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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Definition of ACS

A

STEMI, NSTEMI and unstable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of raised troponin

A
ACS
Congestive heart failure
Sepsis
PE
CKD
Myocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Prognosis of MI

A

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

Earlier perfusion = decreased mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Complications post-MI

A
angina, re-infarct,
heart failure
cardiogenic shock
valve dysfunction 
cardiac rupture
arrhythmia 
PE
Pericarditis
Depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Causes of angina

A
Atherosclerosis
Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Hypertensive heart disease 
Arrhythmias
Anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Management of angina
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
26
Differentials for chest pain
``` 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 ```
27
Prognosis of angina
1 in 10 will have MI within 1 year | Benign
28
Classification of angina
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
29
Identifying high risk ACS patients
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
30
Describe cardiac rehabilitation
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
31
What does a loud first heart sound suggest
Hyperdynamic circulation - Anaemia - pregnancy - hyperthyroidism - mitral stenosis
32
When would you hear a systolic click?
Early or mid-systole aortic stenosis pulmonary stenosis prosthetic heart valve
33
When would you hear an ejection systolic murmur?
Aortic stenosis Pulmonary stenosis Crescendo - decrescendo pattern
34
When would you hear a pansystolic murmur?
Mitral regurgitation | Tricuspid regurgitation
35
When would you hear an early diastolic murmur?
Aortic regurgitation Pulmonary regurgitation Soft blowing decrescendo pattern Best hear when sitting forward in expiration
36
When would you hear a late diastolic murmur?
Mitral stenosis Tricuspid stenosis Associated with opening snap
37
Describe murmur associated with aortic stenosis?
Ejection systolic Crescendo-descrescendo Radiates into neck Best heart at left sternal edge
38
Murmur of mitral regurgitation
``` Pansystolic Blowing Best heard at the apex Radiates to axilla best heard in left lateral position ```
39
Causes of mitral regurgitation
``` Rheumatic fever Degenerative calcification in elderly Congenital SLE RA Infective endocarditits ```
40
What happens to the heart with mitral stenosis?
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
41
Presentation of mitral stenosis
``` Progressive breathlessness Orthopnoea, PND, pulmonary oedema Cough (pulmonary congestion) Chest pain (pulmonary hypertension) Oedema (right heart failure) Fatigue (low cardiac output) AF / Palpitations ```
42
Signs of mitral stenosis
``` 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 ```
43
Investigations and findings in mitral stenosis
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
44
Management of mitral stenosis
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)
45
Epidemiology of heart failure
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 ```
46
Symptoms of heart failure
``` Dyspnoea Fatigue Peripheral oedema Orthopnoea Paroxysmal nocturnal dyspnoea (PND) Noctural cough Pink frothy sputum Wheeze Nocturia Cold peripheries Weight loss Muscle wasing Nausea Anorexia ```
47
Signs of heart failure
``` Peripheral oedema Dyspnoea Raised JVP Cardiomegaly Murmur Crackles on lung auscultation Displaced apex R ventricular heave Hypotension Narrow pulse pressure Tachycardia Tachypnoea ```
48
Aetiology of heart failure
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
49
Pathophysiology of heart failure
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
50
Investigations for heart failure
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
51
Signs of heart failure on CXR
``` Cardiomegaly Prominent upper lobe vessels Bat winging (alveolar oedema) Kerley B lines (interstitial oedema) Pleural effusions ```
52
Management of heart failure
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
53
Classification of heart failure
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
54
Management of acute heart failure
- 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
55
Epidemiology of asthma
``` 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
56
Symptoms of asthma
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.
