Year 3 > Block 31 Week 4 > Flashcards

Block 31 Week 4 Flashcards

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1
Q

which ab can cause QT interval prolongation?

A

macrolides

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1
Q

what is the normal QT interval?

A
  • QT interval needs to be less than half of the R-R interval (less than 500ms)
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2
Q

causes of sinus bradycardia?

A
  • acute MI/ ischemia
  • beta blockers, CCB, digoxin, anticholinergics
  • hypothyroidism
  • hyperkalemia
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3
Q

what could bradycardia suggest?

A
  • RCA supplies SAN so bradycardia could suggest inferior ischemia
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4
Q

Tx for bradycardia?

A
  • atropine
  • noradrenaline
  • isoprenaline
  • dopamine
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5
Q

drug for BB overdose?

A

glucagon

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6
Q

if these drugs don’t work for bradycardia then?

A

pacemaker

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7
Q

positive aVR and broad QRS complexes = Treat as

A

VT unless proven otherwise

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8
Q

Tx of VT?

A
  • amiodarone
  • ICDs
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9
Q

why does aVR become positive in VT?

A
  • current firing around the area of fibrosis in the infract in the ventricle
  • aVR becomes positive
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10
Q

which ab to avoid in a LRTI when the patient is on warfarin?

A

macrolides

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11
Q

infectious HD?

A
  • endocarditis
  • myocarditis
  • pericarditis
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12
Q

New murmur and fever think?

A

endocardititis

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13
Q

RF for endocarditis?

A
  • prosthetic valve
  • elderly patient w degenerated valves
  • IV drug users - tricuspid valve
  • catheters, pacemaker electrodes
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14
Q

Relapse vs reinfection - endocarditis?

A
  • relapse - repeat within 6 months and proven identical pathogen
  • reinfection - new MO or same species but > 6 months
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15
Q

CP of endocarditis?

A
  • fever & systemic disease signs like weight loss
  • murmur
  • septic embolization - brain, kidneys, spleen
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16
Q

most common causes of endo?

A
  • streptoccoi, staphy, enterococci most common causes
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17
Q

less common causes of endocarditis?

A
  • less commonly HACEK
  • haemophilus
  • actinobacillus
  • cardiobacterium
  • eikenella
  • kingella
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18
Q

think ? in resistant cases of endocarditis?

A
  • fungi - candida, aspergillus
  • think fungi in resistant endocarditis
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19
Q

echo (transoesophageal) for endo?

A
  • vegetations/ abscess/ new prosthetic valve dehiscence = specific
  • new regurgitation/ obstruction = not specific
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20
Q

clinical signs of endocarditis?

A
  • splinter haemorrhage
  • roth’s spot on the retina
  • osler’s node
  • janeway lesions
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21
Q

Tx of endo?

A
  • amoxicillin
  • gentamicin
  • MRSA: vancomycin
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22
Q

which type of lung cancer tends to cavitate in the middle?

A

SCC

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23
Q

5 yr survival of lung cancer?

