlines, fluid levels

HRCT - high resolution CT is GOLD STANDARD

  • Bronchial wall dilation
  • Bronchial wall thickening

Sputum microbiology

FBC - raised WCC or polycythaemia

Immune function testing

CF in all under 40 - CFTR genetic mutation analysis or sweat chloride

Lung function tests - FEV1, FVC, peak flow (annual repeat)

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105
Q

Tests for CF

A

CFTR genetic mutation analysis

Sweat chloride

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106
Q

Management of bronchiectasis

A

Smoking cessation
Immunisation against influenza and pneumococcus
Healthy diet and physical exercise

Physiotherapy - airway clearing techniques with or without sterile water

Antibiotics (in acute exacerbations) - amoxicillin or clarithromycin - send of sputum and culture

If more than 3 exacerbations per year requiring antibiotics then long term antibiotics (azithromycin)

Beta 1 agonists and anticholinergic bronchodilators (theophylline and aminophylline)
No steroids. No mucolytics.

Oxygen

Surgery - lung resection if not controlled by medical treatment.

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107
Q

Complications of bronchiectasis

A 
Repeated infection
Decreased lung function
Empyema
Lung abscess
Pneuomothorax
Life threatening haemoptysis
Respiratory failure
Cor Pulmonale
Decreased quality of life
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108
Q

Normal pH

A

7.35-7.45

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109
Q

Base excess

A

-2 to +2
Positive numbers = alkalotic
Negative number - acidosis

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110
Q

ABG findings and causes of respiratory acidosis

A

Low pH < 7.35
Raised pCO2
Normal bicarbonate (if no compensation)
Raised bicarbonate (if compensated)

Lung disease - COPD, late asthma
Respiratory depression
Sleep disordered breathing
Neuromuscular disorders causing decreased muscle ability
Increased CO2 production - seizures, hyperthermia, seizures,
Breath holding

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111
Q

ABG findings and causes of respiratory alkalosis

A

High pH > 7.45
Low CO2
Low bicarbonate (if compensating)

Breathing off too much CO2

  • Fever
  • Sepsis
  • Anxiety
  • Aspirin poisoning
  • Pulmonary oedema
  • Pneumonia
  • Profound anaemia
  • Pleural effusion
  • PE
  • Hyperthyroidism
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112
Q

ABG findings and causes of metabolic acidosis

A

Low pH < 7.35
Low bicarbonate
Low CO2 (if compensating)

DKA
Sepsis
Renal failure
Tissue ischaemia
GI loss of bicarbonate (diarrhoea)
Renal tubular disease 
Uraemia
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113
Q

ABG findings and causes of metabolic alkalosis

A

High pH
Raised bicarbonate
High CO2 if compensating

GI loss of H+ (vomiting)
Renal loss of H+ (loop/thiazide diuretics)
Hypovolaemia

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114
Q

Type 1 respiratory failure and Causes

A

Hypoxaemic respiratory failure
Low O2 with normal or low CO2

COPD
Pneumonia
Pulmonary oedema
Asthma
Pulmonary fibrosis
Pneumothorax
Pulmonary hypertension
PE
Bronchiectasis
ARDS
Obesity
Cyanotic congenital heart disease
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115
Q

Type 2 respiratory failure and causes

A

Hypercapnic respiratory failure
High pCO2 and low O2

COPD
Severe asthma
Drug OD
Myasthenia gravis
Polyneuropathy
Polio
Muscle disorders
Head and neck injury
Pulmonary oedema
ARDS
Hypothyroidism
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116
Q

Non-respiratory causes of respiratory failure

A 
Hypovolaemia
Shock (septic or cardiogenic)
Severe anaemia
Drug OD
Neuromuscular disease
Spinal/head injury
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117
Q

Signs and symptoms of respiratory failure

A 
Dyspnoea
Confusion
Tachypnoea
Cyanosis
Stridor
Accessory muscle use
Anxiety
Headache
Retraction of intercostal spaces
Hypoventilation
Polycythaemia (chronic)
Cor pulmonale
Cardiac arrhythmia
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118
Q

Investigations in respiratory failure

A 
Pulse Oximetry
ABGs
ECG
D-dimer for PE
CXR
Pulmonary function tests
LFTs and U&amp;Es 
TFTs
Echo
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119
Q

Management of respiratory failure

A

ABCDE
Supplemental o2 to sats >90%
Treat underlying cause
BiPap
Intubation and mechanical ventilation - RSI
Bronchidialtors, corticosteroids, antibiotics, opiods

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120
Q

Target O2 saturations

A

94-98%

For COPD 88-92%

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121
Q

Indications for humidifying oxygen prior to delivery

A 
Flow rate > 4l/min for several days
Tracheostomy
CF
Bronchiectasis
Chest infection training secretions
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122
Q

Risk factors for CAP

A 
Extremes of age
Smoking 
Alcohol
Previous recent viral illness (predisposes to strep pneumonia)
Asthma
COPD (increased H. influenza or morexella)
Malignancy
Bronchiectasis
CF
Immunosuppression - AIDS, chemo etc. (increased gram negatives, S.aureus or P.jiroveccii)
IV drug use (S. aureus)
Diabetes
CV disease
Nursing home (H. influenza)

Hospitalisation - hospital acquired

Decreased consciousness, neurological disease = aspiration

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123
Q

Signs and symptoms of pneumonia

A 
Productive cough
Purulent sputum
Breathlessness
Fever
Malaise

Focal chest signs
Increased temperature
Tachypnoea. Tachycardia. 
Bronchial breathing + crepitations
Dullness on percussion
pleural rub
Pleuritic chest pain

Confusion, myalgia, anorexia, fatigue (in elderly)
Non-specific symptoms + abdo pain (children)

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124
Q

Typical pathogens for CAP

A
  • Streptococcus pneumonia (66%)
  • Haemophilus influenzae
  • Klebsiella pneumonia
  • Staphylococcus aureus
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125
Q

Streptococcus pneumonia

A

Gram positive
Diplococci
Common in winter
Common in creasing age, co-morbidities, CV disease, a

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126
Q

Haemophilus influenzae

A

Gram positive

Coccobaccilus

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127
Q

Klebsiella pneumoniae

A

Gram negative
bacillus
More common in men - can cause decreased platelets and leuopaenia

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128
Q

Staph aureus

A

Gram positive
Coccus
More common after influenza like illness

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129
Q

Atypical pathogens for CAP

A

Mycoplasma pneumonia

  • More common in young patients or prior antibiotics
  • Slower onset, neurological complications, dry cough

Chlamydia pneumoniae

  • Initial upper RTI leading to bronchitic or pneumonitic features
  • Cough with scanty sputum
  • Hoarseness, headache

Legionella pneumoniae

  • Sever infection
  • Water sources in Mediterranean
  • Abnormal LFTs, raised CK
  • Mild headache, myalgia, chills, rigors, haemoptysis, GI upset

Pneumocysitic jirovecci
- only in immunocompromised

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130
Q

Investigations for CAP

A

FBC - Raised WCC
Raised CRP
LFTs (decreased albumin)
U&Es - if high urea then poor prognosis
Blood cultures
Urinary antigen tests - legionella or pneumococcus (c-polysaccharide)

CXR
- Consolidation. May have effusions or collapse

Sputum examination and culture
Pulse oximetry or ABGs
Aspiration of pleural fluid for culture

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131
Q

Severity of CAP

A 
CURB65
Confusion
Urea >7
Respiratory rate >30
BP <  90 (systolic)
Age over 65
All worth one point

0 or 1 - LOW
2 = moderate
3 = severe

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132
Q

Management of CAP

A

Smoking cessation
Oxygen for hypoxia
Fluids for dehydration
Analgesics - care with opiates RE respiratory depression

LOW (CURB 0 or 1)

  • Treat at home
  • 5 day course oral amoxicillin
  • If penicillin allergic = clarithromycin or doxycycline

MODERATE (CURB 2)

  • Hospital
  • Amoxicillin and clarithromycin

Severe (CURB 3+)

  • Co-amoxiclav and clarithromycin IV
  • Add levofloxacin if ? legionella
  • ? ITU admission
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133
Q

Complications of CAP

A 
Pleural effusion
Empyema
Lung abscess
pneumothorax
DVT
Bronchiectasis
AKI
Sepsis - pericarditis, endocarditis, osteomyelitis, meningitis
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134
Q

Define hospital acquired pneumonia

A

New radiographic infiltrate in presence of infection with onset 48 hours after admission

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135
Q

RF for hospital acquired pneumonia

A 
Over 70
Chronic lung disease
Co-morbidities
Decreased consciousness
Chest or abdominal surgery
Mechanical ventilation
NG feeding
PHx of antibiotic exposure
Poor dental hygiene
Steroids
Chemotherapy
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136
Q

Causes of hospital acquired pneumonia (bacteria)

A

Gram negative enteric bacilli and pseudomonas

  • Pseudomoas aerginosa - intubation
  • E. Coli
  • Klebsiella

Strep pneumonia and H. influenza
Staph aureus - neurosurgery patients and trauma

Anaerobes e.g. enterobacter after abdo surgery

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137
Q

Antibiotics used in hospital acquired pneumonia

A 
Co-amoxiclav
Ceftriaxome
Tazocin
Carbopenam
Gentamicin
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138
Q

Define pleural effusion

A

Increase in fluid volume between visceral and parietal pleura

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139
Q

Types of pleural effusion

A

Benign (more common) or malignant

Transudate - disruption of hydrostatic and oncotic forces operating across pleural membranes
LOW PROTEIN <30

Exudate - increased permeability of pleural surface - usually due to inflammation
HIGH PROTEIN >30

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140
Q

Causes of transudate pleural effusions

A 
Heart failure
Cirrhosis
Hypoalbuminaemia
Peritoneal dialysis
Atelectasis
Hypothyroidism
Nephrotic syndrome
Mitral stenosis
PE
SVC obstruction
Constrictive pericarditis
Ovarian Hyperstimulation 
Meig's syndrome - benign ovarian tumour, ascites, pleural effusion
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141
Q