57
Signs of asthma
Widespread wheeze on auscultation Low FEV1 or PEFR Peripheral blood eosinophilia
58
Pathophysiology of asthma
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
59
Triggers for asthma
``` Allergens: grass pollen, dander Occupational sensitizers Viral infections Cold air Emotion Irritants: dust, vapour, fumes, smoker Genetic factors Drugs: NSAIDs, beta blockers Atmospheric pollution ```
60
Aspirin sensitive asthma
Symptoms triggered by aspiring These inhibit cyclo-oxygenase which leads to shunting or arachidonic acid metabolism through lipo oxygenase pathway producing cysteinyl leukotrienes
61
Extrinsic vs intrinsic asthma
Extrinsic - atopic individuals. Often starts in childhood | Intrinsic - middle age, non-atopic. More severe
62
Causative agents for occupational asthma
``` Isocyanates - paint sprayers Flour - bakers Colophony and fluxes - soldering and printers latex - medical Animal - vets Aldehydes Wood dust - carpentry ```
63
Investigations in asthma
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
64
Brittle asthma
Exacerbations occur with little or no warning
65
Classification of asthma severity
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
66
Treatment of acute asthma
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 ```
67
Treatment of chronic asthma
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.
68
Asthma in pregnancy
1/3 worsen 1/3 stable 1/3 improve Uncontrolled asthma is biggest risk to foetus
69
ABG finding in asthma
Respiratory alkalosis Hypoxaemia or hypercapnia secondary to hyperventilation
70
Risk factors for cardiovascular disease
``` 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 ```
71
Stages of hypertension
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
72
Relevance of FHx to CV disease
1st degree male under 55, | or female under 65
73
Diagnosing hypertension
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
74
Phaeochromocytoma
``` Labile or severe hypertension headache Palpitations Pallor Diaphoresis ```
75
When should secondary hypertension be considered?
Under 40s Low potassium and high sodium (adrenal disease) Raised creatinine or low GFR (renal disease) Proteinuria or haematuria With labile or worsening HTN
76
Long term complications of hypertension
``` LV hypertrophy CCF CAD Arrhythmias - AF Microvascular disease ``` Increased risk of stroke and dementia Hypertensive retinopathy Hypertensive nephropathy End stage renal disease Glomerular injury
77
Causes of secondary hypertension
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
78
Coarctation of aorta
``` Upper limb hypertension Large difference between arms Absent or weak femoral Radio-femoral delay Suprasternal murmur, radiating to back ```
79
Management of hypertension
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
80
Assessing CV risk
QRISK2 Used up to 84 year olds Age, sex, ethnicity, postcode, smoking, diabetes, FHx, CKD, AF, RA, cholesterol, BMI, BP
81
Diagnostic criteria for metabolic syndrome
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
82
Define COPD
Chronic obstructive pulmonary disease Airflow obstruction, not reversible. Airflow limitation if progressive and encompasses bronchitis and emphysema FEV1
83
Epidemiology of COPD
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 ```
84
Symptoms of COPD
``` Exertional breathlessness Chronic cough Regular sputum production Frequent winter bronchitis Wheeze Weight loss Ankle swelling ```
85
Signs of COPD
``` Tachypnoea Dyspnoea Increased use of accessory muscles Asterixis Confusion Pursed lip breathing Peripheral oedema Cyanosis Wheeze Hyperinflation of chest Quiet vesicular breath sounds ```
86
Pathophysiology of COPD
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
87
Investigations for COPD
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
88
Management of COPD
- 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
89
Complications of COPD
``` Chronic hypoxia Cor pulmonale from pulmonary hypertension Pneumothorax Respiratory failure Arrhythmias - AF Infection Secondary polycythaemia ```
90
MRC dyspnoea grading
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
91
Classifying severity of COPD
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 ```
92
Factors that can destabilise heart failure patient
``` Ischaemia Hypertension Rapid AF Medication initiation Alcohol abuse Non-adherence Active infection PE Anaemia Hyperthyroidism ```
93
Assessing end organ damage from HTN
``` Urinalysis FBC (Hb and Hct) U&Es Fasting glucose Cholestrol work up ECG CXR ```
94
Signs of LV dysfunction
``` Hypotension Soft S1 S3 gallop Decreased volume carotid pulse LV apical enlargement Pulmonary congestion (rales) Mitral regurg ```
95
High risk patients with HTN
``` Older age Diabetes Renal disease LV hypertrophy Vascular disease CHD Cerebrovascular disease ``` Aim for 130/80 vs 140/90
96
Define bronchiectasis
Permanent dilation and thickening of airways characterised by chronic cough, excessive sputum production, bacterial colonisation and recurrent acute infections.
