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week 42: cough > general > Flashcards

general Flashcards

1
Q

an elderly man enters your GP surgery complaining of increasing SOB, has started taking the bus as can only manage to walk 1/2mile before becoming breathless. he has a Hx of ischemic heart disease, TIIDM, HTN, gastro-oesophageal reflux and depression.

a) What are your initial differentials?
b) what red flags should you ask for?
c) what further Ix would you suggest and why?

A

a) - COPD
- asthma
- angina
- heart failure
- infection
- bronchiectasis
- tumour
- interstitial lung disease
- pleural effusion
- ACEi cough

b) haemoptysis, weight loss, chest pain, hoarseness
c) FBC - anaemia can cause breathlessness, secondary polycythaemia can be a consequence of COPD

CXR - COPD changes (hyperinflation, flattened diaphragm and to exclude other resp causes)

ECG - bradycardia, arrhythmia such as AF

echo - heart failure

spirometry - restrictive or obstructive picture

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2
Q

what type of inhalers are salbutamol and increase ellipta?

A

SABA (relived) and LAMA (preventer)

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3
Q

what does a spirometry of FEV1/FVC <0.7 and FEV1 <80% suggest?

A

consistent with airway obstruction

the severity of airflow obstruction can be classified according to the degree of impairment of FEV1 using the global initiative for chronic obstructive lung disease criteria

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4
Q

what’s the most important advice you can give your pt just diagnosed with C|OPD?

A

stop smoking

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5
Q

what are the risk factors of COPD?

A

smoking
air pollution
occupational exposure
alpha-1 antitrypsin deficiency

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6
Q

what medication is given in an acute exacerbation of COPD?

what medication is used if 2days later, the pt is not better/worse?

the pt is no better and is taken to hospital. what are the initial Ix?

A

doxycycline 200mg, followed by 100mg OD and prednisolone 30mg daily for 5 days

+ nebuliser salbutamol (SABA) and ipatropium (SAMA)

CXR, bloods (FBC, U+Es, LFTs, CRP, glucose and lactate), blood +sputum cultures, ABG, insert IV cannula
*pt prescribed 2L/min O2 via nasal cannula as well as nebuliser salbutamol and ipatropiam

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7
Q

ABG show low pO2 and normal pCO2 and pH. what does this suggest?

A

type 1 respiratory failure

  • caused by oxygenation being a problem, for various reasons including infection, pleural effusion or pulmonary oedema. the Tx for this is oxygen
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8
Q

what are the risks of Ox therapy in an acute setting?

A
  • over oxygenation can reduce the hypoxic drive, so that the lungs lose their feedback mechanism to work harder. this can lead to reduced respiratory rate and CO2 retention
  • in principle, pt’s with COPD have a target Ox sat of 88-92% (and all other acutely unwell pt’s SpO2>94%) to minimise the risks of precipitating respiratory failure in susceptible pt’s
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9
Q

a pt, with type 1 resp failure, condition deteriorates. there is increasing breathlessness and confusion. they are agitated and trying to remove the oxygen. you perform an ABG and it shows low pH, low pO2 and high pCO2 and normal bicarbonate - what is the diagnosis?

A

type 2 respiratory failure

there is elevated pCO2 and low pH

this is acute

normal bicarbonate suggests this patient is not normally a chronic retainer of CO2

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10
Q

what is the treatment of acute type 2 resp failure?

A

non-invasive ventilation

the pt needs oxygen but is in resp failure. if they are given more O2 then their acidosis will get worse

bilevel positive airway pressure gives inspiratory and expiratory airwavey pressure. in inspiration in boosts alveolar ventilation and in expiration it prevents alveolar collapse

this has many advantages over invasive mechanical ventilation in that patients are able to communicate, eat and drink, undergo physio and receive nebuliser and oral med more easily, but some its find it difficult to tolerate due to the close-fitting mask

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11
Q

what are the indications and contraindications for long term oxygen therapy?