Meig’s syndrome

A

TRIAD
Pleural effusion
Ascites
Benign ovarian tumour

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142
Q

Causes of exudate pleural effusion

A 
Pneumonia
Malignancy
Pulmonary infarction
PE
Autoimmune - RA
Asbestos exposure
Pancreatitis
TB
Complication of acute MI (Dressler's syndrome)
Drugs - methotrexate, Amiodarone, nitrofurantoin
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143
Q

Signs and symptoms of pleural effusion

A 
SOB
Cough
Dyspnoea
Pleuritic pain
Dullness on percurssion
Decreased breath sounds
Decreased chest expansion
Decreased tactile and vocal fremitus
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144
Q

Investigations for pleural effusion

A

CXR

  • Blunting of costophrenic angles
  • 200ml needed to see PA, 50ml on lateral

Thoracocentesis/pleural aspiration

  • Only if exudate
  • Cytology, protein, LDH, pH, gram stain, culture and sensitivity, lipids, amylase (pancreatitis)
  • Not if bilateral
ESR
CRP
Albumin
Amylase
TFTs
Blood cultures
D-Dimer
CT

CT of thorax +/- abdomen
Pleural biopsy
Thoracoscopy/Bronchoscopy

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145
Q

Causes for bloody thoracocentesis

A 
Malignancy
PE
Infraction
Trauma
benign asbestos
Post cardiac injury syndrome
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146
Q

Causes for low pH or glucose in thoracocentesis

A 
Infection and empyema
RA
SLE
TB
Malignancy
Oesophageal rupture
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147
Q

Management of pleural effusion

A

Aimed at treating underlying cause
If small then observe
If large the tapping fluid can give symptomatic relief and is useful for diagnosis but recurrence common
DO NOT DRAIN MORE THAN 1.5L in one go

Chest drain
(Can use long term indwelling pleural draining in malignant effusions)

Pleurodesis - injection of sclerosing agent to cause pleural adhesion and prevent recurrence - sterile talc, tetracycline, bleomycin

Pleurectomy if all other options failed

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148
Q

Indications for a chest drain

A 
Pneumothorax
Traumatic pneumothorax
Pleural effusion
Haemopneumothorax
Peri-operative - oesophageal or cardiothoracic surgery
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149
Q

Safe triangle for chest drain insertion

A

Between

  • Lateral edge of pec major
  • Base of axilla
  • Lateral edge of lat dorsi
  • Above 5th IC space

If apical pneumothorax - 2nd intercostal space

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150
Q

Process of chest drain

A

Patient lying at 45 degrees. arms raised.
Local anaesthetic
Thoracostomy or seldinger technique used to insert tube
Insert into safe triangle
Aspirate fluid and/or air
Open incision with blunt dissection of deep tissue
Connect drainage system
DO NOT REMOVE MORE THAN 1.5L
Suture to skin
CXR to confirm placement

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151
Q

Complications of chest drain

A

Incorrect placement
Injury to intercostal muscles
Perforation of other vessels
Pain

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152
Q

Define pneumothorax

A

Collection of air in the pleural cavity resulting in the collapse of the lung on the affected side
Extent of collapse depends on amount of air

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153
Q

Types of pneumothorax

A 
Primary spontaneous
Secondary spontaneous
Tramatic
Iatrogenic
Catamenial
Tension
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154
Q

Primary spontaneous pneumothorax

A 
Occurs in healthy people
Increased in:
Tall, thin and healthy
Male
Marfan's 
Prengnacy
Smokers

Occurs from ruptures of blebs and bullae

155
Q

Secondary spontaneous pneumothorax

A

Associated with underlying lung disease
Consequences are greater and management more difficult

Associated with:
Smoking
COPD
Asthma
HIV
TB
Sarcoidosis
CF
Cancer
Idiopathic pulmonary fibrosis
Ehler's Danlos syndrome
RA
Marfan's
FHX
Ankylosing spondylitis
156
Q

Traumatic pneumothorax

A

Follows penetrating chest trauma
Stabbing/gun shot/fractured rib
High risk occupations - diving or flying

157
Q

Iatrogenic pneumothorax

A

Following certain medical procedures

Lung biopsy
Transthoracic needle aspiration
Throacocentesis
Central line insertion
Intercostal nerve block
Tracheostomy
APR
NG tube placement
158
Q

Catamenial pneumothorax

A

At time of menstruation
30-40 years old with pelvic endometriosis
90% in R lung and within 72 hours of onset of menstruation

159
Q

Tension pneumothorax

A

MEDICAL EMERGENCY

Occurs in - ventilated patients, trauma, CPR, lung disease, blocked or clamped chest drain, hyperbaric oxygen treatment

160
Q

Signs and symptoms of pneumothorax

A 
Sudden onset pain - stabbing, radiating to shoulder, increased on inspiration
SOB - depends on size
Cyanosis
Distressed
Sweating
Decreased breath sounds or absent over affected area
Hyper resonance
Trachea deviates AWAY from pneumothorax
Symptoms can be minimal in primary

Tension

  • Hypotension
  • Raised JVP
  • Tachycardia
  • Pulsus paradoxicus (pulse slows on inspiration)
161
Q

Pathophysiology of pneumothorax

A

In normal respiration, pleural space has negative pressure
As chest wall expands, surface tension of pleura expands lung outwards
If pleural space invaded by gas then llung collapses until equilibrium is achieved or rupture sealed
Decreased vital capacity
Decreases PaO2

Tension

  • Injured tissue forms one way valve
  • Air allowed in but not out
  • Increases pressure, lung collapses and hypoxia
  • Decreased venous return to heart
  • Respiratory insufficiency, CV collapse and death
162
Q

Investigations for pneumothorax

A

CXR
- Lung edge and absent lung markings peripherally
- Blunting of ipsilateral costophrenic angle
- Width of rim of air is used to classify size
(Small <2cm, Large >2cm) 2cm= 50% of lung volume

US

Chest CT in complicated or uncertain cases

ABGs - hypoxia more disturbed in secondary
Occasionally hypercapnia

163
Q

Management of pneumothorax

A

Is tension pneumothorax suspected? - YES then immediate needle decompression followed by chest drain insertion

PRIMARY

  • Depth less than 2cm - discharge and follow up
  • > 2cm aspirate. In then under 2cm with clinical improvement then discharge and follow up
  • If no improvement then Admit and fit chest drain

SECONDARY

  • Over 2cm or SOB - admit and fit chest drain
  • Depth 1-2cm - aspirate, if <1cm then admit, high flow O2 and observe, if >1cm then admit and fit chest drain
  • If <1cm then admit, high flow O2 and observe

Aspirate = thoracocentesis

  • 2nd or 3rd intercostal space, midclaviucular line
  • OR 4th or 5th intercostal space over superior rib margin in anterior axillary line
  • Enter just above a rib

Pleurodesis if risk high

Surgery
- If persistent air leak or failure of lung to expand
Open thoracotomy and pleurectomy
OR VATS - video assisted throacoscopic surgery and pleurectomy is better tolerated but higher recurrence

164
Q

Surgical emphysema

A

Also known as subcutaneous emphysema
- Occurs as air tracks below skin under pressure from pleural space
- Results from large air leaks or blocked chest drain
Harmless
treat with high flow oxygen

165
Q

Risk factors for PE

A
  • Major abdo/pelvic surgery
  • Post-op ITU
  • Late pregnancy
  • Malignancy
  • Fractures
  • C-section
  • Varicose vein surgery
  • Decreased mobility
  • Hospitalisation
  • Spinal cord injury
  • IV drug use
  • Major trauma
  • Central venous lines
MINOR
- congenital heart disease
- congestive heart failure
= hypertension
- COCP
- Stroke
- myeloproliferative disorders
- thrombotic disorders
- HRT
- COPD
- Sedentary travel
- Obesity
- IBD
166
Q

Virchows triad

A

Venous stasis
Vessel wall damage
Hypercoagulability

167
Q

Pathophysiology of PE

A

Virchow’s triad - venous stasis, vessel wall damage, hypercoagulability

  • Endothelial damage prmotoed thrombus formation, usually at valves
  • Poor blood flow and stasis also promotes thrombus formation

Thrombus forms and dislodges, becomes trapped in pulmonary vasculature
Obstruction increased pulmonary resistance
Increased work of right ventricle
R ventricle over distension, increased end diastolic pressure and decreased output

168
Q

Symptoms of PE

A 
Dyspnoea
Pleuritic pain
Cough
Haemoptysis
Dizziness
Syncope
Any chest symptoms with signs of DVT
169
Q

Signs of PE

A 
Tachypnoea
Tachycardia
Hypoxia
Pyrexia
Raised JVP
Pleural rub
Hypotension
Cardiogenic shock
Gallop heart rhtyhm
170
Q

Investigations for PE

A

Wells PE Score

  • If more than 4 points then likely then CTPA
  • If 4 or less points then unlikely - D-dimer, if positive then CTPA

CTPA first line

Baseline investigations -

  • O2 sats
  • FBC, U&Es, clotting, troponin

ECG

  • S1Q3T3 deep s waves in I, Q waves in III, inverted T waves in III
  • Right axis deviation
  • RBBB
  • Right ventricular strain
  • Sinus tachycardia
  • AF

CXR - usually normally, may have decreased vascular markings
Late sign = Hampton’s hump

ABGs = low PaO2, low PaCO2 if hyperventilation

D-dimer - raised in VTE, not specific

Leg US - if suspected DVT

If no cause found - need to investigate for an undiagnosed cancer

171
Q

ECG changes in PE

A
  • S1Q3T3 deep s waves in I, Q waves in III, inverted T waves in III
  • Right axis deviation
  • RBBB
  • Right ventricular strain
  • Sinus tachycardia
  • AF
172
Q

Wells PE Score

A

Suspected DVT - 3
Alternative diagnosis less likely than PE - 3
Tachycardia - 1.5
Immobilisation >3 days or surgery in last 4 weeks - 1.5
Hx of DVT or PE - 1
Haemoptysis - 1
Malignancy - 1