97
Classification of bronchiectasis
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.
98
Epidemiology of bronchiectasis
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 ```
99
Aetiology of bronchiectasis
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 ```
100
Pathophysiology of bronchiectasis
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
101
Symptoms of bronchiectasis
``` Vary from intermittent episodes of expectoration to persistent daily expectoration of large volumes of purulent sputum. Dyspnoea Chest pain Haemoptysis Wheezing Cough Rhinosinusitis ```
102
Signs of bronchiectasis
``` 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 ```
103
When should bronchiectasis be considered
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
104
Investigations for bronchiectasis
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)
105
Tests for CF
CFTR genetic mutation analysis | Sweat chloride
106
Management of bronchiectasis
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.
107
Complications of bronchiectasis
``` Repeated infection Decreased lung function Empyema Lung abscess Pneuomothorax Life threatening haemoptysis Respiratory failure Cor Pulmonale Decreased quality of life ```
108
Normal pH
7.35-7.45
109
Base excess
-2 to +2 Positive numbers = alkalotic Negative number - acidosis
110
ABG findings and causes of respiratory acidosis
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
111
ABG findings and causes of respiratory alkalosis
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
112
ABG findings and causes of metabolic acidosis
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 ```
113
ABG findings and causes of metabolic alkalosis
High pH Raised bicarbonate High CO2 if compensating GI loss of H+ (vomiting) Renal loss of H+ (loop/thiazide diuretics) Hypovolaemia
114
Type 1 respiratory failure and Causes
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 ```
115
Type 2 respiratory failure and causes
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 ```
116
Non-respiratory causes of respiratory failure
``` Hypovolaemia Shock (septic or cardiogenic) Severe anaemia Drug OD Neuromuscular disease Spinal/head injury ```
117
Signs and symptoms of respiratory failure
``` Dyspnoea Confusion Tachypnoea Cyanosis Stridor Accessory muscle use Anxiety Headache Retraction of intercostal spaces Hypoventilation Polycythaemia (chronic) Cor pulmonale Cardiac arrhythmia ```
118
Investigations in respiratory failure
``` Pulse Oximetry ABGs ECG D-dimer for PE CXR Pulmonary function tests LFTs and U&Es TFTs Echo ```
119
Management of respiratory failure
ABCDE Supplemental o2 to sats >90% Treat underlying cause BiPap Intubation and mechanical ventilation - RSI Bronchidialtors, corticosteroids, antibiotics, opiods
120
Target O2 saturations
94-98% | For COPD 88-92%
121
Indications for humidifying oxygen prior to delivery
``` Flow rate > 4l/min for several days Tracheostomy CF Bronchiectasis Chest infection training secretions ```
122
Risk factors for CAP
``` 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
123
Signs and symptoms of pneumonia
``` 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)
124
Typical pathogens for CAP
- Streptococcus pneumonia (66%) - Haemophilus influenzae - Klebsiella pneumonia - Staphylococcus aureus
125
Streptococcus pneumonia
Gram positive Diplococci Common in winter Common in creasing age, co-morbidities, CV disease, a
126
Haemophilus influenzae
Gram positive | Coccobaccilus
127
Klebsiella pneumoniae
Gram negative bacillus More common in men - can cause decreased platelets and leuopaenia
128
Staph aureus
Gram positive Coccus More common after influenza like illness
129
Atypical pathogens for CAP
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
130
Investigations for CAP
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
131
Severity of CAP
``` 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
132
Management of CAP
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
133
Complications of CAP
``` Pleural effusion Empyema Lung abscess pneumothorax DVT Bronchiectasis AKI Sepsis - pericarditis, endocarditis, osteomyelitis, meningitis ```
134
Define hospital acquired pneumonia
New radiographic infiltrate in presence of infection with onset 48 hours after admission
135
RF for hospital acquired pneumonia
``` 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 ```
136
Causes of hospital acquired pneumonia (bacteria)
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
137
Antibiotics used in hospital acquired pneumonia
``` Co-amoxiclav Ceftriaxome Tazocin Carbopenam Gentamicin ```
138
Define pleural effusion
Increase in fluid volume between visceral and parietal pleura
139
Types of pleural effusion
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
140
Causes of transudate pleural effusions
``` 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 ```
141
Meig's syndrome
TRIAD Pleural effusion Ascites Benign ovarian tumour
142
Causes of exudate pleural effusion
``` Pneumonia Malignancy Pulmonary infarction PE Autoimmune - RA Asbestos exposure Pancreatitis TB Complication of acute MI (Dressler's syndrome) Drugs - methotrexate, Amiodarone, nitrofurantoin ```