A

O2 is not a Tx for breathlessness but hyperaemia
criteria for referral for further assessment for O2:
- SpO2<92% on air
- FEV1 <30%
- polycythaemia
- peripheral oedema
-cyanosis
- raised JVP
- hospital assessment will include measurement of arterial blood gases and criteria are pO2<7.3kPa or <8.0kPa with cor pulmonate

  • main contraindication is if the pt continue to smoke and the danger of naked flames, such as open fire, due to risk of explosion
  • relative = risk of falls with equipment
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12
Q

describe the conducting and respiratory parts of the bronchial tree

A

trachea -> main bronchi -> lobar bronchi -> segmental brunch -> bronchioles (conducting, terminal, respiratory) -> alveolar ducts -> alveolar sac

anything above the bronchioles is conducting zone and anything below is the respiratory zone

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13
Q

describe the features of the bronchial tubes that become damaged in chronic bronchitis

(infection of the main airways of the bronchi, causing them to become irritated and inflamed. The main symptom is a cough, which may with yellow-grey mucus - chronic = daily productive cough that lasts 3months of the year for at least 2 years)

A
  1. inflamed bronchial tubes produce a lot of mucus –> coughing and difficulty breathing
  2. narrowing of lumens of the conducting part of the bronchial tree due to injury
  3. loss of cilia and accumulation of mucous
  4. coughing, which causes more injury to the bronchial tree
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14
Q

describe the features of the alveolus that become damaged in emphysema

A
  • damage to alveoli causes emphysema
  • over time, the inner walls of the air sacs weaken and rupture. fewer and larger sacs results in decrease SA and less effective gas exchange
  • low O2 sats and pt is SOB
  • lungs can become stretched out as they lose their ‘springiness’
  • air becomes trapped in the lungs, harder to breathe out
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15
Q

what is the clinical presentation of COPD?

A
  • dysponsea
  • wheeze
  • cough
  • sputum production
  • cyanosis
  • raised JVP (hypoxia in alveoli -> vasoconstriction to redirect blood to healthy alveoli -> pulmonary hypertension)
  • peripheral oedema (cor pulmonale)
  • hyper inflated chest
  • cachexia
  • resonant or hyper resonant percussion
  • recurrent infection
  • common in older people. neutrophil driven. characterised by a slow progression of symptoms
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16
Q

what are the 3 changes on spirometer in obstructive lung disease?

A

(air is trapped in expiration –> residual volumes are higher)

  1. reduced FEV1
  2. high FRC
  3. high RV
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17
Q

describe what a pleural effusion is

A

fluid in the pleural space/ between layers of the pleura as a result of increased fluid formation and/or reduced fluid resorption

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18
Q

outline the typical radiographic features and examination findings of pleural effusion

A

initial diagnostic imaging = plain radiograph:
- small effusions blunt the costophrenic angle
- larger ones are seen as water-dense shadows with concave upper borders
- a completely flat horizontal upper border implies that there is also a pneumathorax
- characteristic features:
>blunting of costophrenic angles
>blunting of cardiophrenic angle
> fluid within horizontal or oblique fissures
- eventually a meniscus will be seen
> mediastinal shift in larger volumes away from effusion

presentation:

  • bronchial breathing at the top of the effusion
  • decreased expansion
  • decreased percussion
  • decreased air entry/ diminished breathing sounds
  • won’t hear pt’s voice auscultating. decreased vocal resonance
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19
Q

list common causes of pleural effusion (differentiate between causes of transudates and exudates)

A

broad split into transudates and exudates which really on biochemical analysis of aspirated fluid

transudates (is fluid pushed through the capillary due to high pressure within the capillary):

  • left ventricular failure
  • liver cirrhosis
  • hypoalbuminaemia
  • peritoneal dialysis
  • hypothyroidism
  • nephrotic syndrome

exudates (is fluid that leaks around the cells of the capillaries secondary to infection, inflammation or malignancy):

  • tuberculosis
  • malignancy
  • pulmonary embolism
  • pneumonia
  • RA
  • benign asbestos effusion
  • pancreatitis
  • post-myocardial effusion
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20
Q

describe how Light’s criteria can distinguish between exudate and transudate

A
  • in order to apply lights criteria, the total protein and lactate dehydrogenase (LDH) should be measured in both the blood and pleural fluid

> pleural fluid Is an exudate if one or more of the following criteria are met:

  • pleural fluid protein divided by serum protein is >0.5
  • pleural fluid LDH divided by serum LDH is >0.6
  • pleural fluid LDH >2/3 the upper limits of lab normal value for serum LDH
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21
Q

what is a pneumothorax?