If 4 points or less UNLIKELY (D-dimer)
If OVER 4 points LIKELY (CTPA)

173
Q

Management of a PE

A

Resuscitation - oxygen, IV access, analgesia

Anticoagulation

  • LMWH, fondaparinux ASAP unless renal impairment, significant bleeding risk or haemodynamic instability
  • Continue for 5 days
  • Warfarin or rivaroxiban once confirmed within 24 hours and continue for 3 months
  • Only thrombolysis with alteplase if hypotensive

If not suitable for anticoagulation - IVC filters
Surgical embolectomy if high risk or failed or contraindicated thrombolysis

174
Q

Signs/symptoms of DVT

A

Limb pain and tenderness along line of deep veins
Unilateral swelling of calf or thigh
Pitting oedema
Distension of superficial veins
Increased skin temperature
Skin discolouration (red)
Palpable cord - hard thickened, palpable vein

175
Q

Investigations of DVT

A

Wells score for DVT
Likely 2 or more
Unlikely <2

Likely = Proximal leg vein US
Positive = DVT
Negative D-dimer

Unlikely = D-dimer
If positive then proximal leg vein US

CT/MRI venography
Contrast venogram (old gold standard)

If no diagnosis of cancer and first DVT over 40 - CT abdo and chest + mammogram

176
Q

Wells score for DVT

A

Likely 2 or more
Unlikely <2

Active cancer - 1
Paralysis or immobilisation - 1
Recently bedridden - 1
Localised tenderness in leg veins -  1
Entire leg swelling - 1
Calf swelling >3cm - 1
Unilateral pitting oedema - 1
Previous DVT - 1
Collateral superficial vein - 1

If alterative cause at least as likely - MINUS 2

177
Q

Management of DVT

A

As PE

Anticoagulation

  • LMWH, fondaparinux ASAP unless renal impairment, significant bleeding risk or haemodynamic instability
  • Continue for 5 days
  • Warfarin or rivaroxiban once confirmed within 24 hours and continue for 3 months
  • Only thrombolysis with alteplase if hypotensive

If not suitable for anticoagulation - IVC filters
Consider extending anticoagulant >3m if high risk of recurrence and no increased bleeding risk
Below knee compression stockings after swelling gone down or 1 week

178
Q

Post-thrombotic syndrome

A 
Chronic venous hypertension
Pain
Swelling
Hyperpigmentation
Dermatitis
Ulcers
Gangrene

Post DVT in 20-40%

179
Q

DVT prophylaxis

A

High risk patients -0

  • GA with surgery > 90 minutes
  • Acute surgical admission
  • Decreased mobility
  • 1 or more risk factors for DVT/PE
  • Avoid dehydration
  • Early mobilisation
  • Graduated compression stockings
  • Intermittent pneumatic compression devices
  • LMWH/Fondaparinux/Unfractionated heparin (if CKD)
180
Q

Macule

A

Complelely flat lesion

Smooth small area of colour change <1.5cm

181
Q

Papule

A

Discrete raised palpable lesion <1cm

182
Q

Nodule

A

Discrete raised palpable lesion >1cm

183
Q

Pustule

A

Small raised lesion filled with purulent fluid

184
Q

Plaque

A

Raised area of skin with flat top and clear edge

Circumscribed, superficial, elevated plateau 1-2cm

185
Q

Lichenification

A

Hard thickening of skin with accentuated skin markings

Results from inflammation or rubbing

186
Q

Vesicles

A

Small superficial circumscribed containing serous fluid < 0.5cm

187
Q

Bulla

A

Large superficial circumscribed containing serous fluid > 0.5cm

188
Q

Wheal

A

Transient circumscribed elevated papules or plaques with erythematous borders and pale centres

189
Q

Define psoriasis

A

Chronic T cell mediated autoimmune condition affecting extensor surfaces

Involves hyperproliferation of the keratinocytes in the epidermis with increased cell turnover rate

190
Q

Epidemiology of psoriasis

A

Female 5-10 years
Male 15-19 years
Peak for both in 60-70 years
Genetic influence in younger category

Gender equal
More common in Caucasians
FHx - YES (30%) HLA Cw6

RF
IBD
Immunocompromised

191
Q

Triggers for psoriasis

A 
Streptococcal infection (guttate psoriasis)
Winter
HIV infection
Psychological stresses
Post partum hormonal changes
Smoking
Alcohol
Skin trauma
Drugs - lithium, antimarials, steroid withdrawal, beta blockers, NSAIDs, ACEi, antibiotics
192
Q

Types of psoriasis

A 
90% extensor plaque psoriasis
Flexural
Guttate
Pustular
Unstable
Erythrodermic
Psoriatic arthritis
Napkin
Nail
193
Q

Clinical presentation of psoriasis

A

Commonly extensor surfaces - elbows, knees, scalp, trunk, nails, genitals
Erythematous plaques
Well demarcated, non-coherent silver plaques
Scaling - thickened with masses of adherent shedding white scales
Scratching produces waxy appearance (tache de bougie = candle wax)
Glassy homogeneous erythema
Symmetrical
Can be encircled by paler peripheral zone
nail changes

Kobners reaction - new lesions at site of trauma or injury
Pustules in palmoplantar psoriasis

Auspitz sign - when scales scraped off reveals dilated blood vessels beneath

194
Q

Auspitz sign

A

Psoriasis

when scales scraped off reveals dilated blood vessels beneath

195
Q

Nail changes in psoriasis

A

Oncholysis - nail lifting off bed
Subungal hyperkeratosis - accumulation of chalky material under nail
Pitting
Beau’s lines - transverse lines on nail bed
Splinter haemorrhages

196
Q

Pathophysiology of psoriasis

A

Keratinocytes grow from epidermal base to surface.
In psoriasis there is increased turnover from 23 days to 3-5 days causing thickened skin
Normally lose nuclei but quick progression leads to retained nuclei

Genetic predisposition - HLA Cw6
Combined with precipitating factors

Involvement of IL12, IL23, TNF and IFN gamma

197
Q

Flexural psoriasis

A

Smooth inflamed regions
Without scaling due to moist area
Armpit, groin, under breast and skin folds
Needs to be distinguished from fungal infection

198
Q

Guttate psoriasis

A

Small salmon pink plaques 1-10cm in diameter
Predominantly on trunk
May be scaly
Appears suddenly 2-3 weeks after URTI with group B strep
Usually completely resolves in few weeks but can start chronic psoriasis

199
Q

Pustular psoriasis

A

Sterile pustules on palms and soles
Can be diffuse over the body
It may cycle through: erythema-pustules-scaling
If diffuse then often associated with fever and unwell
Most are smokers
Can be precipitated by oral steroids

200
Q

Unstable or erythrodermic psoriasis

A 
Generalised erythema
Pain
Itching
Fine scaling
Covers nearly all body surface area
Accompanied by fever, chills, hypothermia and dehydration 
Very serious
Systemically unwell
201
Q

Psoriatic arthritis

A

Usually in small joints
Occurs in 5-10%
Stiffness, pain, progressive
Causes permanent joint damage

202
Q

Investigations for psoriasis

A

Diagnosed clinically
Can do biopsy
Would show - basal cell hyperplasia, proliferation of subepidermal vasculature, absence of normal cell maturation and keratinisation

203
Q

Management of psoriasis

A

1st line - topical therapies: corticosteroids, tar, vitamin D analogues
2nd line - phototherapy +/- systemic therapy
3rd line - biological therapy

Topic therapy

  • Regular emollient
  • Topical steroids: short term or intermittent use of beclamethasone (potent)
  • if facial or flexural used moderate potency - clobetasone
  • Vitamin D analogues: used for longer term treatment, improvement in 2-8 weeks. CALCIPOTRIOL
  • Risk of hypercalcaemia, parathyroid hormone suppression
  • Coal Tar
  • Tazarotene gel (vitamin A analogue)

Photochemotherapy

  • PUVA (photosensitive drug) + UVA light
  • 2-3 times per week

Systemic agents
- Methotrexate (ciclosporin if pustular)
- Works in 4-12 weeks
2nd line - hydroxycarbamide, sulfasalazine, azathioprine, leflunomide

Biological therapy

  • etanercept
  • efalizumab
  • adalimumab
  • infliximab
204
Q

Classification of psoriasis

A 
Psoriasis area and severity index (PASI)
For each area calculate:
- % involved
- severity of erythema
- thickness and scaling
205
Q

Define eczema

A

Chronic, relapsing inflammatory skin condition

Characterised by itchy red rash that favours skin creases

206
Q

Epidemiology of eczema

A 
Very common
High prevalence 20% children, 2-18% of adults
Most cases are in under 5s
Equal in gender
Mainly Caucasian
High in developed countries
FHx associated
207
Q

Risk factors for eczema

A

Irritants - soaps and detergents
Skin infections - S.aureus
Contact allergens
Extremes of temperature or humidity
Abrasive factors or fabrics
Dietary factors
Inhaled allergens - dust mites, pollen, dander, moulds
Genetic mutation in production of FILLAGRIN - converts keratinocytes to outmost layer of skin
Stress
Hormonal changes - pre-menstrual changes, flare ups

208
Q

Aetiology of eczema

A

Combination of genetic susceptibility and environmental factors

  • Defects in skins barrier function (FILAGGRIN)
  • Immune dysregulation
  • Allergen exposure
209
Q

Diagnostic criteria for eczema

A

Itchy skin condition plus 3 or more of the following:

  • History of itchiness in skin creases
  • History of asthma or hayfever (or in 1st degree relative if under 4)
  • General dry skin in preceding year
  • Visible flexural eczema
  • Onset in first 2 years of life

Associated disease: asthma, hayfever, allergic rhinitis

210
Q

Types of eczema

A 
Atopic
Pityriasis alba
Eczema herpeticum
Lichen simplex
Asteatotic 
Discoid
Pompholyx
Varicose
211
Q

