respiratory_week_2_20190518190046 Flashcards
what is the hallmarks of remodelling in asthma
thickening of basement membrane, collagen deposition of submucosa and hypertrophy of smooth muscle
how to prevent eosinophilic inflammation in asthma
anti-inflammatory medication - corticosteroids, cromones, theophylline
how to prevent release of mediators and TH2 cytokines in asthma
antileukotrienes, antihistamines or mono-clonal antibodies (anti-IgE or anti-interleukin 5)
how to prevent twitchy smooth muscle (hyperactivity) in asthma
bronchodilators (b2 agonists or muscarinic antagonists)
which drugs worsen asthma
NSAIDs e.g. acetylsalicylic acid or b-blockers
what is the associated atopy with asthma
increased IgE e.g. rhinitis, conjunctivitis and eczema
what is blood eosinophilia in asthma
> 3%
how is asthma diagnosed
history, peak flow, FEV1 / FVC <75%, >15% reversibility to salbutamol, testing: exercise or given histamine, metacholine or mannitol
what contributes to COPD
noxious particles e.g. smoking causes inflammation, mucocilliary dysfunction and tissue damage
distinguish between bronchitis and emphysema
bronchitis - wheezing, emphysema - reduced breath sounds
what is the disease process of COPD
1) activated macrophages - release IL-8 and leukotriene B42) neutrophils and macrophages release proteases that break down connective tissue in lung and cause mucus 3) proteases normally counteracted by a1-antitrypsin, SLPI and tissue inhibitors of metric metalloproteinases - appears to be imbalance between protease and antiproteases
what is the chronic cascade in COPD
impaired alveolar gas exchange leads to respiratory failure which leads to pulmonary hypertension (RV hypertrophy or failure)
what is chronic bronchitis
chronic neutrophilic inflammation of bronchi and bronchioles - partially reversible
what is symptoms of chronic bronchitis
cough, clear mucoid sputum, purulent sputum on infection, increasing breathlessness
what is emphysema
alveolar destruction, loss of bronchial support so irreversible
how to assess COPD
degree of airflow limitation, 2 of more exacerbations in last year or FEV1<50% are high risk
what is non-pharmacological COPD management in extreme or rare cases
venesection, lung volume reduction and stenting
what is rarely given pharmacological treatment in COPD
PDE4 inhibitor - roflumilastmucolytic - carbocisteine antibiotics - azithromycin
what is asthma COPD overlap syndrome (ACOS_
COPD with blood eosinophilia >4%, responds better to ICS with regards to exacerbation reduction, more reversible to salbutamol, difficult to distinguish from asthmatic smokers
what are some skeletal causes of disease
thoracic kyphoscoliosis, ankylosing spondylitis or multiple rib fractures
what are some muscle weakening causes of restrictive disease
intercostal or diaphragmatic e.g. myasthenia gravis, Gullan barre, motor neurone disease and poliomyelitis
what is pathophysiology of DPLD
alveolar barrier to O2 exchange but CO2 exchange unimpaired as alveolar ventilation normal
causes of DPLD caused by fluid in alveolar air space
cardiac pulmonary oedema (raised pulmonary venous pressure) or non-cardiac PO (normal pressure but leaky pulmonary capillaries due to sepsis or trauma)
causes of DPLD caused by consolidation
infective pneumonia, infarction or BOOP (cryptogenic, drugs, rheumatoid disease)
causes of DPLD caused by granulomatous-alveolitis
extrinsic-allergic alveolitis caused by farmers lung and avians,sarcoidosis - caused by lymphadenopathy (presents as rash, uveitis, myocarditis or neuropathy)
causes of DPLD caused by drug induced alveolitis
drugs: amiodarone, bleomycin, methotrexate and gold
causes of DPLD caused by other alveolitis
toxic gases/fumes: chlorinepulmonary fibrosis (scarring)autoimmune: SLE, polyarteritis, wegeners, churg-strauss and bechets
causes of DPLD caused by dust-disease
fibrogenic: asbestos or silicosis non fibrogenic: siderosis (iron), stenosis (tin), baritosis (barium)
causes of DPLD caused by carcinomatosis
due to lymphatics/blood spreadcan also be adenocarcinomatosis e.g. bronchus, breast, prostate, colon or stomach
causes of DPLD caused by eosinophils (type 1/3 allergic response)
drugs: nitrofuratonin fungal: aspergillosis parasites: toxocara, ascaris or filaria autoimmune: charge strauss or polyarteritis
what is the clinical syndrome of DPLD