143
Signs and symptoms of pleural effusion
``` SOB Cough Dyspnoea Pleuritic pain Dullness on percurssion Decreased breath sounds Decreased chest expansion Decreased tactile and vocal fremitus ```
144
Investigations for pleural effusion
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
145
Causes for bloody thoracocentesis
``` Malignancy PE Infraction Trauma benign asbestos Post cardiac injury syndrome ```
146
Causes for low pH or glucose in thoracocentesis
``` Infection and empyema RA SLE TB Malignancy Oesophageal rupture ```
147
Management of pleural effusion
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
148
Indications for a chest drain
``` Pneumothorax Traumatic pneumothorax Pleural effusion Haemopneumothorax Peri-operative - oesophageal or cardiothoracic surgery ```
149
Safe triangle for chest drain insertion
Between - Lateral edge of pec major - Base of axilla - Lateral edge of lat dorsi - Above 5th IC space If apical pneumothorax - 2nd intercostal space
150
Process of chest drain
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
151
Complications of chest drain
Incorrect placement Injury to intercostal muscles Perforation of other vessels Pain
152
Define pneumothorax
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
153
Types of pneumothorax
``` Primary spontaneous Secondary spontaneous Tramatic Iatrogenic Catamenial Tension ```
154
Primary spontaneous pneumothorax
``` Occurs in healthy people Increased in: Tall, thin and healthy Male Marfan's Prengnacy Smokers ``` Occurs from ruptures of blebs and bullae
155
Secondary spontaneous pneumothorax
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
Traumatic pneumothorax
Follows penetrating chest trauma Stabbing/gun shot/fractured rib High risk occupations - diving or flying
157
Iatrogenic pneumothorax
Following certain medical procedures ``` Lung biopsy Transthoracic needle aspiration Throacocentesis Central line insertion Intercostal nerve block Tracheostomy APR NG tube placement ```
158
Catamenial pneumothorax
At time of menstruation 30-40 years old with pelvic endometriosis 90% in R lung and within 72 hours of onset of menstruation
159
Tension pneumothorax
MEDICAL EMERGENCY | Occurs in - ventilated patients, trauma, CPR, lung disease, blocked or clamped chest drain, hyperbaric oxygen treatment
160
Signs and symptoms of pneumothorax
``` 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
Pathophysiology of pneumothorax
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
Investigations for pneumothorax
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
Management of pneumothorax
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
Surgical emphysema
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
Risk factors for PE
- 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
Virchows triad
Venous stasis Vessel wall damage Hypercoagulability
167
Pathophysiology of PE
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
Symptoms of PE
``` Dyspnoea Pleuritic pain Cough Haemoptysis Dizziness Syncope Any chest symptoms with signs of DVT ```
169
Signs of PE
``` Tachypnoea Tachycardia Hypoxia Pyrexia Raised JVP Pleural rub Hypotension Cardiogenic shock Gallop heart rhtyhm ```
170
Investigations for PE
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
ECG changes in PE
- 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
Wells PE Score
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
Management of a PE
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
Signs/symptoms of DVT
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
Investigations of DVT
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
Wells score for DVT
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
Management of DVT
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
Post-thrombotic syndrome
``` Chronic venous hypertension Pain Swelling Hyperpigmentation Dermatitis Ulcers Gangrene ``` Post DVT in 20-40%
179
DVT prophylaxis
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
Macule
Complelely flat lesion | Smooth small area of colour change <1.5cm
181
Papule
Discrete raised palpable lesion <1cm
182
Nodule
Discrete raised palpable lesion >1cm
183
Pustule
Small raised lesion filled with purulent fluid
184
Plaque
Raised area of skin with flat top and clear edge | Circumscribed, superficial, elevated plateau 1-2cm
185
Lichenification
Hard thickening of skin with accentuated skin markings | Results from inflammation or rubbing
186
Vesicles
Small superficial circumscribed containing serous fluid < 0.5cm
187
Bulla
Large superficial circumscribed containing serous fluid > 0.5cm
188
Wheal
Transient circumscribed elevated papules or plaques with erythematous borders and pale centres
189
Define psoriasis
Chronic T cell mediated autoimmune condition affecting extensor surfaces Involves hyperproliferation of the keratinocytes in the epidermis with increased cell turnover rate
190
Epidemiology of psoriasis
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
Triggers for psoriasis