Pityriasis alba

A

Type of eczema

Pale patches of hypopigmentation on face of children

212
Q

Eczema herpeticum

A

Herpes simplex virus infection superimposed onto skin affected by eczema.
History of contact with adult with cold sore
- Areas of rapidly worsening painful eczema
- Clustered blisters consistent with early stage cold sores
- Punched out erosions
- 1-3mm and uniform
- Fever, lethargy or distress

213
Q

Lichen simplex

A

Localised areas of lichenification from rubbing

214
Q

Asteatotic eczema

A

Older people with dry skin on lower legs

Crazy paving

215
Q

Discoid eczema

A 
Intensely pruritic
Coin shaped lesions
Most commonly on limbs
May be vesicular
Frequently colonised by S. aureus
More common in males
216
Q

Pompholyx eczema

A 
Itching vesicles
Fingers, palms and soles
Blisters are small, firm and intensely itchy
Occasionally painful
More common in nickel allergy
217
Q

Varicose eczema

A

Occurs in lower legs with venous insufficiency

Haemosiderin pigmentation

218
Q

Pathophysiology of eczema

A

Impairment in skin barrier function leading to increased sensitisation to cutaneous antigens
Links to genes of EDC - epidermal differentiation complex
Links to FILAGGRIN - mutation leads to poor barrier function
Immune response is predominantly TH2 mediated - IL 4, 5, 13
These interleukins increase production of IgE and eosinophilia
Persistent inflammation and scratching can lead to chronic atopic dermatitis with thick lichenified skin

219
Q

Signs and symptoms of eczema

A

Tendency for dry skin
Flare ups may vary from vesicles to areas of poorly demarcated redness - crusting, scaling, cracking or swelling
Repeated scratching causes thickening of chronic lesions

Infancy - face, scalp, extensor surfaces
Adults - generalised dryness and itching

Can develop bacterial infection - crusting, weeping, postulation, cellulitis

220
Q

Investigations for eczema

A

Not usually required for diagnosis
Mild atopic eczema do not need clinical testing for allergies

Estimation of IgE and RASTs (radioallergosorbent tests) only confirm atopy

RAST and prick testing assess type 1 hypersensitivity

Swab if infection

Assess severity - eczema area and severity index
For each body area - %area, severity score, redness, thickness, scratching, lichenification

221
Q

Management of eczema

A

Avoid provoking factors

Emollients - liberal and frequent

Topical steroids - mild potency on face, potent in lichenified or discoid eczema if on limbs or trunk

  • Once of twice daily
  • Short periods only

Tacrolimus and pimecrolimus
- If not controlled by maximal topical steroid or s/e too great

Treat infections with flucloxacillin

Severe may require

  • Phototherapy
  • Systemic steroids
  • Systemic therapy (azathioprine, ciclosporin)
  • Wet wraps with emollient under
222
Q

When to refer eczema

A 
Diagnosis uncertain
Uncontrolled (1-2 flare ups per month)
On face and not responding
Contact dermatitis
Severe bio/psycho/social issues
Severe and recurrent infections
223
Q

Define contact dermatitis

A

Inflammatory skin reaction in response to an external stimulus acting as an allergen or irritant

224
Q

Risk factors for contact dermatitis

A

More common in females
Most commonly occupational

Working with wet hands, soap and cleaning materials
Florists
hairdressers
Cooks
beautician
Nurses/doctors e,g, gloves
225
Q

Aetiology of contact dermatitis

A

Allergic contact dermatitis - type 4 hypersensitivity reaction. Often occurs after sensitisation and subsequent re-exposure to an allergen

  • cosmetics
  • metal: nickel/cobalt
  • topical medications
  • rubber additives
  • textiles
  • acrylic
  • plants

Irritant contact dermatitis - inflammatory response that occurs after damage to the skin, usually by chemicals. Not an allergy. Can occur in anyone exposed to the irritant. Can be acute or chronic

  • water
  • detergent/soap
  • solvents/abrasives
  • Acids and alkalis
  • Reducing agents
  • Plants
  • Powders, dust and soil
226
Q

Pathophysiology of contact dermatitis

A

Allergic contact dermatitis

  • Requires prior sensitisation to occur
  • Most allergens are HAPTENS than must bind to proteins to become antigenic
  • Hapten protein complex enters the statum corneum and binds to epidermal antigen presenting cells in Langerhans cells
  • These cells process the antigen and present it to CD4 T cells
  • They proliferate into memory and effector T cells which illicit allergic contact dermatitis in 2-4 days
227
Q

Signs and symptoms of irritant contact dermatitis

A 
Burning
Stinging
Soreness
Onset with 48 hours, can be immediate
Rash only in exposed areas
Quick resolution with removal
Commonly associated with atopic eczema
Exposure to soap, water
228
Q

Signs and symptoms of allergic contact dermatitis

A 
Redness, itching, scaling
Delayed onset
Rash not only in exposed areas
Resolution longer
Decreased associated
229
Q

Investigations in contact dermatitis

A

Made on clinical findings and history
Patch testing is gold standard - should always be done if occupational
Occasionally skin biopsy

230
Q

Management of contact dermatitis

A

Avoidance of irritant
Notify HSE all occupational cases
Liberal emollient
Topical corticosteroids - potency depends on severity
In acute severe - short course of oral steroids or if over 20% surface area
2nd line - PUVA + phototherapy, ciclosporin or azathioprine

231
Q

Type 1 Hypersensitivity reaction

A

Mediated by IgE
Allergic reaction provoked by RE-EXPOSURE to a specific type of antigen referred to as an allergen

  • Asthma
  • Anaphylaxis
  • Penicillin allergy
  • Food allergy
232
Q

Type 2 hypersensitivity reaction

A

Cytotoxic reactions which produce haemolysis and purpura
Produced antibodies bind to antigens on patient’s own cell surfaces
B cell mediated - produce antibodies against foreign antigens.
IgG and IgM bind and form complexes - classical pathway of complement activation

  • ABO blood incompatibility
  • Goodpasture’s syndrome
233
Q

Type 3 hypersensitivity

A

Immune complex reactions which result in vasculitis, serum sickness and urticarial

  • Accumulation of immune complexes (antigen antibody complexes) that have not been adequately cleared
  • Giving rise to inflammatory response and attraction of leukocytes
  • SLE
  • RA
  • Post-streptococcal glomerulonephritis
  • Polyarteritis nodosa
  • Reactive arthritis
  • Serum sickness
  • Farmer’s lung
  • Henoch-Schonlein purpura
234
Q

Type 4 hypersensitivity

A

Delayed type reaction with cell-mediated hypersensitivity
CD4 T cells recognise antigen with MHC II complex on surface antigen cells
Secretion of IL2 and interferon gamma, release of cytokines
CD8 cells destroy target cells on contact

  • Allergic contact dermatitis
  • Autoimmune myocarditis
  • Type 1 DM
  • Granulomas
  • Hashimoto’s thyroiditis
  • IBD
  • MS
  • RA
235
Q

Toxic epidermolysis necrolysis (TEN)

A 
Drug induced skin reaction
7-14 days after first drug exposure
Or 3 days after 2nd exposure
Potentially fatal
50% mortality
On spectrum with Steven-Johnson syndrome, SJS if <10% of body, TEN >30%

Burning painful macular or popular rash that spreads from the face
Bullae form and coalesce.
Epidermis slough in sheets
Hyperpyrexia

Causes:

  • Allopurinol
  • Anticonvulsants
  • NSAIDs
  • Penicillin
  • Sulfonamides
236
Q

Stevens-Johnson syndrome

A 
Drug induced skin reaction
10% mortality
Severe mucosal infection
Flu like symptoms
lesions on palms, soles, dorsum of hands, trunk
Macule -> papules, vesicles, bullae

Can be caused by malignancy in adults or viral infection

  • Amoxicillin
  • Allopurinol
  • Carbamazepine
  • Ciprofloxacin
  • Diclofenac/ibuprofen
  • Lamotrigine
  • Phenytoin
  • Penicillin’s
  • Tetracycline’s
237
Q

Acute generalised exanthematous pustulosis

A

Drug induced skin reaction
Acute onset of fever with generalised erythema
Small sterile non follicular pustules

Caused by
antibiotics
Paracetamol
sertraline
diltiazem
furosemide
238
Q

erythema nodosum

A 
Acute nodular erythematous eruption 
Front of shins
Flu like symptoms
Drug reactions
COCP
Penicillin
Sulfonamides

Also associated with: IBD, Streptococcal infection in children, TB, EBV, Sarcoidosis, bechet’s disease, pregnancy, cancer

239
Q

Fixed drug reactions

A

Recur in same area when the same drug is give
- Plaques circular and oedematous
- Resolve to macular hyperpigmentation
- Hands, feet, genitals
Caused by aspirin, antibiotics, NSAIDs, COCP, phenytoin and benzos

240
Q

Investigations for drug induced skin reaction

A

Remove drug
FBC - if serious can have leukopaenia, thrombocytopaenia and eosinophilia
Monitor LFTs and U&Es
2 blood samples for mast cell tryptase if ?anaphylaxis
Prick testing is dangerous - only used for penicillin allergy
Oral provocation tests are gold standard but require strict supervision

241
Q

Impetigo

A 
Child
Usually face and limbs
Highly contagious
Background erythema with yellow crusting and exudates
If bullae = staph aureus
If lymphadenopathy = strep pyogenes
242
Q

Bacterial folliculitis causes

A

Usually legs, bearded area and scalp
Precipitated by waxing and shaving
Staph aureus or pseudomonas aeruginosa

243
Q

Ecthyma

A 
Deep form of impetigo
Mainly on legs
Slow healing
Small bullae with adherent crust overlying ulceration
Group A strep or Staph aureus

Treat with oral penicillin

244
Q

Erysipelas

A

Face or lower leg
Skin infection with strep pyogenes / group A strep
Well demarcated, red, shiny, raised, spreading plaque

245
Q

Management of skin infections

A

Antiseptic skin washes e.g. chlorhexidine hydrochloride
Topical antibiotics - localised infections (fusidic acid) maximum of 2 weeks