A

less than 20%

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24
SCLC is almost always associated w?
active smoking
25
SCC is strongly assoc w
smoking
26
law on radiation exposure?
IRMER
27
Which type of cancer needs referral to coroner?
* Mesothelioma = prescribed disease, needs referral to coroner
28
SVCO leads to
a swollen face
29
What else can be seen w lung cancer?
* hoarse voice * bovine cough * can get seizures when lung cancer metastasised
30
NSCLC has ? on biopsy
genetic tests done
31
Radical vs stereotactic radiotherapy?
* radical radiotherapy isn't aimed specifically like palliative radiotherapy is so you run the risk of losing healthy lung * stereotactic radiotherapy is aimed and has less risk of damaging the rest of the lung e.g. in COPD
32
ALK mutation?
tend to occur in younger non-smoker women
33
obstructive vs restrictive pattern of airflow obstruction?
34
narrowing of large airways vs small airways?
* narrowing of large airways causes early symptoms * major damage can occur to small airways without producing symptoms * resistance inversely proportional to radius
35
obstructive airway diseases?
* asthma * COPD * bronchiectasis
36
asthma?
* variable expiratory airflow limitation * defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity,
37
acute airway changes in asthma?
* SM contraction * mucus hypersecretion * plasma leakage * oedema * sensory nerve activation
38
chronic changes in asthma
* subepithelial fibrosis * smooth muscle hypertrophy
39
asthma diagnosis steps?
- PEFR - testing for variability - testing for oesinophilic inflammation - all patients should have spirometry with a bronchodilator reversibility (BDR) test - all patients should have a FeNO test
40
asthma diagnosis pathway
- spirometry and bronchodilator reversibility - FeNO
41
A - testing for variability methods?
* reversibility * PEF charting * challenge tests
42
methods of testing for oesinophilic inflammation?
* FeNO * blood eosinophils * skin prick test, Ig-E
43
steps of brochodilator reversibility testing?
* 1) Prebronchodilator Spirometry * If possible, withhold usual inhaled therapy before test (SABA ≥ 4 hours, LABA ≥ 15 hours) * 2) Administer short acting beta-2 agonist (400 micrograms salbutamol) * 3) Post-bronchodilator Spirometry * Perform 15 minutes after salbutamol inhalation
44
positive bronchodilator test?
Test considered positive if: * FEV-1 increases by 200mls and 12% * Greater confidence of a positive test if FEV increases by 400mls and 15%
45
Asthma - peak flow monitoring?
* twice daily for 2 to 4 weeks * Calculating variability: * ([Days highest – Days lowest] / mean of days highest and lowest PEFR), averaged over 1 week.
46
peak flow variability that is considered significant?
* >10% (GINA) to 20% (NICE) variability considered significant
47
bronchial challenge testing options?
* hyperpnoea, mannitol, saline
48
mannitol challenge testing?
* highly spec for bronchial hyperresponsiveness consistent w asthma * acts on inflammatory cells to trigger release of mediators like PGD, LTE4, histamine that cause bronchoconstriction in those w hyperactivity
49
FeNO levels supporting an asthma diagnosis?
* NICE say FeNO >40ppb supportive of an asthma diagnosis * Elevated FeNO predicts response to inhaled corticosteroids in asthma
50
peripheral blood oesinophilia?
* more useful in COPD to predict response to inhaled corticosteroids than asthma
51
sputum eosinophilia?
* gold standard * limited to academic centers
52
evidence of atopy in asthma?
* Blood tests - total IgE and specific IgE to aeroallergens (RAST) * Skin prick testing
53
allergic/ atopic asthma?
* Often childhood onset and may be associated with other atopic disease * Associated with eosinophilic airway inflammation. * Identifiable triggers (clinically and objectively)
54
asthma with persistent airflow limitation?
* Some asthma patients develop airflow obstruction that is fixed or incompletely reverses with treatment.
55
asthma and obesity?
* Prominent respiratory symptoms * Little evidence of eosinophilic inflammation
56
COPD?
* persistent resp symptoms and airflow limitation due to airway and/or alveolar abn usually caused by sig exposure to noxious particles or gases * The most common respiratory symptoms include breathlessness, cough and/or sputum production.
57
RF for COPD?
* smoking * genetic factors * abn lung development * accelerated lung aging
58
Causes of COPD?
* Tobacco * Recreational drug use * E-cigarettes * Passive smoking * Chronic asthma * Biofuels * Occupation * Familial
59
emphysema on a CT
looks like holes
60
pathology of chronic bronchitis?