``` 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
Types of psoriasis
``` 90% extensor plaque psoriasis Flexural Guttate Pustular Unstable Erythrodermic Psoriatic arthritis Napkin Nail ```
193
Clinical presentation of psoriasis
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
Auspitz sign
Psoriasis | when scales scraped off reveals dilated blood vessels beneath
195
Nail changes in psoriasis
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
Pathophysiology of psoriasis
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
Flexural psoriasis
Smooth inflamed regions Without scaling due to moist area Armpit, groin, under breast and skin folds Needs to be distinguished from fungal infection
198
Guttate psoriasis
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
Pustular psoriasis
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
Unstable or erythrodermic psoriasis
``` Generalised erythema Pain Itching Fine scaling Covers nearly all body surface area Accompanied by fever, chills, hypothermia and dehydration Very serious Systemically unwell ```
201
Psoriatic arthritis
Usually in small joints Occurs in 5-10% Stiffness, pain, progressive Causes permanent joint damage
202
Investigations for psoriasis
Diagnosed clinically Can do biopsy Would show - basal cell hyperplasia, proliferation of subepidermal vasculature, absence of normal cell maturation and keratinisation
203
Management of psoriasis
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
Classification of psoriasis
``` Psoriasis area and severity index (PASI) For each area calculate: - % involved - severity of erythema - thickness and scaling ```
205
Define eczema
Chronic, relapsing inflammatory skin condition | Characterised by itchy red rash that favours skin creases
206
Epidemiology of eczema
``` 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
Risk factors for eczema
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
Aetiology of eczema
Combination of genetic susceptibility and environmental factors - Defects in skins barrier function (FILAGGRIN) - Immune dysregulation - Allergen exposure
209
Diagnostic criteria for eczema
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
Types of eczema
``` Atopic Pityriasis alba Eczema herpeticum Lichen simplex Asteatotic Discoid Pompholyx Varicose ```
211
Pityriasis alba
Type of eczema | Pale patches of hypopigmentation on face of children
212
Eczema herpeticum
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
Lichen simplex
Localised areas of lichenification from rubbing
214
Asteatotic eczema
Older people with dry skin on lower legs | Crazy paving
215
Discoid eczema
``` Intensely pruritic Coin shaped lesions Most commonly on limbs May be vesicular Frequently colonised by S. aureus More common in males ```
216
Pompholyx eczema
``` Itching vesicles Fingers, palms and soles Blisters are small, firm and intensely itchy Occasionally painful More common in nickel allergy ```
217
Varicose eczema
Occurs in lower legs with venous insufficiency | Haemosiderin pigmentation
218
Pathophysiology of eczema
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
Signs and symptoms of eczema
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
Investigations for eczema
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
Management of eczema
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
When to refer eczema
``` 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
Define contact dermatitis
Inflammatory skin reaction in response to an external stimulus acting as an allergen or irritant
224
Risk factors for contact dermatitis
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
Aetiology of contact dermatitis
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
Pathophysiology of contact dermatitis
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
Signs and symptoms of irritant contact dermatitis
``` 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
Signs and symptoms of allergic contact dermatitis
``` Redness, itching, scaling Delayed onset Rash not only in exposed areas Resolution longer Decreased associated ```
229
Investigations in contact dermatitis
Made on clinical findings and history Patch testing is gold standard - should always be done if occupational Occasionally skin biopsy
230
Management of contact dermatitis
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
Type 1 Hypersensitivity reaction
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
Type 2 hypersensitivity reaction
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
Type 3 hypersensitivity
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
Type 4 hypersensitivity
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
Toxic epidermolysis necrolysis (TEN)
``` 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
Stevens-Johnson syndrome
``` 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
Acute generalised exanthematous pustulosis
Drug induced skin reaction Acute onset of fever with generalised erythema Small sterile non follicular pustules ``` Caused by antibiotics Paracetamol sertraline diltiazem furosemide ```
238
erythema nodosum