Oral antibioics

  • if extensive
  • Staph = flucloxacillin
  • Strep = penicillin
246
Q

Describe phototherapy

A

3 main types:

  • Broadband UVB
  • Narrow band UVB
  • PUVA = psoralen + UVA = photochemotherapy

Uses UV light to decrease inflammation
Given as hospital outpatient 2-5 times per week
Average course = 15-20 treatments
Starting dose calculated using test patch of skin
First dose < 1 minute, up to several minutes

247
Q

Short term side effects of phototherapy

A 
Redness
Folliculitis
Discomfort
Dry itching skin
Blisters
Sunlight induced rash - polymorphic light eruption
248
Q

Indications for phototherapy

A 
Eczema
Psoriasis
Dermatitis
Generalised itching
Cutaneous T cell lymphoma
Vitiligo

These conditions not controlled by topical therapy

249
Q

Contraindications for phototherapy

A 
Can't attend regularly
Made worse by sunlight
Can't stand for 10 minutes
Xeroderma pigmentosum
Hx of skin cancer
Lupus erythematous
Taking methotrexate or ciclosporin
Immunosuppressed
Not PUVA in renal or liver disease
Maximum number of treatments reached
250
Q

Describe wet wrapping

A

Wet bandages wrapped over emollients +/- topical steroids
Useful in erythroderma or hot weeping eczema
Cooling as water evaporates
Moisturisers are deeply absorbed

Decreases itching, scratching, redness, inflammation
Increases rehydration and skin healing
Reduces steroid requirement

251
Q

Describe dermatology shared care

A

Dermatologists provide

  • information for patient
  • pre-treatment assessment
  • Initiate treatment
  • Issue clinic letter to GP
  • Assess response to treatment and make dose adjustments

GP

  • Issues prescription
  • Carry out monitoring stated by dermatologists
  • Contact dermatology for any abnormal results
  • monthly blood checks
252
Q

Define basal cell carcinoma

A

Abnormal controlled lesions that arise from basal cells which line the deepest layer of epidermis.
Slow growing, locally invasive malignancy

253
Q

Epidemiology of basal call carcinoma

A 
Most common skin cancer
80% of non-melanoma skin cancers
More common in men
Increases in age
More common in Caucasians
higher in equatorial areas
254
Q

Risk factors for basal cell carcinoma

A 
Genetic predisposition
Exposure to UV radiation 
Sun exposure as a child
Skin type 1-2 (always burns/rarely tans)
PMHx of BCC
Basal cell naevus (Gorlin's syndrome)
Xeroderma pigmentosa
Immuosuppression
255
Q

Xeroderma pigmentosa

A

rare, autosomal recessive disorder.

There is an impairment of the skin’s ability to repair damage from ultraviolet (UV) light, leading to early skin changes, early sunburn, dry skin and a vastly increased tendency to develop skin tumours and eye damage from UV light.

256
Q

Types of basal cell carcinoma

A

Nodular - solitary, shiny, red nodule with large telangiectasia vessels

Superficial

  • Face, trunk and limbs. Equally distributed
  • Erythematous, well demarcated, scaly plaques
  • Rolled edge

Morphoeic

  • sclerosing or infiltrative BCC
  • More aggressive, prone to recurrence
  • Poorly defined borders, thickened yellow plaques

Pigmented

  • Nodular or superficial histology + brown/blue/grey
  • More common in darker skinned people
257
Q

Gorlin’s syndrome

A 
Multiple BCCs
Autosomal dominant
Jaw cysts
Spine and rib abnormalities
Pitting of palms and soles
Cataracts
Calcification of falx cerebri
258
Q

Pathophysiology of BCC

A

Arises from hair follicles
Tumour infiltrates local tissues through slow irregular growth of subclinical finger like projections

Mutations in p53
Activation of sonic hedgehog signally cascade

259
Q

Presentation of BCC

A 
Sun exposed areas of head or neck
Small, translucent or pearly
Raised areas of telangiectasia
RODENT ULCER - indurated edge
Ulcerated centre
Slow growing
260
Q

Investigations for BCC

A 
Visual inspection 
Removal for histology
All specimens must go to histology
All must be biopsied
No format staging beyond examination for lymphadenopathy
261
Q

Management of BCC

A

Surgery - excision with closure. Excise margin of at least 4mm

  • Moh’s micrographic surgery - best for high risk
  • Curettage and cautery
  • Cryotherapy if small and low risk (need to biopsy first for histology)

Non-surgical

  • Topic imiquimod 5% (can use 5-FU)
  • Photodynamic therapy - minimal side effects with good cosmetic result
  • Radiotherapy if recurrent, incomplete excision or bone/cartilage involvement = 90% cure, poor cosmetic outcome
262
Q

Prognosis of BCC

A

Mets rare
Mortality low
Increased risk of SCC and MM

263
Q

Define squamous cell carcinoma

A

Malignant tumour arising from keratinising cells of epidermis or its appendages
Locally invasive
Has potential to metastasise

264
Q

Epidemiology of SCC

A 
Increases with age
Increased in men
Increased in Caucasians
Increased in equatorial regions
2nd most common (behind BCC)
265
Q

Risk factors for SCC

A 
Chronic UV exposure - holidays, outdoor occupation, sunbeds
Fair Skin
Blond/red hair
Chemical carcinogens
HPV infection
Ionising radiation
Immunodeficiency
Chronic inflammation
Xeroderma pigmentosum
Albinism
Bowen's disease
Actinic keratosis
Ciclosporin
266
Q

Pathophysiology of SCC

A

Arises in keratinocytes that have undergone uncontrolled proliferation
Accumulation of genetic mutations
Decrease levels of PTEN (tumour suppressor)
Can be caused by immunosuppression
Precursor: actinic keratosis

267
Q

Presentation of SCC

A

Indurated (hardened) nodular keratinising or crusting tumour
Non healing ulcer in exposed area
Head and neck
Very variable presentation
Sharply defined red scaling plaques
Bleeding and crusting
As it enlarges the centre becomes necrotic
Can give rise to local mets or spread to local lymoh nodes

268
Q

Investigations for SCC

A 
Incisional biopsy
Full excision under local if possible - take dull depth and wide margins
FNA/Biopsy for any enlarged lymph nodes
CT/MRI if ? spread
Refer for dermatological biopsy
269
Q

Management of SCC

A

Refer to dermatology and skin cancer MDT

  • Complete surgical excision and histopathology
  • Curettage and cautery if small <1cm
  • Cryotherapy if small
  • Topical imiquimod 5%
  • Photodynamic therapy has limited efficacy
  • Radiotherapy if it cannot be treated with surgery
270
Q

Prognosis of SCC

A

Met rate <5% but only 30% survival at 5 years if mets occur

Large size, depth increases risk
As does Bowen;’s disease, radiation area or non-exposed sites
Increased if on ear or lip

271
Q

Epidemiology of malignant melanoma

A

4% of skin tumours
More common in women
Women tend to get on arms and legs, men = head and neck
Increases with age
Superfiical spreading is most common subtype
More common in Caucasians

272
Q

RFs for malignant melanoma

A 
Previous history of melanoma
Naevi = more than 100 common or 2 atypical
Atypical mole syndromes
Naevi on unusual suites
Sun exposure
- Acte in childhood and severe sunburn
- Occupation and leisure - airline, gardener, cricketer
- Host response to UV is more important than dose
- Past sun bed use in under 30s
Skin type 1 or 2
Fhx of melanoma
Solar keratosis
Past pesticide exposure
Higher socioeconomic group
273
Q

Types of malignant melanoma

A

Superficial spreading (50%)

  • Large, flat, pigmented lesion which grows laterally before vertical invasion develops
  • More common in females on lower leg

Nodular melanoma (25%)

  • Most aggressive
  • Rapidly growing pigmented nodule which bleeds or ulcerated
  • More common in males
  • Commonest on trunk
Lentigo melanoma (15%)
- patch of lentigo maligna develops a papule or nodule

Acral lentiginous malignant melanoma

  • Pigmented lesions on palms, soles or under nail
  • presents late, poor prognosis
274
Q

Pathophysiology of malignant melanoma

A

Most common sites to spread:
Lymph, liver, lung, bone, brain

BRAF is an activator of MAP kinase
50% of those with melanoma have BRAF mutations
BRAFV600 therapy is a target

275
Q

Presentation of melanoma

A 
NICE 7 point check lists
Major features - 2 points each
- Change in size
- Irregular colour
- Irregular shape

Minor features - 1 point each

  • Size over 7mm
  • Inflammation
  • Oozing
  • Change in sensation

2 week referral if 3 or more points

ABCDE
Asymmetry, Border irregular, Colour irregular, Diameter >7mm, Evolving

Spontaneous bleeding or ulceration
Altered pigmented lesion

276
Q

Investigations for melanoma

A
  • Full thickness excisional biopsy
  • Dermoscopy: examine lesion
  • Genetic testing: CDKN2A
  • All excised lesions to histology
  • Sentinel lymph node biopsy and removal for staging
  • Scan for mets: CXR/CT chest, CT TAP
  • FBCs, LFTs, LDH
277
Q

Breslow thickness

A

Measurement in mm of distance between granular cell layer to deepest identifiable melanoma cell

278
Q

Management of melanoma

A
  • Refer to dermatology
  • Skin cancer MDT
  • DO NOT REMOVE IN PRIMARY CARE
  • Stage 0 = excise with 0.5cm margin. Consider imiquimod
  • Stage 1 = Excise with 1cm margin
  • Stage 2 = Excise with 2cm margin
  • Stage 3 = lymph node dissection. Palliative care
  • Stage 4 - surgery to control symptoms

Targeted treatment - Dabrefenib if BRAF V600 +
Chemotherapy: dacarbazine

279
Q

Prognosis of melanoma

A

Very poor if mets - survival 6-9 months

5 year survival 80%

280
Q

Define Bowen’s disease

A

Squamous cell carcinoma in situ of the skin
Arises in outer layers of epidermis
Risk of progression to invasive SCC is low 3-5%