A

air in the pleural cavity (interspace between the lung and the chest wall)

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22
Q

outline common causes and risk factors of pneumothorax

A
  • most common is primary spontaneous (especially in young, thin men)
  • other causes are associated with underlying disease (secondary pneumothorax) e.g. asthma, cold, pneumonia, carcinoma, CF, connective tissue disorders (Marfan’s)

risk factors:

  • smoking
  • height/weight
  • age
  • marfans syndrome
  • FHx
  • chest trauma
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23
Q

outline the presentation and evaluation of suspected pneumathorax

A
  • might be asymptomatic (fit, young and small pneumothorax) OR sudden onset dyspnoea +/or sharp pleuritic chest pain
  • sudden deterioration in asthma or copd
  • reduced expansion
  • hyper resonance percussion
  • diminished breathing on the affected side
  • in tension pneumothorax, the trachea will be deviated from the affected side and cyanosis, sweating, severe tachypnoea, tachycardia, hypotension

examination:

  • pulse (tachycardia (>135 suggests tension)
  • BP (hypo, raised JVP)
  • chest exam
  • CXR (confirms Dx; standard erect Xray in inspiration)
  • USS
  • CT
  • ABG (hypoxemia)
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24
Q

outline the Tx options for pneumothorax

A
  • Tension p requires urgent decompression

spontaneous pneumathorax (SP) straight to chest drain if bilateral/haemodynamically unstable.

primary SP:

  • if >2cm +/or breathless -> needle aspirate -> consider discharge review in 2-4 weeks if successful; chest drain +admit if not
  • discharge and review if <2cm and not breathless

secondary SP:

  • if >2cm or breathless -> chest drain and admit
  • <2cm and not breathless -> aspirate if 1-2cm -> chest drain if unsuccessful; if successful admit

admit + high flow oxygen +observe for 24hrs

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25
Q

what is the appropriate diagnosis for the following?

a) bronchial breathing middle right lung field
b) stony dull percussion left lung base
c) tracheal deviation to the left
d) hyper-resonant percussion note left lung
e) tracheal deviation to the right (not large pneumothorax)

A

a) small right sided pleural effusion
b) left sided pleural effusion
c) right sided tension pneumothorax
d) small left sided pneumothorax
e) right sided collapse

26
Q

how does percussion note differ between pneumothorax and pleural effusion?

A

is hyper-resonant in pneumothorax and dull (often describes as ‘stony’) in pleural effusion

(flat or dull = pleural effusion or lobar pneumonia

resonant = normal healthy lung or bronchitis

hyper resonant = emphysema or pneumothorax)

27
Q

discuss some other ways to differentiate pneumothorax and effusion

A

large effusion or pneumothorax can cause a shift in the mediastinal and trachea away from the side where the pathology is. conversely, collapse causes tracheal deviation towards the side of the abnormality as it is pulled across due to volume loss on the affected side

both pleural effusion and pneumothorax will cause diminished breath sounds on auscultation. sometimes, bronchial breathing can be heard on top of the pleural effusion

28
Q

which of the following are causes of transudate pleural effusion?

nephrotic syndrome
heart failure
mesothelioma
peritoneal dialysis
RA
cirrhosis
pneumonia
A

nephrotic syndrome
heart failure
peritoneal dialysis
cirrhosis

29
Q

You are an FY1 doctor helping the respiratory consultant in assessing a patient with a unilateral pleural effusion. A sample of pleural fluid is obtained for analysis and you are asked to send the sample to the lab. Which of the following laboratory tests are required to apply Light’s criteria to distinguish between an exudate and transudate?