breathless on exertion, cough but no wheeze, clubbing and central cyanosis, lung crackles, fibrosis at end stage
what is the basic ways to diagnose DPLD
history, reduced lung volume, reduced gas diffusion (DLCO) and arterial oxygen desaturation (reduced PaO2 and SaO2) at rest and exercise
what are the most invasive tests in the diagnosis of DPLD
test for antibody against avian and fungal disease (serum ACE and Ca raised in sarcoid)CXR for bilateral diffuse alveolar infiltrates HRCT to compare inflammatory ground glass and fibrotic nodular component of alveolar infiltrates
what is treatment of DPLD
remove trigger, treat reversible alveolitis (ground glass) by immunosuppressives
what is 1st line drug treatment in DPLD
systemic steroids (oral prednisolone)
what is 2nd line drug treatment in DPLD
oral azathioprine (steroid sparing)
what is treatment for IPF
anti-fibrotic agents: pirfenidone and nintedanib
how is inspiration controlled
pre-botzinger complex excites dorsal neurones, fire in bursts leading to contraction of muscles and when firing stops - passive expiration
how is active expiration (hyperventilation) controlled
increased firing of dorsal excites second group: ventral (located below dorsal) which excites internal intercostals
what is the role of the pons and where is it located
located above dorsal neurones, contains PC whose stimulation (when dorsal neurones fire) terminates inspiration so modify rhythm - without it, prolonged breathing with inspiratory gasps - apneusis
stretch receptors are respiratory centre stimuli; where are they located and what is their role
in walls of bronchi and bronchioles (hering-breur reflex)activated at >1 tidal volumes and may prevent over inflation of lungs during hard exercise
J receptors are respiratory centre stimuli: how are they stimulated?
stimulated by pulmonary capillary congestion, pulmonary oedema and pulmonary emboli
joint receptors are respiratory centre stimuli: how are they stimulated
movement
baroreceptors are respiratory centre stimuli: how are they stimulated
increased BP and cause ventilatory increase
what is role of peripheral chemoreceptors
sense tension of oxygen and carbon dioxide gases as well as [H+] in blood also role in adjusting acidosis caused by addition of non-carbonic acid H+ to blood
what does the stimulation of peripheral chemoreceptors cause
hyperventilation and increases elimination of CO2 from body (reduced H+)
where are central chemoreceptors situated
near surface of medulla of brainstem
what do central chemoreceptors respond to
[H+] of cerebral fluid: blood brain barrier impermeable to H+ and HCO3- but CO2 diffuses readily
what causes hypoxia at high altitudes
result of decreased partial pressure of inspired oxygen (PiO2)
what is acute response of hypoxia at high altitudes
hyperventilation and increased cardiac output
what is the symptoms of hypoxia at high altitudes
headache, fatigue, nausea, tachycardia, dizziness, sleep disturbance, exhaustion and shortness of breath
what adaptations take place during hypoxia at high altitudes
increased RBC (polycythaemia), increased 2,3 BPG, increased capillaries, increased mitochondria and kidneys conserve acid so pH decreases
what is result of spirometry in asthma
still breathe out but full capacity takes longer FVC - preserved
what is result of spirometry in COPD
FVC - impaired
what is result of spirometry in restrictive
FEV1 is reduced in proportion to FVC
what are the different kinds of bronchial challenge testing
exercisemetacholine, histamine and mannitol allergens and chemicals
what does decreased FEV1 and PEV (peak flow) suggest
asthma
what does decreased SaO2 during exercise suggest
interstitial lung disease
what is static lung volume testing
helium dilution / N2 washout
what is the result of static lung volume testing in emphysema
increase in total lung capacity
what is result of static lung volume testing in restrictive lung disease
decrease in total lung capacity
PERF
decrease in obstructive normal in restrictive
FEV1
decrease in both
FVC
normal in asthma, reduced in COPD, reduced in restrictive
FEV1/FVC
<75% in obstructive, >75% in restrictive
gas transfer (TLCO)
decrease in emphysema, normal in asthma, decrease in restrictive
FEV1 response to B2 agonist
> 15% in asthma, <15% in COPD, no response in restrictive
where is RBC developed and what do they have that mature RBC dont
bone marrownucleus need vitamin B12 and folate