* Mucus gland hypertrophy * Smooth muscle hypertrophy * Goblet cell hyperplasia * Inflammatory cell infiltrate * Excess mucus
61
emphysema =
* Abnormal enlargement of airspace distal to the terminal bronchiole accompanied by destruction of their walls and without obvious fibrosis
62
why does emphysema cause airflow obstruction?
* Alveolar pressure reflects sum of pleural pressure + elastic recoil * Combination of reduced radial traction and reduced intraluminal pressure leads to airway narrowing/collapse
63
COPD and cycle of inactivity
64
asthma vs COPD age of onset?
* asthma usually childhood but can be any age, COPD usually >40yrs
65
asthma vs COPD symptoms?
* asthma: symptoms vary over time, often triggers * COPD: chronic and continous symptoms with good and bad days
66
Asthma vs COPD - bronchodilator response?
* asthma: Variable airflow limitation. Bronchodilator reversibility * COPD: Post bronchodilator FEV1/FVC <0.7
67
A vs COPD - history?
* asthma: Often have personal or family history of asthma * COPD: Relevant exposure (cigarette smoke)
68
A vs C - reversible?
* asthma: reversible and can resolve * COPD: progressive
69
Asthma vs COPD X ray changes?
* asthma: X ray usually normal * COPD:Hyperinflation and other chronic changes
70
asthma vs COPD type of inflammation?
* asthma: inflammation is usually eosinophilic * COPD: typically neutrophilic
71
Asthma and COPD overlap syndrome?
72
why airflow obstruction causes hypoxia?
* Ventilation / perfusion mismatch. Many alveoli will be poorly ventilated because of bronchial narrowing * Emphysema also reduces the surface area of the gas exchanging part of the lung impairing diffusion of gasses.
73
consequences of pulm hypertension - cor pulmonale?
* Right sided heart failure as a result of chronic lung disease. * Right heart failure leads to raised venous pressure and oedema
74
bronchiectasis can be divided into?
* CF * non-CF
75
what is bronchiectasis?
* Abnormal dilatation of the airways * Chronic purulent sputum production * Recurrent infection
76
causes of bronchiectasis
* Many causes – most commonly idiopathic * Cystic fibrosis is the most common fata genetic disease
77
how is the diagnosis of bronchiectasis confirmed?
* Diagnosis of bronchiectasis is confirmed using high resolution CT (HRCT)
78
airflow obstruction in bronchiectasis?
* Paradox of airway narrowing in a disease defined by dilatation of one or more bronchi * Secretions and fibrosis affecting predominantly small airways causes airflow obstruction
79
Asthma vs COPD spirometry results?
* Reversibility can be established using before and after measurements after an inhaled beta-agonist( after 30 minutes) or taking oral prednisolone (after 2 weeks). * A positive response is increase in FEV1by 15% and >200ml = ASTHMA, less than this is COPD
80
COPD FEV1/ FVC ratio?
has to be less than 70%
81
COPD grading?
* FEV1 - 60-80% predicted:mild * FEV1 - 40-60% predicted:moderate * FEV1  -<40%    predicted :severe
82
regular cough and sputum in a smoker usually indicates?
chronic hypersecretory bronchitis
83
features of COPD?
* Dyspnoea varying from mild (exertional) to severe at rest * Cough and sputum if CHB * Recurrent exacerbations * Respiratory failure if severe
84
Chronic features of COPD?
* Respiratory failure if severe * Odema, secondary polycythaemia - as a result of chronic hypoxia * Pulmonary hypertension (and cor pulmonale)
85
other features of COPD?
* weight loss * depression and social isolation * premature retirement
86
Smoking cessation?
* only intervention that can halt decline in FEV1 * nicotine replacement therapy, bupropion and vareninicline can be used in a smoking cessation package
87
inhaled bronchodilators in COPD?
* Usually combine inhaled beta-agonist (sabutamol) and anticholinergic agent (ipatropum and tiotropium) * often in a nebuliser * Large measurable response usually suggests an asthmatic component.
88
Steroids in COPD?
* useful if reversibility testing suggests asthmatic component to airflow obstruction * short course of oral steroids can also be used in exacerbations
89
Carbocysteine in COPD?
mucolytic, reduce cough and sputum production
90
pulm rehab for COPD?
* Pulmonary rehabilitation is the most effective treatment for reducing dyspnoea and disability * It is best delivered as a multidisciplinary and exercise based programme (combined with emotional and nutritional support)
91
recognition of COPD exacerbations?
* Increased dyspnoea,sputum volume or purulence * More wheezy * Peripheral odema * Fever or symptoms of upper respiratory tract infection * Confusion or drowsiness (implies respiratory failure)
92
Causes of Copd exacerbations?