a. pleural fluid glucose
b. pleural fluid LDH
c. serum protein
d. pleural fluid protein
e. pleural fluid amylase
f. serum LDH
g. pleural fluid pH

A

b. pleural fluid LDH
c. serum protein
d. pleural fluid protein
f. serum LDH

30
Q

A 22 year old medical student develops sudden onset dyspnoea during a lecture. His symptoms persist through the morning and he also notices some right sided pleuritic chest pain. He has no past medical history of note and is a non-smoker. He is advised by one of his tutors later that day to attend ED. On examination, he is comfortable at rest with RR 20 and complains of ongoing dyspnoea. Oxygen saturations are 96% on air. BP is 115/70, pulse is 80. There is reduced air entry over the right lung field with a hyper-resonant percussion note. CXR shows a right sided pneumothorax. The ED trainee measures the interpleural distance to be just more than 2cm. Which one of the following is the most appropriate next step?

a. refer to respiratory team for chest drain insertion
b. discharge and review in 2 weeks in the respiratory clinic
c. aspirate with 16-18G cannula

A

c. aspirate with a 16-18G cannula
* likely to be a primary spontaneous pneumothorax in a previously fit and well student. management should take into account symptoms in addition to radiological and other features. In this case, the student has ongoing breathlessness

  • pt’s with PSP or SSP and significant breathlessness associated with any size of pneumothorax should undergo active intervention
  • > observation is the Tx of choice for small PSP without significant breathlessness
  • > selected asymptomatic pt’s with a large PSP may be managed by observation alone
  • > pt’s with a small PSP without breathlessness should be considered for discharge with early outpatient review. these pt’s should receive clear written advice to return in the event of worsening breathlessness
31
Q

list 3 causes of iatrogenic pneumothorax

A
  1. central line insertion (esp if using subclavian vessels)
  2. thoracocentesis
  3. pleural biopsy
  4. mechanical ventilation including NIV
32
Q

describe the meaning of the term ‘immunocompromise’

A

attenuated or absent immunity, leaving the patient more vulnerable to invasion and damage by pathogens than others in the population

33
Q

relate defects of each component of the human immune system to relevant infection risks

A

compromised innate IS (early response; antigen presenting cells, macrophages and dendritic cells, are used to prime the adaptive immune system)

  • > broken skin - cellulitis and abscesses (e.g. psoriasis often has breaks in the skin)
  • > base of skull fracture - trauma can present unusual routes for infections into the CNS such as pneumococcal meningitis
  • > ciliary dysfunction - increased respiratory infection
  • > bladder outflow obstruction - stagnent urine can lead to UTI
  • > chemotherapy - bone marrow suppression and neutropenia

compromised adaptive IS (advance cellular response that kicks in later)

  • > HIV - depletes cellular components of adaptive IS (esp. helper CD4 Tcells)
  • > Drugs (e.g. autoimmune disease/post-transplant) - deliberate targeted suppression of specific immune activities
34
Q

give examples of when specific immune organs are compromised

A

specific organs with primary immunological function:

  1. thymus - key organ of T-cell development, esp in children. failures to develop or dysfunction cause T-cell deficiency. the adaptive IS requires T-cell synthesis
  2. bone marrow - site of WBC synthesis. dysfunction (e.g. leukaemia, drugs) causes neutropenia and other cell subset deficiencies. these cells are required fro robust immune response

secondary immune organs: spleen and lymph nodes
1. spleen - synthesises antibodies, removes antibody-coated bacteria, stores monocytes and lymphocytes. loss increases the risk of sepsis from encapsulated bacteria

35
Q

what is the difference between primary and secondary immunodeficiency?