``` 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
Fixed drug reactions
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
Investigations for drug induced skin reaction
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
Impetigo
``` Child Usually face and limbs Highly contagious Background erythema with yellow crusting and exudates If bullae = staph aureus If lymphadenopathy = strep pyogenes ```
242
Bacterial folliculitis causes
Usually legs, bearded area and scalp Precipitated by waxing and shaving Staph aureus or pseudomonas aeruginosa
243
Ecthyma
``` 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
Erysipelas
Face or lower leg Skin infection with strep pyogenes / group A strep Well demarcated, red, shiny, raised, spreading plaque
245
Management of skin infections
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
Describe phototherapy
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
Short term side effects of phototherapy
``` Redness Folliculitis Discomfort Dry itching skin Blisters Sunlight induced rash - polymorphic light eruption ```
248
Indications for phototherapy
``` Eczema Psoriasis Dermatitis Generalised itching Cutaneous T cell lymphoma Vitiligo ``` These conditions not controlled by topical therapy
249
Contraindications for phototherapy
``` 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
Describe wet wrapping
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
Describe dermatology shared care
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
Define basal cell carcinoma
Abnormal controlled lesions that arise from basal cells which line the deepest layer of epidermis. Slow growing, locally invasive malignancy
253
Epidemiology of basal call carcinoma
``` 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
Risk factors for basal cell carcinoma
``` 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
Xeroderma pigmentosa
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
Types of basal cell carcinoma
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
Gorlin's syndrome
``` Multiple BCCs Autosomal dominant Jaw cysts Spine and rib abnormalities Pitting of palms and soles Cataracts Calcification of falx cerebri ```
258
Pathophysiology of BCC
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
Presentation of BCC
``` Sun exposed areas of head or neck Small, translucent or pearly Raised areas of telangiectasia RODENT ULCER - indurated edge Ulcerated centre Slow growing ```
260
Investigations for BCC
``` Visual inspection Removal for histology All specimens must go to histology All must be biopsied No format staging beyond examination for lymphadenopathy ```
261
Management of BCC
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
Prognosis of BCC
Mets rare Mortality low Increased risk of SCC and MM
263
Define squamous cell carcinoma
Malignant tumour arising from keratinising cells of epidermis or its appendages Locally invasive Has potential to metastasise
264
Epidemiology of SCC
``` Increases with age Increased in men Increased in Caucasians Increased in equatorial regions 2nd most common (behind BCC) ```
265
Risk factors for SCC
``` 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
Pathophysiology of SCC
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
Presentation of SCC
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
Investigations for SCC
``` 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
Management of SCC
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
Prognosis of SCC
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
Epidemiology of malignant melanoma
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
RFs for malignant melanoma
``` 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
Types of malignant melanoma
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
Pathophysiology of malignant melanoma
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
Presentation of melanoma
``` 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
Investigations for melanoma
- 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
Breslow thickness
Measurement in mm of distance between granular cell layer to deepest identifiable melanoma cell
278
Management of melanoma
- 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
Prognosis of melanoma
Very poor if mets - survival 6-9 months 5 year survival 80%
280
Define Bowen's disease
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
Epidemiology of Bowen's disease
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
Presentation of Bowen's disease
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
Management of Bowen's disease
Cryotherapy - often first line Topical 5FU Curettage Surgical excision
284
Define actinic keratoses
Also known as solar keratoses | UV light induced lesions on the skin and are the most common lesions with malignant potential into SCC
285
Epidemiology of actinic keratoses
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
Presentation of actinic keratoses
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
Investigations for actinic keratoses