281
Q

Epidemiology of Bowen’s disease

A

More common in women (75%)
Common in 60-70 years ]
Higher in Caucasians

RFs
- Sun damage
- Irradiation damage
- Carcinogens
- HPV infection (usually HPV16)
Immunosuppression (AIDs, organ transplant)
Chronic skin injury
282
Q

Presentation of Bowen’s disease

A

Slowly growing erythematous patch or plaque
Sharply demarcated, scaling or hyperketatoic with red/pink surface
May be a small erosion
Generally asymptomatic but can bleed
Most on limbs, head and neck (sun exposed areas)

283
Q

Management of Bowen’s disease

A

Cryotherapy - often first line
Topical 5FU
Curettage
Surgical excision

284
Q

Define actinic keratoses

A

Also known as solar keratoses

UV light induced lesions on the skin and are the most common lesions with malignant potential into SCC

285
Q

Epidemiology of actinic keratoses

A

Increase with age
More common in men
More common in Caucasians
Increased in equatorial areas

RFs
Outdoor lifestyle
Sun beds
Working outside
Immunosuppressed
Skin type 1 or 2
286
Q

Presentation of actinic keratoses

A

Sun exposed areas
Telangiectasis, elastosiss
Small rough spots, more easily felt than seen
Enlarge over time becoming red and scaly
Can be pigmented, have horn like projection or be thickened
Flare and erythematous when immunosuppressed
10% undergo malignant change

287
Q

Investigations for actinic keratoses

A 
None unless malignancy suspected
Biopsy if:
- pronounced hyperkeratosis or erythema
- recurring lesions
- unresponsive to treatment
- confluent lesions
- transplant recipient
- past history of SCC
288
Q

Management of actinic keratoses

A

Mild = emollient or no therapy

Topical 5FU
Phototherapy if superifical
Curettage or excisional surgery for histological information

Refer if multiple confluent AKs, organ transplant patient or unclear diagnosis

289
Q

Seborrhoeic keratosis

A

Flat topped warty looking lesions that appear stuck on
Usually pigmented
Well circumscribed
Surface pitted and irregular with visible keratin dots giving a rough and glandular appearance
Most common on trunk
Usually asymptomatic

290
Q

Skin types

A 
1 - always burns, never tans
2 - always burns, sometimes tans
3 - somestimes burns, always tans
4 - never burns, always tans
5- brown skin (Asian)
6 - Black skin
291
Q

FEV1

A

Volume of air the patient is able to exhale in the first second of forced expiration

292
Q

FVC

A

Forced vital capacity

Total volume of air a patient can forcibly exhale in 1 breath

293
Q

FVC and FEV1 in Obstructive lung disease

A

FEV1<80%

FEV1/FVC <70%%

294
Q

FVC and FEV1 in Restrictive lung disease

A

FEV1<80%
FVC<80%
FEV1/FVC>70%

295
Q

Define TB

A

Notifiable disease
Chronic granulomatous disease caused by Mycobacterium tuberculosis
It is spread via inhalation of infected droplets

296
Q

Epidemiology of TB

A

14 per 100,000
Increased in ethnic minorities
Increased in elderly
Increased in Non UK born population

RDs

  • Healthcare worker
  • Alcoholic
  • Close contact of TB patient
  • Homeless / poor housing / over crowding
  • Poverty
  • Drug use
  • Malnutrition
  • Prison
  • Immunocompromised
  • HIV (60% have TB)
  • Haematological cancers
  • Diabetes
  • long term steroids
  • Silicosis
297
Q

Aetiology of TB

A

Causes by mycobacterium tuberculosis

Can be
Multi-drug resistant - resistant to more than 1 drug
Extensively drug resistant = resistant to more than 3 drugs

298
Q

Pathophysiology of TB

A
  • Primary infection host macrophages in lung engulf organisms and carry to hilar lymph nodes which forms GHON FOCUS
  • Some organisms disseminate via lymph nodes to distant sites
  • Small granulomas are formed around the body to contain the bacteria
  • 80% heal spontaneously and bacteria are eliminated
  • OR bacterial remain encapsulated in defensive barrier but persist
  • DORMANT DISEASE

Secondary TB - activation of dormant disease
usually preceded by immunosuppression, malnutrition, aids.
Reactivation usually occurs in APEX of lungs and can spread

299
Q

Miliary TB

A

When primary infection is not adequately contained it enters the blood stream and causes severe disease

300
Q

Presentation of TB

A

Most cases occur from latent infection from previous exposure
Onset is insidious
1y infection - asymptomatic
2y infection is variable and non-specific

TB can affect all organs and body systems

  • General symptoms: fatigue, weight loss, anorexia, pyrexia
  • Pulmonary symptoms: chronic productive cough +/- haemoptysis, lobar collapse, bronchiectasis, pleural effusion, pneumonia, pneumothorax
  • GU: most common site outside of lung. infertility, pyuria, swelling of epididymis
  • MSK: pain, arthritis, osteomyelitis, nerve compression
  • CNS: meningitis
  • GI: ileocecal regions: abdo pain, bloating, obstruction
  • Lymph nodes: tender, firm, discrete
  • Skin
  • pericardial effusion
301
Q

Investigations for TB

A

CXR (even if no pulmonary symptoms)

  • Primary: central apical portion + lower lobe infiltrate or effusion
  • Severe = millet seeds
  • patchy nodular shadows
  • upper zones
  • Loss of volume
  • fibrosis +/- cavitation

Microbiology - 3 sputum samples for culture

  • Analysed using Ziehl-Neelson stain to test for acid/alcohol fast bacteria
  • 4-8 weeks for culture as slow growth

lab tests for HIV, Hep B and C

FBC, U&Es, CRP, ESR, U&Es

302
Q

What is the Ziehl- Neelson stain used for?

303
Q

Screening and vaccination for TB

A

Mantoux test or IGRA (interferon gamma release assay)

If had vaccine: Mantoux +, IGRA -
If have TB - Mantoux +, IGRA +
If no vaccine, no TB - Mantoux -, IGRA -

Mantoux measures response to tuberculin - <5mm is negative, 5-10mm is positive, 10-15mm is strongly positive

For contact screening use Mantoux

304
Q

Management of TB

A

Notify public health
Most managed as outpatients but some need admitting to monitor drug adherence.
Well ventilated single room, away from immunocompromised

  • 6 months, 4 drugs
  • Isoniazide, rifampicin
  • Ethambutol and pyrazinamide (only for first 2 months)
  • If meningeal then 12 months with 2-3 weeks of steroids
  • Regularly check LFTs due to drug toxicity
  • Avoid ethambutol in renal failure
  • Compliance is a large problem
305
Q

Fibroepithelial polyps

A

Skin tags/acrochordons
- small pedunculated skin coloured papules
occur most frequently with skin folds
0.2-0.5mm

306
Q

Causes of lung fibrosis in upper zones

A 
TB
Extrinsic allergic alveolitis
Coal workers pneumoconiosis
Silicosis
Sarcoidosis
Ankylosing spondylitis
Histocytosis
307
Q

Causes of lung fibrosis in lower zones

A

bleomycin
idiopathic pulmonary fibrosis
Connective tissue disorder
Drug induced - methotrexate, Amiodarone, asbestosis

308
Q

Epidemiology of aortic stenosis

A

Most common valve disease
2-7% of population over 65, 10% over 80s
Can be congenital
Aged 30-60 in rheumatic disease, 50-60 with bicuspid valves, 70-90 with calcific changes

309
Q

Aetiology of aortic stenosis

A

Congenital aortic stenosis
Congenitally biscuspid valve
Rheumatic disease
Degenerative - calcified

310
Q

Pathophysiology of aortic stenosis

A

Cardiac output is maintained at the expense of steadily increasing gradient
LV becomes hypertrophied and coronary blood flow may then become inadequate
Fixed outflow obstruction limits and increase in cardiac output with exercise
Eventually LV cannot overcome obstruction and pulmonary oedema occurs

311
Q

Presentation of aortic stenosis - symptoms

A

Tend to be asymptomatic for years and deteriorate rapidly
SOB on exertion
Angina
Dizziness
Syncope (on exertion)
Predisposition to angina - 50% have coronary artery disease
Risk of sudden death so avoid exertion

TRIAD - chest pain, heart failure and syncope
Episodes of acute pulmonary oedema

312
Q

Signs of aortic stenosis

A 
Ejection systolic murmur
Radiates to carotids
Most commonly heard in aortic area
Slow rising pulse - pulsus parvus et tardus
Narrow pulse pressure
Thrills
4th heart sound if severe
Thrusting apex beat from LV pressure overload
Crepitations from pulmonary oedema
313
Q

Investigations for aortic stenosis

A

ECG: LVH and LBBB
Left ventricular strain pattern, down slowing ST segments, ST depression, T wave inversion

CXR - may be normal
Cardiomegaly, enlarged LV and dilated ascending aorta

Echo: calcified valve with restricted opening, hypertrophied LV
Doppler to measure degree of stenosis

Cardiac catheterisation - identify coronary artery disease and measure gradient across the valve

No exercise testing unless they are asymptomatic

CT and cardiac resonance imaging for quantifying calcification and used in prognosis

314
Q

Management of aortic stenosis

A

Avoid heavy exertion
Early surgical intervention as no medical management can improve outcome

  • Statins
  • Modify atherosclerotic risk factors
  • Digoxin, diuretics and ACEi if awaiting or not suitable for surgery
  • Manage hypertension and maintain sinus rhythm
  • If severe, monitor every 6 months and echo, mild-moderate review yearly

Aortic valve replacement
- Definitive therapy, mortality 1-3%,

Balloon valvuplasty
- NICE recommended but restenosis and deterioration occurs within 6-12 months for most paitnets, only used if unsuitable for replacement

Transcatheter aortic valve implantation

  • Under general or local
  • Balloon valvuoplasty followed by insertion of specialised valve device
  • Fluoroscopy guided
315
Q

Complications of aortic stenosis

A 
LV dysfunction
Heart failure
Infective endocarditis
Small systemic emboli
Sudden death
316
Q