A

immune deficiency = increased predisposition to infection. key components of their physiology can’t respond to threats.

primary (congenital):

  • rare
  • often hereditary (Ar or X-linked)
  • > 95 syndromes recognised
    e. g. Di George’s syndrome, X-linked agammaglobulinaemia
  • usually detected early in life as affect the ability to fight infection (e.g. recurrent ear/sinus/chest infections)

secondary (acquired):

  • common
  • multiple causes e.g. extremes of age, cancer, diabetes, organ failure, HIV, splenectomy, immune suppressive medication
36
Q

give examples of primary immunodeficiencies

A

T-cell def:

  • e.g. Di George syndrome
  • AD deletion of chromosome 22 –> failure of 3rd +4th pharyngeal arches develop
  • parathyroid glands, aortic arch and thymus dont develop
  • dysmorphic facies and hypo-PTH
  • increased incidence of fungal + protozoan infection
  • calcium supplementation, correction of cardiac abnormalities, prophylactic antibiotics, thymus transplantation

B-cell def:

  • e.g. X-linked agammaglobulinaemia (XLA)
  • presents after maternal IgG protection falls
  • X chromosomes loss of function mutation presenting B cell development
  • early mortality from lung and CNS infections. later risk of lung disease and lymphoma
  • lifelong IV Ig

T+B cell def:

  • e.g. severe combined immunodeficiencies (SCID)
  • heterogeneous group of rare disorders
  • most common is X-linked defect in IL-2 receptor gamma chain
  • Tx = stem cell transplant

neutrophil def:

  • e.g. chronic granulomatous disease (CGD)
  • rare, X-linked
  • normal/ increase neutrophils but impaired respiratory burst (release of reactive oxygen species to kill phagocytksed bacteria)
  • usually onset at toddler age - recurrent deep-seated bacterial infections
  • Tx with antimicrobials, immunotherapy, stem cell transplant
37
Q

give examples of secondary immunodeficiencies

A

HIV:

  • low CD4 count
  • susceptible to bacterial infections, candidiasis and as count gets lower and lower (<200) susceptible to tuberculosis (isoniazid preventive therapy), pneumocystitis pneumonitis (PCP) (co-trimozazole prophylaxis), toxoplasmosis , cryptococcal disease (fluconazole secondary prophylaxis), CMV
  • use preventer therapy: antibiotic prophylaxis: low dose co-trimoxazole. reduce risk of TB with antibiotic isoniazid. prophalyse against other infections with fluconazole (anti fungal)
  • also ART to reverse cd4 count
  • live vaccines contra-indicated

malignancy:

  • neutropenia, common in oncology pt’s post chemo, radio or due to bone marrow infiltration.
  • mild (1-1.5x10-9), moderate (0.5-1x10-9) or sever <0.5x10-9)
  • risk of bacterial infection
  • sever neutropenia Is associated with temp>38C = at risk of septicaemia or bacteriaemia
  • neutropenic sepsis
  • sepsis 6 + ABs in first hour (gentamicin (or meropenem) + pipercillian taszebactum)

drugs:

  • corticosteroids
  • DMASDs (azathiprone, hydrochloroquine, methotrexate, sulfasalazine)
  • biological (infliximab, rituximab)
  • organ transplant and anti-rejection meds (cyclosporin, tacrolimus)

splenectomy:

  • trauma, infarct, surgery
  • highest risk is sepsis from capsulated organisms
  • vaccinate (pneumococcal, h.influenza b, meningococcal)
  • preventive antibiotics at least 2yrs
  • apparent infection with fever - rapid sepsis 6

copd:

  • smoking, ciliary impairment
  • altered innate and adaptive IS
  • recurrent antibiotics and corticosteroids
  • stop smoking! influenza and pneumococcal vaccines

diabetes:

  • increased risk of UTIs, skin, soft tissue, bone and joint infections
  • optimise glycaemic control
  • influenza and pneumococcal vaccines

liver, heart and kidney disease:

  • vaccine as above
  • also hep B and C in liver disease
38
Q

what organisms is associated with chronic lung disease and can quickly become AB resistant?