``` None unless malignancy suspected Biopsy if: - pronounced hyperkeratosis or erythema - recurring lesions - unresponsive to treatment - confluent lesions - transplant recipient - past history of SCC ```
288
Management of actinic keratoses
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
Seborrhoeic keratosis
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
Skin types
``` 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
FEV1
Volume of air the patient is able to exhale in the first second of forced expiration
292
FVC
Forced vital capacity | Total volume of air a patient can forcibly exhale in 1 breath
293
FVC and FEV1 in Obstructive lung disease
FEV1<80% | FEV1/FVC <70%%
294
FVC and FEV1 in Restrictive lung disease
FEV1<80% FVC<80% FEV1/FVC>70%
295
Define TB
Notifiable disease Chronic granulomatous disease caused by Mycobacterium tuberculosis It is spread via inhalation of infected droplets
296
Epidemiology of TB
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
Aetiology of TB
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
Pathophysiology of TB
- 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
Miliary TB
When primary infection is not adequately contained it enters the blood stream and causes severe disease
300
Presentation of TB
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
Investigations for TB
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
What is the Ziehl- Neelson stain used for?
TB
303
Screening and vaccination for TB
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
Management of TB
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
Fibroepithelial polyps
Skin tags/acrochordons - small pedunculated skin coloured papules occur most frequently with skin folds 0.2-0.5mm
306
Causes of lung fibrosis in upper zones
``` TB Extrinsic allergic alveolitis Coal workers pneumoconiosis Silicosis Sarcoidosis Ankylosing spondylitis Histocytosis ```
307
Causes of lung fibrosis in lower zones
bleomycin idiopathic pulmonary fibrosis Connective tissue disorder Drug induced - methotrexate, Amiodarone, asbestosis
308
Epidemiology of aortic stenosis
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
Aetiology of aortic stenosis
Congenital aortic stenosis Congenitally biscuspid valve Rheumatic disease Degenerative - calcified
310
Pathophysiology of aortic stenosis
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
Presentation of aortic stenosis - symptoms
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
Signs of aortic stenosis
``` 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
Investigations for aortic stenosis
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
Management of aortic stenosis
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
Complications of aortic stenosis
``` LV dysfunction Heart failure Infective endocarditis Small systemic emboli Sudden death ```
316
Epidemiology of aortic regurgitation
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
Aetiology of aortic regurgitation
``` Rheumatic disease Bicuspid aortic valve Infective endocarditis Collagen vascular disease Degenerative aortic valve disease Aortic dilatation - Marfan's, aneurysm, dissection, ankylosing spondylitis ```
318
Pathophysiology of aortic regurgiation
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
Symptoms of aortic regurgitation
``` Often asymptomatic Palpitations breathlessness Angina PND Peripheral oedema ```
320
Signs of aortic regurgitation
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
Musset's sign
Head bobbing with each pulse | Seen in aortic regurgitation
322
Quincke's sign
Capillary pulsation in nail beds | Seen in aortic regurgitation
323
Investigations in aortic regurgitation
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
Management of aortic regurgitation
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
Types of mitral regurgiation
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
Epidemiology of mitral regurgitation
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
Aetiology of mitral regurgitation
``` 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
Pathophysiology of mitral regurgitation
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
Symptoms of mitral regurgitation
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
Signs of mitral regurgiation
Pansystolic murmur best heard at apex, radiates to axilla Cardiomegaly AF or atrial flutter Signs of pulmonary venous congestion - creps, effusions
331
Investigations for mitral regurg
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
Management of mitral regurgitation
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
Complications of mitral regurgitation
Pulmonary hypertension LV dysfunction AF Thromboembolism due to AF
334
Define aortic aneurysm
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
Epidemiology of aortic aneurysms
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
Aetiology of aortic aneurysms
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
Pathophysiology of aortic aneurysms
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
Presentation of unruptured aortic aneurysm
