AF & COPD Flashcards

1
Q

what is atrial fibrillation

A

A type of supraventricular tachyarrhythmia. Characterized by uncoordinated atrial activity on the surface ECG with fibrillatory waves of varying shape, amplitude, and timing associated with irregularly irregular ventricular response when atrioventricular conduction is intact

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2
Q

pathophysiology of atrial fibrillation

A
  • Rapidly firing ectopic foci located inside 1 or more pulmonary veins
  • Abnormal atrial tissue substrate - ↑ atrial pressure, ↑ atrial muscle mass, atrial fibrosis, inflammation and infiltration of the atrium
  • Only a proportion of electrical impulses in the atria reach the ventricles  electrical re-entry which then results in atrial fibrillation
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3
Q

what are the different types of atrial fibrillation

A

initial episode - AF > 30 second diagnosed by ECG

paroxysmal - recurrent 2 or more episodes that terminate within 7 days

peristent - continuous > 7 days or AF > 48 in which a decision is made to perfrom CV

long standing - continuous AF for > 12 months

permanent - joint decision by patient and clinician to cease further attempts to restore or maintain sinus rhythm

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4
Q

aetiology of AF?

A
  • in developed country most common  HTN, coronary artery disease and MI
  • in developing country most common  congestive heart failure, HTN and rheumatic valvular disease
  • Cardiac conditions  Sinus sick syndrome (electrophysiological abnormalities), Wolff-Parkinson-White syndrome, Cardiac surgery, congenital heart disease, tumour near heart
  • Infections  pericarditis, amyloidosis, myocarditis
  • Alcohol intoxication/Caffeine/Drugs
  • Hyperthyroidism/thyrotoxicosis
  • Lung cancer/PE
  • Diabetes
  • Obesity
  • Idiopathic – 11%
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5
Q

clinical features of AF

A
palpitations 
tachycardia 
irregularly irregular pulse 
SOB 
chest pain 
dec exercise capacity/fatigue 
stroke as 1st presentation 
elevated JVP 
hypotension - AF induced haemodynamic instability
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6
Q

investigation for AF

A

feels for irregularly irregular pulse

ECG - if AF, will show fibrillation, irregular ventricular rate (RR intervals), no clear P waves, QRS rhythm is rapid and irregular

if paroxysmal AF is suspected and no AF recorded in initial ECG –> 24 hour ambulatory ECG

FBC, U&E, TFTs

CXR to exclude HF or resp. causes

Transthoracic echocardiography in those confirmed with AF - find any structural heart causes and baseline for long-term management

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7
Q

when will you admit a person with AF to hospital

A

if severe symptoms/serious complication

  • pulse > 150
  • BP < 90
  • LOC / severe dizziness/ongoing chest pain/inc SOB
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8
Q

mx of acute AF

A
cardiovesion - electrical DC shock/IV drugs if 
- new-onset AF (<48 hours) 
- AF with a reversible cause 
- heart failure a cause 
\+ atrial flutter
  • If unstable  electrical DC shock + IV amiodarone after
  • If stable  either DC shock of IV amiodarone at a later stage
  • A transesophageal echo is done to look for clots in heart before cardioversion otherwise it can dislodge and case a stroke or anti-coag for 4 weeks before cardioversion

Rate control - B-blocker, CCB or digoxin

Rhythm control - amiodarone

Anti-coag - after CHA2DS2-VASc and HAS-BLED

  • DOAC as 1st line
  • warfarin if mechanical valve, aortic stenosis or rheumatic fever
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9
Q

mx of chronic AF

A
  • Rate controlling drugs – beta blockers, Ca channel blockers
  • Antiarrhythmic drug – Quinidine, Beta blockers, amiodarone
  • CHA2DS2-VASc for stroke assessment + HAS-BLED for bleeding risks
  • Oral anticoagulant e.g. warfarin, NOACs – need to be calculated by the CHA2DS2-VASc scoring system
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10
Q

what is discussed in AF annual review

A
  • Follow up 1 week after starting rate control treatment
  • Check symptoms at rest and during exercise/assess HR
  • If not controlled consider increasing dose/combining any 2 of beta blockers/digoxin/diltiazem (check this + beta blocker with specialist)
  • If still not controlled refer within 4 weeks to cardiologist
  • Side effects
  • HR/BP
  • Calculate TTR to ensure an INR of between 2 and 3 with warfarin
  • Exclude measurements taken within the 1st 6 weeks of treatment
  • Calculate over a maintenance period of at least 6 months
  • If poor control then attempt to correct contributing factors/switch to NOACs
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11
Q