A

pseudomonas aeruginosa

mycobacterium abscesses (->Related to TB but somewhat diff. invade and damage lungs of pts with underlying lung disease. Advanced immunocompromised pts. Difficult to Tx )

39
Q

discuss the health impact of smoking in relation to copd

A
  • higher mortality
  • most important preventable cause of ill-health
  • 80% of Americans with COPD are or were smokers

*smoking is the biggest contributor to early mortality and health inequalities in Scotland, and is implicated in most cases of COPD

40
Q

consider environmental hazards relating to copd and their interaction with smoking

A
  • occupation/ exposure to biomass fuel, industrial pollution, agriculture, brick making, flour or grain work, plastics, textiles etc
  • air pollution esp. in big cities
  • exposure to second hand smoke
  • indoor smoke from wood etc
  • climate change

*smoking interacts with other exposures to greatly increase risk

41
Q

list some wider environmental factors influencing health and health inequalities

A

lead too resp. illness:

  • unable to afford heating
  • living near pollutants
  • working among pollutants
  • inadequate housing
  • increase risk of smoking
  • occupational and environmental hazards also cause significant proportion of COPD cases, especially in low and middle income countries
  • inequalities mean that risk of ill health from environmental hazards is unevenly distributed
42
Q

how can environmental hazards that play in disease be tackled?

A
  • smoking ban, public spaces, in cars etc
  • policy changes e.g. ultra low emission London
  • travel polices e.g. care share initiatives
  • city designs
  • the right to breathe clean air campaign 2017
43
Q

what is involved in an occupational Hx?

A
  • social Hx
  • do you work? what do you do?
  • what does it involve?
  • what jobs have you done in the past?
  • ## other jobs and hobbies?
44
Q

list some of the main workplace hazards (something with the potential to cause harm to health)

A

physical:

  • noise
  • vibration
  • radiation
  • manual handling
  • dust
  • slips, trips, falls

chemical:

  • gas - chlorine or carbon monoxide
  • liquid - cleaning chemicals
  • spray - paint
  • fumes - welding, hot rubber

biological:
- bugs/organisms/ parasites
- e.g. healthcare workers, famers, sewerage workers, lab workers, foresters

psychological:

  • demands
  • control
  • support
  • role
  • relationships
  • change
45
Q

list some of the main legislation around control of workplace hazards

A
  • risk assessments are a legal requirement
  • health and safety at work act, COSHH
  • specific legislations such as asbestos, lead, vibration
  • equality act 2010
46
Q

what are some of the positive impacts work can have on health and wellbeing

A
  • promotes recovery
  • aids rehabilitation
  • better health outcomes: improves quality of lives and well being; reduces social exclusions and equality, minimises harmful, mental, physical and social consequences of long term wordlessness
47
Q

how is worklessness bad for health?

A
  • higher consultation, hospital admissions and prescription rates
  • 2-3 times increased risk of poorer general health
  • 2-3 times increase risk of worse mental health
  • 20% excess mortality
  • 6x increase risk of suicide
  • the longer you are off work the less likely you will get back to work (e.g. 50% after 6months, close to 0% by 2yrs)
48
Q

what are the main principles involved in assessing fitness for work

A
  • the long-term consequences of advising or agreeing a pt stays off work may be greater than original health problem. danger is a drift into long-term sickness

assess the person:

  • stamina
  • mobility
  • agility (dexterity, posture)
  • rational (mental state)
  • treatment (SEs)
  • intellectual (cognitive abilities)

assess the job:

  • demands of the job
  • environment
  • tempora (shift work, early start)
  • travel
  • organisational (Lon-worker or customers)
  • layout (ergonomic aspect of workstation, work equipment)

fit not prescription - can be phase return, amend duties, alter hours

give advice:
- encourage pt to keep in touch with work, reduce hours, change patter, change tasks, adapt workplace, reduce the pace of work

49
Q

what are the 2 types of respiratory failure

A

type 1:
PO2 <8kPA
- infection (CAP), airway disease, interstitial lung disease
-pulmonary oedema (CHF), pneumonia, pulmonary haemorrhage

type 2:
PO2 <8kPA and PCO2 >8kPa
- ventilation failure, restrictive lung disease, pulmonary oedema
- asthma attack, cold, drug overdose, chest injury (flair chest)