what is microcytic anaemia and what is its cause
smaller cellscause: iron deficiency (chronic blood loss)
what is macrocytic anaemia and what is its cause
larger cellscause: vitamin B12 / folate deficiency (nuclear defects), alcohol excess, liver disease, hyperthyroidism (membrane defects)
what is normocytic anaemia and what is its cause
normal cells - acute blood losscause: anaemia of chronic diseases due to change in iron supply to RBC
when does neutrophil increase (neutrophilia)
increase in common bacteria infection increase during steroid use (re-distributed in blood)
when does lymphocytes increase (lymphocytosis)
increase in common viral infectionno granules
when does monocytes increase (monocytosis)
increase in atypical infections and cancers (monocytosis)no granules
when does eosinophils increase (eosinophilia)
increase in parasitic infection and allergies
when does basophils increase (basophilia)
allergic reactions
what is non genuine thrombocytopenia (low platelets)
clumps form in collection tube and confuse analyser
what is genuine thrombocytopenia (low platelets)
caused by liver disease, consumption (auto immune) or trapping (enlarged spleen)
what is haemostasis
arrest of bleeding and maintenance of vascular potency
what is requirements of haemostasis
permanent state of readiness, prompt response, localised response and protection against unwanted thrombosis by fibrinolysis or anticoagulant defences
what is primary haemostasis
formation of platelet plug
what is secondary haemostasis
formation of fibrin clot
what is coagulation screen and what are the different times
measures time taken to form fibrin clot types: prothrombin time (PT) and activated partial thromboplastin time (aPTT)
what causes prolongation of coagulation
multiple coagulation factor deficiencies e.g. liver disease (production problem) or disseminated intravascular coagulation (consumption problem)
where can increased fibrinolysis be found
thrombosis, inflammation, malignancy and heart failure
what are D-dimers and how are measurements used
fibrin degradation product, used in conjunction with clinical features to decide on probability of venous thromboembolism
where is increased plasma viscosity found
systemic inflammation and less commonly, haematological malignancies producing abnormal protein
what is respiratory acidosis and how is it caused
increase [H+] due to increased PCO2 caused by choking, bronchopneumonia, COAD
what is metabolic acidosis and how is it caused
increase [H+] due to decreased HCO3- caused by impaired H+ excretion, increased H+ production
what is respiratory alkalosis and how is it caused
decreased [H+] due to decreased PCO2caused by over breathing, raised intracranial pressure
what is metabolic alkalosis and how is it caused
decreased [H+] due to increased HCO3-caused by loss in H+ in vomit, alkali ingestion, potassium deficiency
response of too much H+
this mops up HCO3- so lungs need to lose CO2
response of too much CO2
kidneys get rid of H+ to regain HCO3-
response of too little H+
reaction pulled to left
response of too little CO2
reaction pulled to right
what is type 1 respiratory failure
short of O2
what happens to good lungs in type 1 respiratory failure
increased tidal volume and respiratory rate which results in normal PaO2 but decreased PaCO2
what happens to bad lungs in type 1 respiratory failure
decreasing PO2 and normal PCO2
what is type 2 respiratory failure
short of O2 and too much CO2
what is the Bohr effect on type 2 respiration
PO2 curve moves to right more so they have low SpO2 (O2 saturation)
why is having too much O2 a bad idea
once dissociation curve flattens off, FiO2 drops from 120 to 80, O2 saturation remains 100% so big drop go undetected
how do people retain O2?
V / Q mismatch as long as V directly proportional to Q then lungs happy but when too much O2 given, this not the case
what is the hypoxic drive
form of respiratory drive in which body uses O2 chemoreceptors instead of CO2 receptors to regulate respiratory cycle
what is chronic hypercarbia
loses sensitivity of chemoreceptors
what is signs of hypoxaemia
altered mental state, cyanosis, dyspnoea, tachypnoea, arrhythmias
at which kPa does hyperventilation, loss of consciousness and death occur
hyperventilation: PO2 <5.3kPaloss of consciousness: 4.3kPadeath: 2.7kPa
what does oxygen actually treat
hyperaemia, not breathlessness