pathophysiology of COPD

A

poorly reversible airflow limitation that is usually progressive

associated with persistent inflammatory response of the lungs

chronic bronchitis
- airway narrowing
- hypertrophy and hyperplasia of mucus secreting glands
- bronchial wall inflammation
- mucosal oedema
- epithelial cell later may ulcerate
squmaous epithelium may replace columnar epithelium when ulcers heal –> squamour metaplasia

emphysema

  • dilatation and destruction of the lung tissue distil to the terminal bronchioles
  • loss of the elastic coil
  • expiratory airflow limitation and air trapping
  • smoking > 20 years
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12
Q

what scale is used to classify COPD

A

Medical Research Council Dyspnoea Scale

Grade 1 - breathless on strenuous exercise
Grade 2 - breathless on walking up hil
Grade 3 - breathless that slows walking on the flat
Grade 4 - stop to catch their breath after walking 100 meters on the flat
Grade 5 - unable to leave the house due to SOB

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13
Q

investigation of COPD?

A

MRC Dyspnoea Scale
spirometry - PEV1/FVC ratio < 0.7
CXR - hyperinflation and to exclude other diagnosis

FBC - anaemia, inc haematrocrit, polycythaemia, eosinophil count, 
sputum culture
BMI 
ECG 
ECHO 
BNP 
Alpha 1 antitrypsin
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14
Q

what is used to assess the severity of COPD?

A

GOLD framework

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15
Q

what is the single most important diagnostic test for COPD

A

spirometry with bronchodilator reversibility test

  • FEV1/FVC < 0.7
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16
Q

what are the different stages of COPD?

A

Stage 1, mild — FEV1 80% of predicted value or higher. With these values, a diagnosis of COPD can only be made on the basis of respiratory symptoms.

Stage 2, moderate — FEV1 50–79% of predicted value.

Stage 3, severe — FEV1 30–49% of predicted value.

Stage 4, very severe — FEV1 less than 30% of predicted value.

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17
Q

what is considered to be asthma features

A

previous diagnosis of asthma or of atopy, a higher blood eosinophil count, substantial variation in FEV1 over time (at least 400ml) or substantial diurnal variation in peak flow (at least 20%)

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18
Q

management of COPD without asthma features

A

1) SABA or SAMA PRN

2) LABA + LAMA

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19
Q

management of COPD with asthma features

A

1) SABA or SAMA PRN
2) ICS + LABA
3) if still exacerbations –> ICS + LAMA + LABA

20
Q

what is pleura effusion

A

collection of fluid in the pleural cavity

21
Q

what are the 2 types of pleural effusion

A

exudative - high protein count (>3g/L), protein leaking out of the tissues into the pleural space

transudative - relatively low protein count (< 3g/L protein), fluid moving across into the pleural space

22
Q

aetiology of o exudative pleural effusion

A

local inflammation

  • lung cancer
  • penumonia
  • TB
  • PE
  • post CABG
  • systemic disease eg RA
23
Q

aetiology of transudative pleural effusion

A

systemic shift in fluid

  • congestive heart fialure
  • cirrhosis, nephromatic syndrome
  • Meig’s syndrome - R sided pleural effusion with ovarian malignancy
24
Q

clinical features

A

SOB
cough - can be productive or not
dullness to percussion over the effusion
tracheal deviation away from the effusion - if massive
reduced breath sounds
improving pneumonia with a/onging fever - suspect empyema

25
Q

investigation of pleural effusion?

A
CXR - 1st line 
•	Blunting of the costophrenic angle
•	Fluid in the lung fissures
•	Larger effusions will have a meniscus
•	Tracheal and mediastinal deviation – massive effusion

USS - more sensitive than CXR

  • Thoracentesis
  • High protein count, pH<7.2, ↓ glucose, ↑ LDH = empyema
  • Blood = malignancy, PE with infarction, trauma
  • Light’s criteria is used when the pleural fluid is between 25-30g/L to differentiate between exudate and transudate
26
Q

what is the light’s criteria for pleural effusions

A

it looks into protein and LDH to differentiate between exudate and transudate pleural effusion

Transudate

  • protein (pleura/serum) < 0.5
  • LDH (pleural/serum) <0.6
  • pleura LDH < 2/3 of upper limit of normal serum LDH

Exudate

  • protein (pleura/serum) > 0.5
  • LDH (pleural/serum) >0.6
  • pleura LDH > 2/3 of upper limit of normal serum LDH
27
Q

management of pleural effusion?

A

small - conservative management

larger - pleural aspiration and chest drain

empyema (pH<7.2) - chest drina + ABx

28
Q

what cancer most commonly mets to the lungs

A
breast 
colorectal
renal 
bladder 
prostate
29
Q

where does lung cancer most commonly mets to?