50
Q

what is acute respiratory distress syndrome (ARDS) and outline investigation principles

A
  • acute diffuse inflammation lung injury caused by alveolar injury (e.g. smoking, infection, burns) or capillary inflammation and leakage (e.g. organ infarct and vesicular contents flow in vv. to via right sided heart to lungs)
  • causes pulmonary oedema, damage to type II pneumocystis (decreased surfactant), decreased diffusion, scarring over time
  • signs = hypoxaemia, bilateral lung opacities, physiological dead space (physiological shunt due to hyoxaemia), decreased lung compliance (stiff and difficult to ventilate), fibrosis over time of alveolar-capilary membrane (last steps of inflammatory process is deposition of fibrin)
Ix:
first line =
- Hx + exam - prejudge
- blood tests (eosinophils)
- CXR
- ECG (cardiac cause or pulmonary; evidence of right heart strain)
- ABG
- spirometry, PEFR
- sputum

2nd line =

  • extended bloods according to disease
  • allergen testing
  • skin prick tests
  • CT chest
  • perfusion scan
  • PET
  • lung function tests
  • bronchoscopy

3rd line| =

  • cardiopulmonary exercise testing
  • right heart catheter studies
  • sleep studies
  • cryobiopsy
  • radial EBUS
  • navigation bronchoscopy
  • transpulmonary nodal biopsy

4th:
MDT
accepting probability and risk
trails of Tx

51
Q

what is the likely cause of an ABG with the following results:

pH = normal
pCO2 = normal
pO2 = low
bicarbonate = low
A

type 1 respiratory failure of metabolic origin

52
Q

describe the role of respiratory function test in Dx resp disease and the patterns associated

A

*non-invasive tests that show how well the lungs are working. The tests measure lung volume, capacity, rates of flow, and gas exchange.

PEFR:

  • simple bedside test
  • persons maximum speed of expiration
  • can be useful to see how well asthma is controlled

spirometry:

  • measure how much air you inhale, exhale and how quickly you exhale
  • used to diagnosing asthma, copd and other resp conditions
  • determine obstructive vs restrictive lung disease

bronchial provocation test:

  • looks to see is lung airways are more sensitive than normal
  • use mannitol, methacholine, exercise to challenge airways and see If bronchodilator is effective afterward

FeNO :

  • exhaled NO
  • way of determining how lung inflammation is present in pt with allergic or eosinophilic asthma
53
Q

how would you systematically review a ABG?

A

1) identify if it is acidosis or alkalosis by looking at the pH
2) identify if it is respiratory or metabolic by looking at the CO2 and HCO3
3) identify if it is compensated (pH is normal and both CO2 and HCO3 are abnormal - can asses from pt Hx/exam), partial compensated (PH is abnormal and CO2 and HCO3 are abnormal) or uncompensated (pH abnormal, CO2 OR HCO3 is abnormal)

54
Q

what do we know about copd (common, preventable and treatable disease, characterised by persistent respiratory symptoms and airflow limitation - due to airflow +/or alveolar abnormalities, usually caused by significant exposure to noxious particles or gases)?

A
  • fixed airway obstruction, with little-to-no response to inhaled steroids
  • exacerbations are reduced with steroids (oral prednisolone - 30mg for 5days, may need osteoporosis prophylaxis)
  • management is based in symptom control
  • FEV declines, inexorably
  • 3 inhaler therapies: LAMA (trotropium) -> LABA (salmeterol) -> ICS (beclomethasone)
  • bronchodilators relax smooth muscle, improve airflow, improve breathlessness
  • inhaled steroids reduce inflammation, and so exacerbation
  • has to be a host factor that modifies the initial stimulus (smoking) -> lung inflammation (neutrophil process) -> oxidative stress -> copd
55
Q

what are the treatment goals and prognosis of COPD?