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
Presentation of ruptured aortic aneurysm
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
Grey Turners sign
Flank bruising (due to retroperitoneal bleeding)
341
Investigations for AAA
``` 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
Management for aortic aneurysm
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
Complications and prognosis of aortic aneursym
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
Normal electrical activity in the heart
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
Define sinus bradycardia | Causes
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
Symptoms of sinus bradycardia
Often asymptomatic Fatigue Lightheadedness Syncope
347
Management of sinus bradycardia
Normally responds to IV atropine | If recurrent or persistent then cardiac pacing
348
Causes of sinus tachycardia
Sinus >100bpm ``` Anxiety Fever/Sepsis Thyrotoxicosis Anaemia Phaeochromocytoma heart failure Drugs - beta agonists Pregnancy Exercise ```
349
Sick sinus syndrome
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
Atrial ectopic beats
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
Atrial flutter
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
AF
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
Causes of AF
``` Idiopathic MI Valvular heart disease (particularly mitral disease) Hypertension SA node disease Hyperthyroidism Alcohol Cardiomyopathy Congential heart disease Chest infection PE Pericardial disease ```
354
Symptoms of AF
``` Palpitations Breathlessness Fatigue Lightheadedness Chest pain (if coronary artery disease) May have reduced BP ``` Often asymptomatic Stroke/TIA
355
Investigations for AF
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
Management of AF
- 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
Assessing risk of stroke in AF
``` 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
Complications of AF
Stroke Can precipitate acute heart failure or aggravate established heart failure Cardiomyopathy Premature death
359
Management of acute AF
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
Types of AF
Paroxysmal - intermittent episodes that self-terminate in 7 days Persistent - prolonged episodes which can be terminated with chemical or electrical cardioversion Permanent
361
Atrioventricular nodal re-entrant tachycardia
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
Wolff-Parkinson White syndrome | ECG changes
Shortened PR interval Slurred initial deflection of QRS - DELTA WAVE Broad QRS complex
363
Wolff-Parkinson White syndrome
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
Describe ventricular ectopics
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
Bigeminy
Alternating between ventricular ectopics and sinus rhythm between on each beat S - E - S - E - S - E
366
When are ectopic beats more common
At rest In patients with heart failure and cardiomyopathy Increases in age Digoxin toxicity
367
ECG findings in VT
Tachycardia, rate over 120bpm Broad, abnormal QRS complexes Marked left axis deviation Can be difficult to distinguish between this and SVT with BBB
368
VT
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
Symptoms and features in keeping with VT
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
Management of VT
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
ECG findings in Torsade de Pointes
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
Causes of long QT and Torsade de pointes
``` Bradycardia Hypokalaemia Hypomagnesaemia Hypocalcaemia Class 1a and class 1c anti-arrhythmic drugs Amitriptyline and other TCAs Chlorpromazine Congenital syndromes ```
373
Congenital long QT syndromes
Long QT1 - triggered by exercise Long QT2 - triggered by sudden noise Long QT3 - common during sleep
374
Management of torsade de points
Treat underlying cause IV magnesium in all cases Atrial pacing If very long >500ms then implanted defibrillator
375
Brugada syndrome
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
First degree heart block
AV conduction delayed | Prolonged PR interval > 200ms
377
Second degree heart block
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
Third degree heart block
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
Causes of 3rd degree heart block
``` Congential Idiopathic fibrosis MI Inflammation - infective endocarditis, sarcoidosis, Chaga's disease Cardiac surgery Drugs - Digoxin, beta blockers ```
380
Stokes-Adams attacks
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
Causes of RBBB
``` Normal variant Right ventricular hypertrophy or strain PE Congenital heart disease e.g. atrial septal defect Coronary artery disease ```
382
Causes of LBBB
Coronary artery disease Hypertension Aortic valve disease Cardiomyopathy
383
Bundle branch block
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
Reversible causes of cardiac arrest
``` Hypovolaemia Hypoxia Hydrogen ions (acidosis) Hypothermia Hypokalaemia/ hyperkalaemia Hypoglycaemia ``` ``` Toxins Tamponade (cardiac) Tension (pneumothorax) Thrombosis (coronary or pulmonary) Trauma ```