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respiratory_week_2_20190518190046 Flashcards

1
Q

what is the hallmarks of remodelling in asthma

A

thickening of basement membrane, collagen deposition of submucosa and hypertrophy of smooth muscle

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2
Q

how to prevent eosinophilic inflammation in asthma

A

anti-inflammatory medication - corticosteroids, cromones, theophylline

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3
Q

how to prevent release of mediators and TH2 cytokines in asthma

A

antileukotrienes, antihistamines or mono-clonal antibodies (anti-IgE or anti-interleukin 5)

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4
Q

how to prevent twitchy smooth muscle (hyperactivity) in asthma

A

bronchodilators (b2 agonists or muscarinic antagonists)

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5
Q

which drugs worsen asthma

A

NSAIDs e.g. acetylsalicylic acid or b-blockers

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6
Q

what is the associated atopy with asthma

A

increased IgE e.g. rhinitis, conjunctivitis and eczema

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7
Q

what is blood eosinophilia in asthma

A

> 3%

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8
Q

how is asthma diagnosed

A

history, peak flow, FEV1 / FVC <75%, >15% reversibility to salbutamol, testing: exercise or given histamine, metacholine or mannitol

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9
Q

what contributes to COPD

A

noxious particles e.g. smoking causes inflammation, mucocilliary dysfunction and tissue damage

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10
Q

distinguish between bronchitis and emphysema

A

bronchitis - wheezing, emphysema - reduced breath sounds

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11
Q

what is the disease process of COPD

A

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

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12
Q

what is the chronic cascade in COPD

A

impaired alveolar gas exchange leads to respiratory failure which leads to pulmonary hypertension (RV hypertrophy or failure)

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13
Q

what is chronic bronchitis

A

chronic neutrophilic inflammation of bronchi and bronchioles - partially reversible

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14
Q

what is symptoms of chronic bronchitis

A

cough, clear mucoid sputum, purulent sputum on infection, increasing breathlessness

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15
Q

what is emphysema

A

alveolar destruction, loss of bronchial support so irreversible

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16
Q

how to assess COPD

A

degree of airflow limitation, 2 of more exacerbations in last year or FEV1<50% are high risk

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17
Q

what is non-pharmacological COPD management in extreme or rare cases

A

venesection, lung volume reduction and stenting

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18
Q

what is rarely given pharmacological treatment in COPD

A

PDE4 inhibitor - roflumilastmucolytic - carbocisteine antibiotics - azithromycin

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19
Q

what is asthma COPD overlap syndrome (ACOS_

A

COPD with blood eosinophilia >4%, responds better to ICS with regards to exacerbation reduction, more reversible to salbutamol, difficult to distinguish from asthmatic smokers

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20
Q

what are some skeletal causes of disease

A

thoracic kyphoscoliosis, ankylosing spondylitis or multiple rib fractures

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21
Q

what are some muscle weakening causes of restrictive disease

A

intercostal or diaphragmatic e.g. myasthenia gravis, Gullan barre, motor neurone disease and poliomyelitis

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22
Q

what is pathophysiology of DPLD

A

alveolar barrier to O2 exchange but CO2 exchange unimpaired as alveolar ventilation normal

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23
Q

causes of DPLD caused by fluid in alveolar air space

A

cardiac pulmonary oedema (raised pulmonary venous pressure) or non-cardiac PO (normal pressure but leaky pulmonary capillaries due to sepsis or trauma)

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24
Q

causes of DPLD caused by consolidation

A

infective pneumonia, infarction or BOOP (cryptogenic, drugs, rheumatoid disease)

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25
Q

causes of DPLD caused by granulomatous-alveolitis

A

extrinsic-allergic alveolitis caused by farmers lung and avians,sarcoidosis - caused by lymphadenopathy (presents as rash, uveitis, myocarditis or neuropathy)

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26
Q

causes of DPLD caused by drug induced alveolitis

A

drugs: amiodarone, bleomycin, methotrexate and gold

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27
Q

causes of DPLD caused by other alveolitis

A

toxic gases/fumes: chlorinepulmonary fibrosis (scarring)autoimmune: SLE, polyarteritis, wegeners, churg-strauss and bechets

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28
Q

causes of DPLD caused by dust-disease

A

fibrogenic: asbestos or silicosis non fibrogenic: siderosis (iron), stenosis (tin), baritosis (barium)

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29
Q

causes of DPLD caused by carcinomatosis

A

due to lymphatics/blood spreadcan also be adenocarcinomatosis e.g. bronchus, breast, prostate, colon or stomach

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30
Q

causes of DPLD caused by eosinophils (type 1/3 allergic response)