Epidemiology of aortic regurgitation

A

Most commonly caused by rheumatic disease
Peak age 40-60
2%

RFs
Marfan's
SLE
Ehler's Danlos syndrome
Turners
Ankylosing spondylitis 
Reactive arthritis
Takayasu's disease
Behcet's disease
Acute severe follows infective endocarditis or aortic dissection
317
Q

Aetiology of aortic regurgitation

A 
Rheumatic disease
Bicuspid aortic valve
Infective endocarditis
Collagen vascular disease
Degenerative aortic valve disease
Aortic dilatation - Marfan's, aneurysm, dissection, ankylosing spondylitis
318
Q

Pathophysiology of aortic regurgiation

A

LV dilated and hypertrophies to compensate for regurg
Stroke volume can be doubled/tripled
As disease progresses, LV diastolic pressure rises and causes breathlessness

319
Q

Symptoms of aortic regurgitation

A 
Often asymptomatic
Palpitations
breathlessness
Angina
PND
Peripheral oedema
320
Q

Signs of aortic regurgitation

A

Early diastolic murmur
best heard in aortic area
Sitting forward in expiration
Austin Flint murmur
Wide pulse pressure with sudden collapse of pulse at the end
Water hammer/Corrigan pulse
head bobbing with each pulse - Musset’s sign
Pulsus bisferienes (double peak of pulse)
Bounding peripheral pulses
Femoral bruit (Duroziez’s sign)
Capillary pulsation in nail beds - Quincke’s sign
Displaced apex beat
Creps

321
Q

Musset’s sign

A

Head bobbing with each pulse

Seen in aortic regurgitation

322
Q

Quincke’s sign

A

Capillary pulsation in nail beds

Seen in aortic regurgitation

323
Q

Investigations in aortic regurgitation

A

ECG - initially normal, then LV hypertrophy and T wave inversion

CXR - cardiac dilatation, features of left heart failure

Echo - dilated LV, hyperdynamic LV, fluttering anterior mitral leaflet

Cardiac resonance imaging/ CT if enlarged aorta on echo e.g. Marfan’s

Can do cardiac catheterisation - dilated LV, aortic regurg, dilated aortic root

324
Q

Management of aortic regurgitation

A

If acute - urgent surgical intervention
Mild-moderate - monitor annually, echo every 2 years
Severe every 6 months, echo every year

Vasodilators and inotropic agents - short term
ACEi in chronic severe

Surgery if symptomatic

  • Aortic valve replacement
  • Valve sparing aortic replacement is becoming more common
  • Operative mortality 1-4%
325
Q

Types of mitral regurgiation

A

Primary
Intrinsic lesions affect one or several components of the valve
Degenerative mitral regurgitation is the most common cause
Acute can be caused by papillary muscle rupture, infective endocarditis or trauma

Secondary (functional)
Valve leaflets normal but MR results from distortion of subvalvular apparatus due to LV enlargement
May be due to cardiomyopathy

326
Q

Epidemiology of mitral regurgitation

A

2nd most prevalent valve disease after aortic stenosis
Increased in females
increases with age

RFs

  • Lower BMI
  • Renal dysfunction
  • Prior MI
  • Prior mitral stenosis or mitral valve prolapse
327
Q

Aetiology of mitral regurgitation

A 
Coronary artery disease (papillary muscle dysfunction)
Infective endocarditis
Following mitral valve surgery
Myxomatous degeneration - Ehler's Danlos, Marfan's, SLE, scleroderma
Cardiac tumours - atrial myxoma
Rheumatic fever
Acute LV dysfunction
Congenital heart disease
Drug related
328
Q

Pathophysiology of mitral regurgitation

A

Chronic mitral regurg causes gradual dilation of LA with little increase in pressure causing few symptoms
LV dilates slowly and LV diastolic and LA pressures increase gradually as a result of chronic volume overload

329
Q

Symptoms of mitral regurgitation

A

If acute, rapid pulmonary oedema which can be fatal and requires emergency valve repair

Chronic

  • Heart failure
  • breathlessness
  • Pansystolic murmur best heard at the apex
  • Radiates into axilla
  • Dyspnoea (pulmonary venous congestion)
  • Fatigue (low cardiac output)
  • Palpitations
  • Oedema, ascites (R sided HF)
330
Q

Signs of mitral regurgiation

A

Pansystolic murmur best heard at apex, radiates to axilla
Cardiomegaly
AF or atrial flutter

Signs of pulmonary venous congestion - creps, effusions

331
Q

Investigations for mitral regurg

A

CXR
Enlarged LA, enlarged LV, pulmonary venous congestion, pulmonary oedema if acute

ECG
Left atrial hypertrophy, broad P wave, LV hypertrophy

Echo: dilated LA, LV. structural abnormalities of mitral valve

Cardiac catheterisation - dilated LA, LV, mitral regurg, pulmonary hypertension, co-existing coronary artery disease

Angiography for CAD

332
Q

Management of mitral regurgitation

A

Surgery if signs of LV dysfunction, new onset AD or pulmonary hypertension

Follow up yearly with echo every 2 years, severe every 6 months with echo annually

Medical
- Nitrates, diuretics, positive ionotropic agents (Digoxin)- Anticoagulation if AF present

Surgery

  • urgent if acute severe
  • valve replacement, repair where possible
  • Percutaneous not recommended
333
Q

Complications of mitral regurgitation

A

Pulmonary hypertension
LV dysfunction
AF
Thromboembolism due to AF

334
Q

Define aortic aneurysm

A

Permanent and irreversible dilation of the aorta by at least 50% its normal diameter
Normal diameter of the aorta is 2cm, but increases with age
AAA is >3cm
Most arise from above the renal arteries

335
Q

Epidemiology of aortic aneurysms

A

1-12% of the population
More common in men
Symptomatic in 25/100,000

RFs
Hypertension
Fhx (minimal)
Severe atherosclerotic changes to vessel wall
Smoking
COPD
Hyperlipidaemia
336
Q

Aetiology of aortic aneurysms

A

Most have no specific cause

  • Trauma
  • Infection - HIV, TB, Brucellosis, salmonellosis
  • Inflammatory disease - behcet’s and takaysau’s
  • Connective tissue disorders - Marfan’s, Ehler’s Danlos syndrome
337
Q

Pathophysiology of aortic aneurysms

A

Degradation of elastic lamellae
Leukocytic infiltrate
Enhanced proteolysis
Smooth muscle cell loss
Dilation affects all 3 layers of the cell wall
The larger the AAA the larger the growth rate and the greater the risk of rupture

338
Q

Presentation of unruptured aortic aneurysm

A

Most have no symptoms
Incidental finding on examination
Can have pain in back, abdomen or groin (? due to pressure on nearby structures)
Pulsatile abdominal swelling
Distal embolization can produce features of limb ischaemia
Hydronephrosis
Abdominal bruits

339
Q

Presentation of ruptured aortic aneurysm

A

Hypotension
Atypical abdominal symptoms
Sudden and severe abdominal pain (or back or loin)
Syncope
Shock or collapse
Cold, sweaty, faint
Vomiting
Degree of shock depends on site of rupture and whether it is contained
Retroperitoneal bleeding may cause Grey Turner’s sign - flank bruising

TRIAD - pain in flank or back, hypotension, abdominal pulsatile mass

If thoracic - then chest pain, cardiac tamponade and haemoptysis

340
Q

Grey Turners sign

A

Flank bruising (due to retroperitoneal bleeding)

341
Q

Investigations for AAA

A 
Bloods - FBC, clotting screen, renal function, LFTs, cross match units for surgery
ESR or CRP if ? inflammatory cause
ECG
CXR
Lung function tests

Scans
US
CT - crescent sign (blood within thrombus which may predict immanent rupture)
MRI angiography

342
Q

Management for aortic aneurysm

A

If UNCOMPLICATED:
- Monitor if <5.5cm, consider surgery in over 5.5cm
- US monitoring frequency depends on size, 3-4.5 every year, >4.5 every 3 months
- Change RFs where possible
Surgery
- If over 5.5
- High risk of rupture
- Rapid expansion
- Symptomatic
Open repair with aortic and iliac clamping, replacement of segment with prosthetic graft
OR endovascular repair: stent-graft system through femoral arteries

343
Q

Complications and prognosis of aortic aneursym

A

Death
AKI
Multi-organ failure
Respiratory failure

Risk determined by diameter
2.4% mortality with elective repair
20% annual survival rate if over 5.5vm
80% mortality with ruptured AAA

344
Q

Normal electrical activity in the heart

A

Initiated by electrical discharge in SA note
Atria and ventricles depolarise sequentially.
SA node acts as pace maker, intrinsic rate determined by autonomic nervous system
Passes through AV node, into bundles of His then pirkinje fibres

345
Q

Define sinus bradycardia

Causes

A

HR under 60bpm in sinus rhythm

MI
Sinus node disease (sick sinus syndrome)
Hypothermia
Hypothyroidism
Cholestatic jaundice
Raised ICP
Drugs - beta blockers, digoxin, verapamil

NORMAL in athletes

346
Q

Symptoms of sinus bradycardia

A

Often asymptomatic

Fatigue
Lightheadedness
Syncope

347
Q

Management of sinus bradycardia

A

Normally responds to IV atropine

If recurrent or persistent then cardiac pacing

348
Q

Causes of sinus tachycardia

A

Sinus >100bpm

Anxiety
Fever/Sepsis
Thyrotoxicosis
Anaemia
Phaeochromocytoma
heart failure
Drugs - beta agonists
Pregnancy
Exercise
349
Q

Sick sinus syndrome

A

Also referred to as Sinoatrial Disease

  • Most common in elderly
  • Underlying pathology can be fibrosis, degenerative changes or ischaemia
  • Characterised by a number of arrhythmias
  • May have palpitations, dizzy spells, syncope
  • Intermittent tachycardia, bradycardia or pauses with no atrial or ventricular activity

Features:

  • Sinus bradycardia
  • Sinoatrial block
  • Paroxysmal AF
  • Paroxysmal atrial tachycardia
  • AV block