* infections * other - reflux
93
Tx of COPD exacerbations?
* ab to cover H influenza/ S pneumoniae/M catarrhalis * increase bronchodilator dose (nebulized) if worsening airflow obstruction * steroids
94
when is admission for COPD required?
* Admission required if severely breathless, suspicion of respiratory failure,need to exclude other conditions,social factors
95
type 1 resp failure?
hypoxia (under 8kPa) and normal to low CO2
96
type 2 resp failure?
hypoxia and hypercapnia - CO2 over 6kPa
97
which type of resp failure are ppl usually in during exacerbations?
* most people have type 1 failure during exacerbations and then when stable and then type 2 in exacerbations and then permanently
98
mechanisms of hypoxia - low inspired oxygen
e.g. altitude
99
mechanisms of hypoxia - hypoventilation?
opiate overdose
100
mechanisms of hypoxia - diffusion defect?
lung fibrosis (alveoli abn, initially hypoxic only on exercise but as it progresses gas exchange becomes worse causing severe hypoxia which needs a lot of oxygen to correct)
101
mechanisms of hypoxia - V/Q mismatch?
COPD or asthma
102
mechanisms of hypoxia - right to left shunt?
- pulmonary AVM: deox blood enters the LA bypassing alveoli so it doesn't get oxygenated, blood leaving via arteries is still deoxygenated
103
Mechanisms of hypercapnia?
* Same as those that lower paO2 apart from altitude * The CO2 dissociation curve is steeper and more linear than for oxygen so carbon dioxide elimination is more ventilation dependent
104
how can oxygen worsen hypoxia in COPD?
* In acute exacerbations of COPD uncontrolled oxygen can worsen hypercapnoea by reducing hypoxic drive,causing a degree of hypoventilation and worsening V/Q mismatch by reversing hypoxic vasoconstriction in poorly perfused lung units
105
management of resp failure - oxygen?
* pulse oximetry and blood gas * Controlled oxygen –aim for paO2>6.5-8kPa
106
management of resp failre - pharm?
* Improve ventilation with high dose combination bronchodilators (salbutamol + ipatropium) and mobilising secretions(physiotherapy)
107
resp failure - ventilation
* consider non-invasive positive pressure ventilation or intubation with mechanical ventilation in ICU (level 3 care) if the patient doesn't improve and has T2F with acidosis
108
symptoms of resp failure?
* confusion, * agitation, * headache, * drowsy, * coma.
109
signs of resp failure?
* cyanosis * bounding pulse - high volume radial pulse very suggestive of CO2 retention * flapping tremor.
110
O2 therapy for COPD?
* acute for Tx of exacerbations * short burst to relieve dyspnoea * ppts can have portable cylinders to relieve breathlessness e.g. to improve exercise tolerance
111
LTOT for COPD?
* LTOT is the only treatment shown to prolong survival in COPD patients with chronic respiratory failure. * Patients should use oxygen for >15 hrs/day and oxygen is provided from a concentrator.
112
What is type 1 resp failure?
* Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa / 60mmHg) with normocapnia (PaCO2 <6.0 kPa / 45mmHg)
113
what is type 2 resp failure?
* Type 2 respiratory failure involves hypoxaemia (PaO2 <8 kPa / 60mmHg) with hypercapnia (PaCO2 >6.0 kPa / 45mmHg)
114
why does type 1 resp failure occur?
* usually occurs due to V/Q mismatch - volume of air flowing in and out of the lungs isn't matched w flow of blood to lung tissue * as a result of the mismatch, PaO2 falls and PaCO2 rises * The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 
115
examples of type 1 resp failure?
* Reduced ventilation and normal perfusion (e.g. pneumonia, pulmonary oedema, bronchoconstriction) * reduced perfusion and normal ventilation e.g. PE
116
type 2 resp failure is caused by?
* It occurs as a result of alveolar hypoventilation, which prevents patients from being able to adequately oxygenate and eliminate CO2 from their blood. * This leads to PaO2 falling (due to lack of oxygenation) and PaCO2 rising (due to lack of ventilation and elimination of CO2).
117
why can hypoventilation occur?
* Increased resistance as a result of airway obstruction (e.g. COPD) * Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity) * Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease) * Reduced respiratory drive (e.g. opioids and other sedatives)
118
normal PaO2 on high glow oxygen
this is abnormal as you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy.
119
A ‘very low’ PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations:
this is likely a venous sample.
120
PaO2 on room air in a healthy ppt?
* PaO2 should be >10kPa when oxygenating on room air in a healthy patient
121
PaO2 of a patient on oxygen therapy should be?