A

bone
liver
adrenals
brain

BLAB

30
Q

clinical features of lung mets

A

enlarged axillary lymph nodes
bone pain
ascites

31
Q

investigations of lung mets

A

CT chest abdo pelvis

PET-CT - for distant mets (not useful for brain, kidney or bladder)

MRI

32
Q

what is mesothelioma

A

neoplasma arising from the lining of the lung

commonly caused by asbestos exposure, aged 60-85, male

33
Q

what are the management of lung mets

A

bone - single fraction radiotherapy for bone mets, denosumab - prevent skeletal-related events from bone mets

Liver - peritoneal catheter drainage system for treatment resistant, recurrent malignant ascties

adrenal - surgical and replacemetn of cortisol and alderstone and androgen

brain - 1x met –> chemo/immuno otherwise stereotactic radiosurgery/radiotherapy
- if > 1x mets –> stereotactic radiosurgery/radiotherapy

34
Q

what are the different types of lung cancer?

A

non small cell lung cancer

small cell lung cancer

35
Q

what is sarcoidosis

A

granulomatous (nodules of macrophages) inflammatory condition commonly affecting the lungs, skin and eyes

36
Q

aetiology of sarcoidosis

A

unknown

most commonly affect - women, black, young adulthood, > 60 yrs old

37
Q

clinical faetures of sarcoidosis

A

CNS - diabetes inspidius, encepahlopathy

PNS - facial nerve palsy, mononeuritis multiplex

eye - uveitis, conjunctivitis, optic neuritis

lung - dry cough, SOB, wheeze, mediastinal lymphadenopathy, pulmonary fibrosis

heart - bundle branch block, heart block

liver - cirrhosis, cholestasis

skin - erythema nodosum, lupus pernio, granuloma development in scar tissues

systemic - fever, fatigue, weight loss

kidney - kidney stones, hypercalcaemia, nephrocalcinosis, interstitial nephritis

MSK - arthralgia, arthritis, myopathy

38
Q

aetiology of sarcoidosis

A

unknown

most commonly affect - women, black, young adulthood, > 60 yrs old

39
Q

management of sacroidosis

A

no/mild symptoms - no treatment

moderate symptoms

1) orla steriod - indicated for parenchymal lung disease/uveitis/hypercalacemia/neurological/cardiac involvment
2) bisophophonates for boen protection

3) methotrexate/azathioprien

severe lung transplant

40
Q

what genetic mode of transfer is cystic fibrosis

A

autosomal recessive - gene mutation in the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7

most common variant = delta F508

41
Q

clinical features of cystic fibrosis

A

meconium ileus

recurrent LRTI

chronic cough

nasal polyps esp if bilateral

thick sputum production

crackles/wheeze on auscultation

salty sweat

finger clubbing

FFT 
abdo pain 
abdo distension 
pancreatitis 
steatorrhoea
42
Q

what genetic mode of transfer is cystic fibrosis

A

autosomal recessive - gene mutation in the cystic fibrosis transmembrane conductance regulatory gene on chromosome 7

43
Q

management of cystic fibrosis

A

MDT approach

chest physio with nebulised saline - twice daily
salbutamol
Nebulised DNase
ABx - prophylactic flucloxacillin

CFTR modulators eg ivacaftor (G551D mutation only)
vaccine - pneumococcal, influenza, varicella

transplants - lung, liver

high calorie diet, CREON tablets

44
Q

investigation for cystic fibrosis

A

1) newborn screening via guthrie test (majority diagnosed here) + typical clinical symptosm/FHX of sibling
2) sweat test - gold standard - diagnostic if > 60 on 2 separate occasions

or genetic testing for CFTR gene during pregnancy by aminocentesis, CVS

45
Q

clinical features of TB

A
persistent productive cough
SOB 
Haemoptysis - late features 
weight loss 
fever 
night sweats 
malaise 

extra-pulmonary involvement
- headache, vomiting, irritability, confusion, cranial nerve abnor - TB meningitis
- lymphadenopathy - cervical and supraclavicular lymph nodes
- SOB, chest pain, ankle swelling - TB pericarditis
- abdo/pelvic pain, constipation, bowel obstruction
sterile pyuria - renal TB
- skin lesions - erythema nodosum, lupas vulgaris - cutaneous TB
- bone/joint/back pains, joint swelling

46
Q

investigation of TB

A

Active TB
• CXR
• 3x early morning sputum samples – acid fast bacilli +ve
• If active extrapulmonary, arrange scanning of the relevant areas

Latent TB
• Mantoux test – tuberculin injected and skin reaction after 2-3 days = +ve test
• Interferon gamma release assay (IGRA) test
• HIV/Hep B/Hep C testing
• CXR – calcified Ghon complex

47
Q

management of TB

A

• Notifiable disease + immediate contact tracing

6 months (or 3 months if latent) of isoniazid with pyridoxine and rifampicin, supplemented in the first 2 months with pyrazinamide and ethambutol