Treat symptomatic patients with pacing

350
Q

Atrial ectopic beats

A

Extrasystoles, premature beats
usually causes no symptoms
ECG shows a premature but otherwise normal QRS
If the visible p wave has a different morphology, from abnormal site

No consequence, however, very frequent atopics can lead to onset of AF

351
Q

Atrial flutter

A

Large re-entry circuit within the R atrium
Atrial rate 300bpm, usually associated with 2:1, 3:1 or 4:1 block (producing HR 150, 100 or 75)
- Saw tooth flutter waves
- Should always be suspected if narrow complex with 150bpm
-
Management
- Carotid sinus pressure or IV adenosine can slow rate to see sawtooth waves
- Treat with digoxin/beta blockers/verapamil
- Can try to restore rhythm through DC cardioversion or IV Amiodarone
- Beta blocker or Amiodarone can help prevent recurrence
- Catheter ablations can give chance of complete cure and is treatment of choice with persistent symptoms

352
Q

AF

A

Most common sustained cardiac arrhythmia
0.5% prevalence, increases to 9% in over 80s
Abnormal automatic firing with presence of multiple atrial re-entry circuits
Becomes sustained after re=entry conduction

Atria beat rapidly, ineffectively and in-coordinated
Ventricles activated irregularly determined by conduction through AV node

Irregularly irregular pulse
Normal but irregular QRS
No p wave

Can be paroxysmal or permanent
Initial physical changes - electrical remodelling
After a few months - structural remodelling with atrial fibrosis and dilation

353
Q

Causes of AF

A 
Idiopathic
MI
Valvular heart disease (particularly mitral disease)
Hypertension
SA node disease
Hyperthyroidism
Alcohol
Cardiomyopathy
Congential heart disease
Chest infection
PE
Pericardial disease
354
Q

Symptoms of AF

A 
Palpitations
Breathlessness
Fatigue
Lightheadedness
Chest pain (if coronary artery disease)
May have reduced BP

Often asymptomatic
Stroke/TIA

355
Q

Investigations for AF

A

12 lead ECG

  • Irregular QRS
  • No p waves
  • Fast ventricular rate 120-160, slows with chronic

Bloods

  • FBC (anaemia may precipitate)
  • U&Es (potassium is a culprit)
  • LFTs and coag screen prior to anticoagulation
  • TFTs

CXR - may show structure causes

Echo - baseline needed for longer term management, if considering cardioversion or high risk of functional or structural heart disease

356
Q

Management of AF

A
  • Treat any underlying cause
  • Control of arrhythmia (rate and rhythm)
  • Thromboprophylaxis

Rate control is first line unless: reversible cause of AF, heart failure caused by AF or new onset AG

  • beta blocker or rate limiting CCB
  • Consider digoxin if permanent AF and sedentary patient
  • If monotherapy fails, try combining
  • No Amiodarone

Rhythm control - if AF continues post rate control or unsuccessful

  • Cardioversion (electrical, Amiodarone therapy for 4 weeks before and 12 months after to maintain sinus)
  • Drug treatment:
  • 1st line: beta blocker
  • Dronedarone or Amiodarone is LV impairment of HF
  • Left atrial ablation if drugs unsuccessful
  • Pacing and ablate strategy

Anticoagulation

  • Apixaban, rivaroxaban or warfarin or dabigatran
  • Use CHA2DS2-Vasc score
357
Q

Assessing risk of stroke in AF

A 
CHA2DS2 Vasc score
Congestive heart failure 
Hypertension
Age>75 - 2 points
Diabetes
past Stroke or TIA - 2 points

Vascular disease
Age 65-75 - 1 point
Sex - female

If males score 1 or more, or females 2 or more - start anticoagulation, proving consideration of bleeding risk

HAS-BLED

358
Q

Complications of AF

A

Stroke
Can precipitate acute heart failure or aggravate established heart failure
Cardiomyopathy
Premature death

359
Q

Management of acute AF

A

If life threatening haemodynamic instability then emergency electrical cardioversion and resuscitation]
Rhythm control if within 48 hours of start, rate control if unsure or longer

360
Q

Types of AF

A

Paroxysmal - intermittent episodes that self-terminate in 7 days

Persistent - prolonged episodes which can be terminated with chemical or electrical cardioversion

Permanent

361
Q

Atrioventricular nodal re-entrant tachycardia

A

Re-entry circuit involving AV node and its 2 right atrial input pathwyas

  • Produces tachycardia at 120-140bpm
  • Occurs in absence of structural disease
  • Rapid, forceful regular heart beat
  • Chest discomfort
  • Breathlessness
  • Lightheadness
  • Tachycardia with normal QRS complexes
  • Adenosine or verapamil will restore sinus rhythm in most cases
362
Q

Wolff-Parkinson White syndrome

ECG changes

A

Shortened PR interval
Slurred initial deflection of QRS - DELTA WAVE
Broad QRS complex

363
Q

Wolff-Parkinson White syndrome

A

Abnormal band of conducting tissue connects atria and ventricles
Accessory pathway - bundle of Kent contains rapidly conducting fibres rich in sodium channels
As the AV node and accessory pathway have different conduction speeds and refractory periods - therefore a re-entry circuit can develop causing tachycardia

  • If AF occurs very dangerous as no rate limitation from AV node (emergency)
364
Q

Describe ventricular ectopics

A

Broad, premature and bizarre QRS complexes
Ventricles are activated sequentially and not simultaneously

Unifocal or multifocal

Pulse irregular with weak or missed beats
Generally asymptomatic but can have irregular hearbeat, missed beats or unusually strong beats

More prominent at rest and decreases with exercise
No treatment unless symptomatic - use beta blockers or catheter ablations

365
Q

Bigeminy

A

Alternating between ventricular ectopics and sinus rhythm between on each beat

S - E - S - E - S - E

366
Q

When are ectopic beats more common

A

At rest
In patients with heart failure and cardiomyopathy
Increases in age
Digoxin toxicity

367
Q

ECG findings in VT

A

Tachycardia, rate over 120bpm
Broad, abnormal QRS complexes
Marked left axis deviation
Can be difficult to distinguish between this and SVT with BBB

368
Q

VT

A

Ventricular tachycardia

  • Occurs most commonly in MIs and cardiomyotahty, where there is extensive ventricular disease
  • May cause haemodynamic compromise and progress to VF
  • It is caused by abnormal automaticity or triggered activity in ischaemic tissue
369
Q

Symptoms and features in keeping with VT

A

Symptoms:

  • Syncope
  • Palpitations
  • Lightheadedness
  • Dyspnoea

Features

  • History of MI
  • AV dissociation
  • Capture or fusion beats
  • Extreme left axis deviation
  • Very broad QRS > 140ms
  • No response to carotid sinus massage or IV adenosine
370
Q

Management of VT

A

Prompt action to restore sinus rhythm

  • DC cardioversion if BP<90
  • IV Amiodarone if arrhythmia well tolerated
  • Correct: hypokalaemia, hypoxia, hypomagnesaemia, acidosis
  • Avoid class 1c anti-arrhythmic
371
Q

ECG findings in Torsade de Pointes

A

Rapid irregular complexes the oscillate from upright to inverted position and twists around the baseline as mean QRS axis changes

Non sustained, repetitive, but can degenerate into VF

Prolonged QT interval

372
Q

Causes of long QT and Torsade de pointes

A 
Bradycardia
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
Class 1a and class 1c anti-arrhythmic drugs 
Amitriptyline and other TCAs
Chlorpromazine
Congenital syndromes
373
Q

Congenital long QT syndromes

A

Long QT1 - triggered by exercise
Long QT2 - triggered by sudden noise
Long QT3 - common during sleep

374
Q

Management of torsade de points

A

Treat underlying cause
IV magnesium in all cases
Atrial pacing
If very long >500ms then implanted defibrillator

375
Q

Brugada syndrome

A

Genetic disorder which can present with polymorphic VT or sudden death
Due to a defect in the sodium channel function
RBBB and ST elevation in V1 and V2 with no prolongation of QT interval

376
Q

First degree heart block

A

AV conduction delayed

Prolonged PR interval > 200ms

377
Q

Second degree heart block

A

2:1
Mobitz type 1 Wenckeback
PR interval increases until QRS dropped

2:2 - mobitz type 2
PR interval remains constant but some QRS complexes are not conducted, Regular p waves

378
Q

Third degree heart block

A

QRS and p waves do not correlate

Occurs when AV conduction fails completely
Slow regular pulse 25-50bpm
Pulse does not vary with exercise

379
Q

Causes of 3rd degree heart block

A 
Congential
Idiopathic fibrosis
MI
Inflammation - infective endocarditis, sarcoidosis, Chaga's disease
Cardiac surgery
Drugs - Digoxin, beta blockers
380
Q

Stokes-Adams attacks

A

Episodes of ventricular asystole that can complicate 3rd degree or mobitz type 2 heart block
Sudden loss of consciousness that occurs without warning and results in collapse
Brief anoxic seizure if prolonged
Pallor and death like appearance during attack followed by characteristic flushing
Rapid recovery unlike epilepsy

381
Q

Causes of RBBB

A 
Normal variant
Right ventricular hypertrophy or strain
PE
Congenital heart disease e.g. atrial septal defect 
Coronary artery disease
382
Q

Causes of LBBB

A

Coronary artery disease
Hypertension
Aortic valve disease
Cardiomyopathy

383
Q

Bundle branch block

A

Depolarisation goes through a smaller myocardial route rather than fast Purkinje fibres
Causes delayed conduction into one of the ventricles

Broad QRS > 120ms
WilliaM - LBBB has W in V1 and M in V6
MarroW - RBBB has M in V1 and W in V6

384
Q

Reversible causes of cardiac arrest

A 
Hypovolaemia
Hypoxia
Hydrogen ions (acidosis)
Hypothermia
Hypokalaemia/ hyperkalaemia
Hypoglycaemia

Toxins
Tamponade (cardiac)
Tension (pneumothorax)
Thrombosis (coronary or pulmonary)
Trauma

Year 3 (6 decks)

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