approximately 10kPa less than the % inspired concentration FiO2
122
nasal cannulae?
* nasopharynx used as a resevoir for oxygen * oxygen flow rate of 2-6 L/min
123
simple face masks?
* O2 flow rate of 5-10L/min * These masks should not be used with flow rates less than 5L/min - risk of CO2 retention due to rebreathing
124
non rebreather masks?
* Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at a flow rate of 10–15 l/min. * The concentration is not accurate and will depend on the flow of oxygen as well as the patient’s breathing pattern.
125
when should NBM be used?
most suitable for trauma and emergency use where carbon dioxide retention is unlikely.
126
NRB - flow rate of under ? leads to risk of CO2 retention due to rebreathing?
12L/min
127
fixed performance devices?
venturi mask
128
Venturi mask?
* gives accurate conc of oxygen to the patient * They are suitable for all patients needing a known concentration of oxygen,
129
COPD venturi mask?
* 24% and 28% Venturi masks are particularly suited to those at risk of carbon dioxide retention (e.g. patients with chronic obstructive pulmonary disease)
130
venturi mask valve colours?
* blue delivers the least Oxygen and green the most
131
when should flow rate on a venturi be increased?
* BTS guidelines recommend that if the patient has a RR>30 that the flow rate on the Venturi mask is increased above the flow rate given on the adapter, to compensate for the patient’s increased respiratory flow. * This will not increase the FiO2 being delivered to the patient.
132
advanced O2 delivery systems?
* capable of delivering upto 100% humidified and heated oxygen at a flow rate of uto 60L/min * The high flow rate also creates a small amount of PEEP (positive end-expiratory pressure), which helps to keep the alveoli open at the end of expiration
133
pH values?
* Acidotic: pH <7.35 * Normal: pH 7.35 – 7.45 * Alkalotic: pH >7.45
134
changes in ? = respiratory
* changes in CO2 - respiratory * changes in HCO3 - metabolic
135
respiratory acidosis vs respiratory alkalosis?
Respiratory acidosis: low pH and high CO2 Respiratory alkalosis: high pH and low CO2
136
respiratory acidosis w metabolic compensation?
pH low, high CO2, high bicarb
137
resp alkalosis with metabolic compensation?
high pH, low CO2, low bicarb
138
metabolic acidosis?
pH and HCO3- low, CO2 normal
139
metabolic alkalosis?
high pH and bicarb, normal CO2
140
metabolic acidosis with resp compensation:
low ph, low bicarb, low CO2
141
metabolic alkalosis with resp compensation:
high pH, high bicarb and high CO2
142
Mixed alkalosis and acidosis?
* e.g. respiratory and metabolic acidosis * CO2 and HCO3– will be moving in opposite directions (e.g. ↑ CO2 ↓ HCO3– in mixed respiratory and metabolic acidosis).
143
causes of resp acidosis?
* inadequate alveolar ventilation leading to CO2 retention * Respiratory depression (e.g. opiates) * Guillain-Barre: paralysis leads to an inability to adequately ventilate * Asthma and COPD * Iatrogenic (incorrect mechanical ventilation settings)
144
why does resp alkalosis occur?
* caused by excessive alveolar ventilation  (hyperventilation) resulting in more CO2 than normal being exhaled. * As a result, PaCO2 is reduced and pH increases causing alkalosis.
145
causes of resp alkalosis?
* Anxiety (i.e. panic attack) * Pain: causing an increased respiratory rate. * Hypoxia: resulting in increased alveolar ventilation in an attempt to compensate. * Pulmonary embolism * Pneumothorax * Iatrogenic (e.g. excessive mechanical ventilation)
146
2 methods that metabolic acidosis can occur through?
* Increased acid production or acid ingestion. * Decreased acid excretion or increased rate of gastrointestinal and renal HCO3– loss.
147
examples of metabolic acidosis?
* diabetic ketoacidosis * lactic acidosis * aspirin overdose * renal failure * diarrhoea * renal tubular disease or Addinsons disease
148
metabolic alk occurs as a result of?
* occurs as a result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.
149
Met alk - GI loss of H+ ions e.g.
(e.g. vomiting, diarrhoea)
150
met alk - renal loss of hydrogen ions?
e.g. loop and thiazide diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn’s syndrome
151
met alk - iatrogenic?
e.g. addition of excess alkali such as milk-alkali syndrome
152
Causes of mixed respiratory and metabolic acidosis?
* cardiac arrest * multi organ failure
153
target O2 sats?
* target sats 94%-98% * unless risk of CO2 retention 88-92%
154
variable performance devices?