A

drugs: nitrofuratonin fungal: aspergillosis parasites: toxocara, ascaris or filaria autoimmune: charge strauss or polyarteritis

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31
Q

what is the clinical syndrome of DPLD

A

breathless on exertion, cough but no wheeze, clubbing and central cyanosis, lung crackles, fibrosis at end stage

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32
Q

what is the basic ways to diagnose DPLD

A

history, reduced lung volume, reduced gas diffusion (DLCO) and arterial oxygen desaturation (reduced PaO2 and SaO2) at rest and exercise

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33
Q

what are the most invasive tests in the diagnosis of DPLD

A

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

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34
Q

what is treatment of DPLD

A

remove trigger, treat reversible alveolitis (ground glass) by immunosuppressives

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35
Q

what is 1st line drug treatment in DPLD

A

systemic steroids (oral prednisolone)

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36
Q

what is 2nd line drug treatment in DPLD

A

oral azathioprine (steroid sparing)

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37
Q

what is treatment for IPF

A

anti-fibrotic agents: pirfenidone and nintedanib

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38
Q

how is inspiration controlled

A

pre-botzinger complex excites dorsal neurones, fire in bursts leading to contraction of muscles and when firing stops - passive expiration

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39
Q

how is active expiration (hyperventilation) controlled

A

increased firing of dorsal excites second group: ventral (located below dorsal) which excites internal intercostals

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40
Q

what is the role of the pons and where is it located

A

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

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41
Q

stretch receptors are respiratory centre stimuli; where are they located and what is their role

A

in walls of bronchi and bronchioles (hering-breur reflex)activated at >1 tidal volumes and may prevent over inflation of lungs during hard exercise

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42
Q

J receptors are respiratory centre stimuli: how are they stimulated?

A

stimulated by pulmonary capillary congestion, pulmonary oedema and pulmonary emboli

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43
Q

joint receptors are respiratory centre stimuli: how are they stimulated

A

movement

44
Q

baroreceptors are respiratory centre stimuli: how are they stimulated

A

increased BP and cause ventilatory increase

45
Q

what is role of peripheral chemoreceptors

A

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

46
Q

what does the stimulation of peripheral chemoreceptors cause

A

hyperventilation and increases elimination of CO2 from body (reduced H+)

47
Q

where are central chemoreceptors situated

A

near surface of medulla of brainstem

48
Q

what do central chemoreceptors respond to

A

[H+] of cerebral fluid: blood brain barrier impermeable to H+ and HCO3- but CO2 diffuses readily

49
Q

what causes hypoxia at high altitudes

A

result of decreased partial pressure of inspired oxygen (PiO2)

50
Q

what is acute response of hypoxia at high altitudes

A

hyperventilation and increased cardiac output

51
Q

what is the symptoms of hypoxia at high altitudes

A

headache, fatigue, nausea, tachycardia, dizziness, sleep disturbance, exhaustion and shortness of breath

52
Q

what adaptations take place during hypoxia at high altitudes

A

increased RBC (polycythaemia), increased 2,3 BPG, increased capillaries, increased mitochondria and kidneys conserve acid so pH decreases

53
Q

what is result of spirometry in asthma

A

still breathe out but full capacity takes longer FVC - preserved

54
Q

what is result of spirometry in COPD

A

FVC - impaired

55
Q

what is result of spirometry in restrictive

A

FEV1 is reduced in proportion to FVC

56
Q

what are the different kinds of bronchial challenge testing

A

exercisemetacholine, histamine and mannitol allergens and chemicals

57
Q

what does decreased FEV1 and PEV (peak flow) suggest

A

asthma

58
Q

what does decreased SaO2 during exercise suggest

A

interstitial lung disease

59
Q

what is static lung volume testing

A

helium dilution / N2 washout

60
Q

what is the result of static lung volume testing in emphysema

A

increase in total lung capacity

61
Q

what is result of static lung volume testing in restrictive lung disease

A

decrease in total lung capacity

62
Q

PERF

A

decrease in obstructive normal in restrictive

63
Q

FEV1

A

decrease in both

64
Q

FVC

A

normal in asthma, reduced in COPD, reduced in restrictive

65
Q

FEV1/FVC

A

<75% in obstructive, >75% in restrictive

66
Q

gas transfer (TLCO)

A

decrease in emphysema, normal in asthma, decrease in restrictive

67
Q

FEV1 response to B2 agonist

A

> 15% in asthma, <15% in COPD, no response in restrictive

68
Q

where is RBC developed and what do they have that mature RBC dont

A

bone marrownucleus need vitamin B12 and folate

69
Q

what is microcytic anaemia and what is its cause

A

smaller cellscause: iron deficiency (chronic blood loss)