A
  • reduce the symptoms - improve symptoms, exercise tolerance, health status
  • reduce risk - disease progression, exacerbation and mortality
  • untested there will be disease progression and decline in FEV
  • rate of decline according to FEV%
  • consider cigarette +ve vs. inhaler deficient
  • exacerbation frequency associated with mortality
56
Q

how do you diagnose COPD?

A
  1. clinical features and Hx, trial of treatment (e.g. repeated benefits from steroids +/or antibiotics or used family member meds and had a benefit )
  2. pulmonary function tests
    - non-invasive tests that show how well the lungs are working. The tests measure lung volume, capacity, rates of flow, and gas exchange.
  3. spirometry (obstructive FEV/FVC <0.70 = less vol out in 1sec and less vol out overall)/ categorise into mild/moderate/severe
  4. lung volumes (gas trapping, RV/TLC)
  5. gas transfer (reduced efficiency of alveolar transfer)
    - oxygen saturation (92% lower of abnormal), desaturation
  6. imaging
    - CXR (specific, but not sensitive)
    - CT is very sensitive, but carries risk - radiation (will show emphysema)
    - (neither should be the main driver)
    - NB you can have normal FEV but severe emphysema! therefore, guide treatment based on ABCD assessment tool which considers risk and symptoms
  7. use ABDC and cold scale to assess severity and diagnose
57
Q

what tool should you use to guide treatment of copd?

A

ABCD assessment tool + Gold scale (FEV1 % predicted)

y-axis is grading of risk (based on exacerbation and hospital admissions)

x-axis is graded on symptoms (MRC and CAT = both grading of breathlessness tools)

*do this to judge essentially what we do with them/ guide therapy (also the level of airflow limitation, impact of disease on the pt’s health status, risk of future events or death)

58
Q

broadly, how do you manage copd based on the ANCD method (drug therapy)

A 
group A (MRC of 0-1, CAT <10 and 0-1 exacerbation history):
- bronchodilator
group B (MRC of >2, CAT >10 and 0-1 exacerbation history):
- a long-acting bronchodilator (LABA or LAMA)

group C (MRC of 0-1, CAT <10 and >2 exacerbation Hx OR >1 exacerbation Hx leading to hospital admission):

  • LABA and LAMA
  • can add ICS here

group D (MRC of >2, CAT >10 and >2 exacerbation Hx OR >1 exacerbation Hx leading to hospital admission):

  • LAMA + LABA + ICS
  • LTRA - roflumilast tablet in continued exacerbations
  • macrolide (clarithromycin, erythromycin etc) have anti-inflammatory immunomodulatory effects

*should be giving steroid if high eosinophils, why are you if not high?

59
Q

what 3 areas can tablets help with?

A
  1. inflammation:
    - leukotriene-receptor antagonists e.g. montelukast, roflumilast
    - theophylline e.g. phyllocontin, uniphyllin
  2. breathlessness:
    - concurrent palliative care
    - opiates
    - benzodiazepines - oral, sublingual
    - furosemide
  3. infection:
    - maintanece antibiotics e.g. azithromycin, clarithromycin
    - pseudomonas (is a problem)
    - haemophilus influenzae

*systemic administration therefore systemic SEs. variable tolerance

60
Q

what management option has the most important impact on copd?

A

pulmonary rehabilitation!
+ smoking cessation

(other important options = vaccinations, oxygen therapy, palliative care, ACP)

61
Q

in a disease that cannot be cured (copd) we havve to mange what drives it. what are these?

A

co-morbities:

  • CVD
  • GORD
  • micro-aspiration
  • frailty
  • psychosocial care
  • anxiety and depression
62
Q

what is the emergency treatment for respiratory failure (PaO2 <8kPa)?

A

type 1 RF (PaO2 <8kPa):

  • infection, airways disease, sepsis
  • Tx = high flow O2 therapy, intubation, CPAP

type 2 (PaO2 <8kPA and PaCO2 >8pKA)

  • ventilatory failure, classic decompensated COPD
  • Tx = No high flow O2!! usually not intubation –> Non-invasive ventilation - BiPAP

week 42: cough (1 decks)

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