* Variable performance devices deliver variable FiO2 depending upon several variables, including the oxygen flow rate and the patient’s ventilation pattern. * These devices do not provide all the gas required for minute ventilation; each breath will include a proportion of inspired air and the oxygen supplied. * nasal cannulae, simple facemasks, non rebreather masks
155
examples of critical illnesses requiring high levels of oxygen?
* cardiac arrest/ resus * shock * sepsis * major pulmonary haemorrhage * status epileptica * major head injury
156
? poisoning requires as much oxygen as possible
CO
157
Critical illnesses requiring high levels of oxygen - which delivery device to use?
* 15L/min via NRB * Patients at risk of hypercapnic respiratory failure (e.g., COPD) who develop a critical illness should have target saturations of 94-98% until proven, on an ABG, that they need controlled oxygen therapy with target saturations of 88-92%
158
BTS table for critical illnesses requring a lot of oxygen
159
illnesses requiring moderate levels of supplemental oxygen if patient is hypoxaemic:
* acute hypoxaemia * asthma * pneumonia * lung cancer * pneumothorax * PE * pleural effusions * acute HF * post op dyspnoea
160
O2 therapy for the illnesses requiring moderate levels of oxygen?
Initial oxygen therapy will be: - 2-6L/min via nasal cannula - or 5-10L/min via simple face mask, if sats not maintained oxygen delivery to 15L/min via NRM * For patients not at risk of hypercapnic respiratory
161
sats below 85%?
treat as a critical illness and use 15L/min via NRB mask targeting 94-98
162
BTS table for moderate levels of oxygen
163
conditions where monitoring is required but oxygen not needed unless ppt is hypoxaemic:
* MI/ ACS * Stoke * hyperventilation * poisoning and drug overdoses (unless CO poisoning)
164
O2 delivery device for when o2 not required unless ppt is hypoaemic?
* If Hypoxaemic aim saturations 94-98%, give 2-6L/min via nasal cannula or 5-10L/min via simple face mask unless saturations are below 85% (use 15L/min via NRB)
165
BTS table for when oxygen is only required when ppt is hypoxaemic
166
COPD oxygen?
* Prior to an ABG use a 24% venturi mask at 2-3L/min or 28% venturi at 4L/min or 1-2L/min via nasal cannula aiming target saturations of 88-92%
167
sudden cesation of oxygen therapy?
can cause life-threatening rebound hypoxaemia with a rapid fall in oxygen saturations below the starting oxygen saturation prior to the start of supplementary oxygen therapy.
168
phases of a cough?
* inspiratory phase - negative flow phase * closed glottis * expiratory phase - positive flow phase
169
acute vs chronic cough?
* acute: <3 weeks * subacute: 3-8 weeks * chronic: 8+ weeks
170
receptors for the cough reflex?
* larynx, tracheo-bronchial tree and the carina have the most sensitive receptors * polymodal receptors - respond to mechanical, pharm, chemical stimulation
171
common causes of acute cough?
* pneumonia * acute on chronic bronchitis * pertussis
172
parenchymal diseases that can cause a cough?
* chronic intersitital lung fibrosis * emphysema * sarcoidosis
173
tumours that can cause a cough?
* bronchogenic carcinoma * mediastinal tumours * aveolar cell carcinoma
174
other causes of a cough?
* foreign bodies * middle ear pathology in children and elderly
175
CVD causes of a cough?
* LVF * pulmonary infarction * aortic aneurysm
176
GI causes of a cough?
* reflux oesophagitis * recurrent aspiration
177
Ix for a cough?
* spirometry * CXR * FeNO/ eosinophils
178
cough hypersentitivity syndrome?
* airways * upper airways cough syndrome * reflux
179
which ab can be used in bronchiectasis prophylactically?
* azithromycin can be used as a prophylactic ab in for its anti-inflammatory and immunomodulatory effects bronchiectasis
180
what can be seen on a TB CXR?
* reticular nodular shadowing in TB on CXR
181
What can be seen on a CXR for bronchiectasis?
'dirty' lung fields
182
CT findings of bronchiectasis - ? sign?
* signet ring - airways more dilated than vessels
183
resp consequences from excessive cough?
* pneumothorax * pneumomediastinum * pneumoperitoneum * laryngeal damage
184
CV conseuquences of excessive cough?
* cardiac dysarrythmias * subconjunctival haemorrhage * loss of conciousness
185
CNS consequences of chronic cough?
- syncope - headaches - central air embolism
186
Tx of cough?
* codeine, morphine, dimorphine are good antitussive agents * dextrromethophan (synthetic morphine)
187
obstructive vs restrictive lung diseaseS?
* obstructive: FEV1/ FVC ratio of <70% * restrictive: FEV1/FVC >70%
188
examples of restrictive lung diseases?
- pulm fibrosis - obesity - chest wall deformities - NM disorders
189
spirometry findings on an obstructive disease
190
COPD epidemology?