70
Q

what is macrocytic anaemia and what is its cause

A

larger cellscause: vitamin B12 / folate deficiency (nuclear defects), alcohol excess, liver disease, hyperthyroidism (membrane defects)

71
Q

what is normocytic anaemia and what is its cause

A

normal cells - acute blood losscause: anaemia of chronic diseases due to change in iron supply to RBC

72
Q

when does neutrophil increase (neutrophilia)

A

increase in common bacteria infection increase during steroid use (re-distributed in blood)

73
Q

when does lymphocytes increase (lymphocytosis)

A

increase in common viral infectionno granules

74
Q

when does monocytes increase (monocytosis)

A

increase in atypical infections and cancers (monocytosis)no granules

75
Q

when does eosinophils increase (eosinophilia)

A

increase in parasitic infection and allergies

76
Q

when does basophils increase (basophilia)

A

allergic reactions

77
Q

what is non genuine thrombocytopenia (low platelets)

A

clumps form in collection tube and confuse analyser

78
Q

what is genuine thrombocytopenia (low platelets)

A

caused by liver disease, consumption (auto immune) or trapping (enlarged spleen)

79
Q

what is haemostasis

A

arrest of bleeding and maintenance of vascular potency

80
Q

what is requirements of haemostasis

A

permanent state of readiness, prompt response, localised response and protection against unwanted thrombosis by fibrinolysis or anticoagulant defences

81
Q

what is primary haemostasis

A

formation of platelet plug

82
Q

what is secondary haemostasis

A

formation of fibrin clot

83
Q

what is coagulation screen and what are the different times

A

measures time taken to form fibrin clot types: prothrombin time (PT) and activated partial thromboplastin time (aPTT)

84
Q

what causes prolongation of coagulation

A

multiple coagulation factor deficiencies e.g. liver disease (production problem) or disseminated intravascular coagulation (consumption problem)

85
Q

where can increased fibrinolysis be found

A

thrombosis, inflammation, malignancy and heart failure

86
Q

what are D-dimers and how are measurements used

A

fibrin degradation product, used in conjunction with clinical features to decide on probability of venous thromboembolism

87
Q

where is increased plasma viscosity found

A

systemic inflammation and less commonly, haematological malignancies producing abnormal protein

88
Q

what is respiratory acidosis and how is it caused

A

increase [H+] due to increased PCO2 caused by choking, bronchopneumonia, COAD

89
Q

what is metabolic acidosis and how is it caused

A

increase [H+] due to decreased HCO3- caused by impaired H+ excretion, increased H+ production

90
Q

what is respiratory alkalosis and how is it caused

A

decreased [H+] due to decreased PCO2caused by over breathing, raised intracranial pressure

91
Q

what is metabolic alkalosis and how is it caused

A

decreased [H+] due to increased HCO3-caused by loss in H+ in vomit, alkali ingestion, potassium deficiency

92
Q

response of too much H+

A

this mops up HCO3- so lungs need to lose CO2

93
Q

response of too much CO2

A

kidneys get rid of H+ to regain HCO3-

94
Q

response of too little H+

A

reaction pulled to left

95
Q

response of too little CO2

A

reaction pulled to right

96
Q

what is type 1 respiratory failure

A

short of O2

97
Q

what happens to good lungs in type 1 respiratory failure

A

increased tidal volume and respiratory rate which results in normal PaO2 but decreased PaCO2

98
Q

what happens to bad lungs in type 1 respiratory failure

A

decreasing PO2 and normal PCO2

99
Q

what is type 2 respiratory failure

A

short of O2 and too much CO2

100
Q

what is the Bohr effect on type 2 respiration

A

PO2 curve moves to right more so they have low SpO2 (O2 saturation)

101
Q

why is having too much O2 a bad idea

A

once dissociation curve flattens off, FiO2 drops from 120 to 80, O2 saturation remains 100% so big drop go undetected

102
Q

how do people retain O2?

A

V / Q mismatch as long as V directly proportional to Q then lungs happy but when too much O2 given, this not the case

103
Q

what is the hypoxic drive

A

form of respiratory drive in which body uses O2 chemoreceptors instead of CO2 receptors to regulate respiratory cycle

104
Q

what is chronic hypercarbia

A

loses sensitivity of chemoreceptors

105
Q

what is signs of hypoxaemia

A

altered mental state, cyanosis, dyspnoea, tachypnoea, arrhythmias

106
Q

at which kPa does hyperventilation, loss of consciousness and death occur

A

hyperventilation: PO2 <5.3kPaloss of consciousness: 4.3kPadeath: 2.7kPa

107
Q

what does oxygen actually treat

A

hyperaemia, not breathlessness

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