* costs the NHS £1.2bn/ annum * 2% of the whole population have COPD * 25,000 deaths/ year in the UK
191
COPD RF?
* Cigarette smoke * occupational dust and chemicals * indoor and outdoor air pollution * genes
192
mechanisms underlying airflow limitation in COPD - small airways disease?
* airway inflammation and fibrosis, luminal plugs * increased airway resistance
193
mechanisms underlying airflow limitation in COPD - parenchymal destruction?
* loss of alveolar attachments * decrease of elastic recoil
194
air trapping in COPD?
* Inflammation and thickened airway (SM hypertrophy and constriction) * loss of alveolar attachments * loss of elasticity (emphysema) * airway closure
195
mucosal changes of COPD?
* mucosal oedema * mucus hypersecretion * loss of alveolar SA and attachments
196
other changes seen in COPD (3)?
* hyperinflation and gas trapping * increased work of breathing * V/Q mismatch
197
systemic effects of COPD
* IHD * cardiac failure * osteoporosis * diabetic metabolic syndrome * normocytic anemia * depression
198
how is COPD diagnosed?
* spirometry required to make the diagnosis: the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation.
199
vaccinations that should be offered to COPD patients?
* pneumonia * influenza
200
palliative care for COPD?
* opiates, NMES * nutritional supplementation can improve resp strength and overall health in malnourished patients * fatigue can be improved by self managament, pulm rehab, nutritional support
201
LTOT COPD?
* for patients w an SaO2 level below 88% * or if O2 is higher but there's evidence of pulmonary hypertension, peripheral edema suggesting congestive cardiac failure, or polycythemia
202
COPD bronchodilators?
* increase radius of the small airways and so reduce the resistamce of the airflow during breathing * Airflow is inversely proportional to the radius of the small airway to the power of four
203
anti-inflammatory therapies in COPD - steroids?
* ICS - but increased risk of pneumonia * oral glucocorticoids
204
anti-inflammatory therapies in COPD - PDE4 inhibitors?
* PDE4 inhibitors - in patients w chronic bronchitis. severe COPD and a history of exacerbations
205
anti-inflammatory therapies in COPD - mucolytics?
* carbocysteine
206
COPD - airflow obstruction -> inhaler?
* airflow obstruction -> LAMA/ LABA combination inhaler * eosinophilic airway inflammation -> ICS
207
bronchiectasis =
Persistent or recurrent bronchial sepsis, related to irreversibly damaged and dilated bronchi
208
presentation of bronchiectasis?
* cough * sputum - excessive volume * haemoptysis * dyspnoea * chest pain * recurrent chest infections
209
CXR of bronchiectasis
210
CT features of bronchiectasis?
- HRCT is the gold standard for bronchectasis
211
Cystic vs non tapering bronchiectasis on CT
212
signs associated with bronchiectasis?
* bronchial wall thickening * mucus impaction * mosaic perfusion/ air trapping on expiratory CT
213
Allergic bronchopulmonary aspergillosis (ABPA)?
* causes 4% of bronchiectasis in the UK * Can get proximal bronchiectasis and high attenuation mucus plugging
214
who should bronchiectasis be suspected in?
215
diagnosing ABPA?
* associated clinical deterioration - inc cough, wheeze, increased sputum production, worsening lung function * high total IgE >500 * Either positive Aspergillus-specific IgE or immediate reaction on skin prick testing * mucus plugging/ proximal bronchiectasis on imaging
216
immune dysfunction as a cause of bronchiectasis?
* investigate for primary B cell immunodeficiency - IgG replacement therapy * check serum ab & electrophoresis * measurement of baseline spec ab levels against capsular polysaccharides of strep pneumoniae
217
bronchiectasis - CVID?
* Cardinal feature: recurrent pulm infections with encapsulated organsisms * GI infection with Giardia and enteric pathogens is a common complication of CVID
218
CVID ix?
* reduced IgG and IgA/IgM * impaired resp to test immunisation
219
Kartagener's syndrome:
* chronic sinusitis * dextrocardia * bronchiectasis
220
Causes of bronchiectasis?
- primary ciliary dyskinesia - CF - youngs syndrome
221
Primary ciliary dyskinesia - are likely to have?
* history going back to childhood * upper and lower RT infections * chronic rhinosinusitis * recurrent otitis media * situs inversus
222
which condition has a strong association with bronchiectasis?
RA
223
in which adults shoukd CF be investigated in?
224
cf?
* newborn screening * AR * Caucasian population * CFTR dysfunction
225
Youngs syndrome?
* Azoospermia(obstructive) * Chronic rhinosinusitis * Bronchiectasis * No ciliary beat frequency or ultrastructural abnormalitiss
226
Bronchiectasis management - airway clearance teachiques?
* chest clearance techniques to keep airways free of secretion * resp physio effective in stable patients
227
Bronchiectasis Mx - breathing and devices?
* active cycle of breathing, autogenic drainage, use of positive expiratory pressure devices
228
bronchiectasis - rehab?
* pulm rehab * improved excercise tolerance and health related QOL
229
Prior to starting long term macrolides:
* avoid in patients w prolonged QT interval * azithromycin 3x a week for bronchiectasis * caution when patient has hearing loss
230
atopic triad?
asthma, eczema, and hay fever
231
ashma affects ? adults
1 in 12
232
pathiphys of asthma?
* mural inflammation - eosinophils, mast cells, lymphocytes * wall thickening by oedema, hyperaemia, fibrosis * SM thickening and spasm * mucous plugs
233
which variation is exacerbated in asthma?
diurnal variation
234
Ix of asthma?
* PEF * to assess severity at that time * or to show patterns of disease * peak flow diary * spirometry * FEV1/ FVC ratio of under 0.7
235
beta agonists in asthma?
* salbutamol and terbutaline - stimulation of SNS -> bronchodilation * inhaled route normally except in severe and life threatening exacerbartions when the use of nebulisers is recommended
236
occupations at risk of asthma?
237
NIV?
* used in NM disease (resp muscle weakness), morbid obesity, kyphoscoliosis * resp support to a spontaneously breathing patient using a tight fitting face mask and is an effective alternative to intubation with an endotracheal tube and mechanical ventilation in ICU
238
CPAP?
- not the same as NIV - used to treat obstructive sleep apnoea by preventing collapse of upper airway during sleep, but this does not blow air into the lungs
239
NIV is indicated for COPD when?
* indicated for acidotic T2RF in a COPD exacerbation in a patient who isn't responding to drug Tx
240
how does NIV work?
* increases alveolar ventilation and CO2 elimination through resting fatigued respiratory muscles and decreasing the work of breathing * opens airways
241
+ of NIV?
* lower risk of nosocomial pneumonia * no sedation required * patient can talk ,eat, cough * ICU bed not usually needed, reduced costs
242
NIV involves a ?
small portable ventilaor
243
overlap syndrome?
* The combination of morbid obesity and COPD (often with an element of sleep apnoea) is called overlap syndrome and is a common cause of type 2 respiratory failure
244
Intubation (invasive ventilation) is used when?
* safer if patient unconscious, vomiting, severe acidosis, unable to protect upper airway, cardiovascular instability * better access to airway (particularly important in patients with copious secretions) * patient cooperation not required so greater scope to alter ventilator
245
AS features
An ejection systolic murmur and splitting of the second heart sound are both signs
246
Heart sound in heart failure?
third
247
pulsus paradoxus?
In cardiac tamponade, there will be an abnormally large drop in BP during inspiration, known as pulsus paradoxus
248
LV free wall rupture
A patient develops acute heart failure 10 days following a myocardial infarction. On examination he has a raised JVP, pulsus paradoxus and diminished heart sounds - left ventricular free wall rupture
249
AHF management
IV furosemide
250
CHF management?
1: ACEi AND BB 2: aldost antagonist such as spironolactone and elpernone 3: ivabradine, valsartan, hydralazine, nitrate, digoxin, cardiac resync therapy
251
SGLT2 inhib?
- in management of HF w rEF
252
digoxin?
does not improve mortality in HF
253
ralazine in combination with nitrate
this may be particularly indicated in Afro-Caribbean patients
254
CRT
indications include a widened QRS (e.g. left bundle branch block) complex on ECG
255
Other Tx of HF?
offer annual influenza vaccine offer one-off pneumococcal vaccine
256
Initial Mx of ACS?
- Aspirin - O2 if sats under 94% - morphine in severe pain - nitrates - but not if hypotensive
257
STEMI Tx?
- PCI if present within 24 hours and can be done within 2 hrs - if not fibrinolysis within 12 hours of onset of symptoms
258
PCI AP THERAPY?
- aspirin - plus prasugrel if not alr taking an AC - clopidogrel if already taking an AC
259
Drug therau during PCI?
- UFH with gylcoprotein inhibitior as a bailout
260
Fibrinolysis?
- give antithombin -
261
NSTEMI mX?
- aspirin and fondaparinux if no immediate PCI planned - calc GRACE score
262
NSTEMI - low GRACE RISK
- <3% - give ticagrelor - conservative management
263
PCI for NSTEMI?
- >3% GRACE risk - give prasuregl or ticareglor - give UFH
264
NSTEMI - if ppt alr on AC awap?
praugrel/ ticareglor for clopidrogel
265
Year 3
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