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Phase 2a > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is pneumonia?

A

inflammation of the lung parenchyma caused by a lower RTI after a upper RTI as epithelial cells have been damaged

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2
Q

What are the signs and symptoms of pneumonia?

A

fever, confusion, chills, rigor, tachycardia, tachyponea, productive cough, vomiting, diarrhoea, dyspnea, pleuritic chest pain, punilent sputum, dull percussion, cyanosis, resp failure, speticaemia

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3
Q

Risk factors for pneumonia?

A

> 65, smokers, malnourished, underlying lung disease, medications, recent RTI, infants, COPD, immunocompromised, nursing home residents, impaired swallowing, alcoholics, drug users

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4
Q

How do the lungs prevent against infection?

A

mucus lining the bronchiole, sterile lower resp tract, alveolar macrophages, mucociliary escalator, cough, IgA antibody, microflora, node hairs (mouth acidity)

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5
Q

What is the epithelium of the bronchi?

A

ciliated columnar epithelium

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6
Q

What does the epithelium of the bronchi secrete for immunoprotection?

A

mucus and IgA to eliminate microorganisms

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7
Q

What are the causative pneumonia agents?

A

bacteria: streptococcus pneumonia, haemopholus influenza, legionella pneumonia, staph aureus, mycoplasma
virus: influenze, RSV
fungi: (not common - most likely in immunocompromised)

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8
Q

What kind of impaired pulmonary defenses can cause pneumonia?

A

loss of cough reflex, injured mucocillary apparatus, decreased alveolar macro-phages, pulmonary congestion, odemea, accumulation of secretions

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9
Q

How does bacteria cause pneumonia?

A

bacteria enter alveoli causing immune response, leading to vasodilation and increasing vascular permeability so fluid shifts from vascular space into alveoli causing congestion

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10
Q

How do viruses cause pneumonia?

A

infect the respiratory cell, and release its genetic material and uses the respiratory cell proteins to replicate and make new viral particle, so the respiratory cells lysis causing immune response in the alveoli

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11
Q

How does fungi cause pneumonia?

A

the spores are inhaled and it grows into a fungal ball (seen in imaging), this can then spread to vasculature, causing systemic effects

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12
Q

What makes up a fungal ball?

A

fungus, mucus, cellular debris

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13
Q

What is seen in an alevoli in pneumonia?

A

fluid filled alveoli (congestion/consolidation), constriction, increase in mucus secretion

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14
Q

What is consolidation?

A

When the alveoli are fluid filled, causing a backflow of fluid into other alveolis, until the whole lobe is full of fluid, pus, blood and cells, resulting in lobar diffuse opacity

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15
Q

What is lobar pneumonia?

A

When there is consolidation in a lobe, starts distally and spreads throughout

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16
Q

What is broncho pneumonia?

A

when there are patches of consolidation throughout both lungs, starts proximally and moves distally towards the alveoli

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17
Q

What are the signs of pneumonia?

A

fever, raised HR, raised RR, low BP, signs of consolidation, decrease in chest expansion on affected side, bronchal breath sounds, vocal resonance, caitation, pleural effusion

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18
Q

What are the four stages of lobar pneumonia?

A

congestion, red hepatization, grey hepatization, resolution

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19
Q

When to hospitalise a pneumonia patient?

A

use CURB-65 severity criteria, if >2, needs to be hospitalised

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20
Q

What does CURB-65 stand for in pneumonia severity?

A

confusion, urea >7mmol/L, RR >30/min, BP 65years (1 point for each)

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21
Q

how many points match each stage in CURB-65 pneumonia?

A 
mild = 0-1
moderate = 2
severe = 3 or more
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22
Q

What is the transmission of pneumonia?

A

inhalation, aspiration of organisms that colonise the oropharnyx, aspiration of stomach contents, hematological spread, direct innoculation

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23
Q

What mainly causes a community acquired pneumonia?

A

bacterial or viral normally from an upper RTI infection of a viral origin, main organisms are strep pneumonia, H.influenza, Morexaella cateralis, influenza, RSV

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24
Q

What is hospital acquired pneumonia?

A

pneumonia that is not incubating at time of admission and develops in a patient who is hospitalized for more than 48 hours

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25
Q

What organisms mainly cause hospital acquired pneumonia?

A

enterobacterzae, pseudomonas species and staphylococcus aureus and MRSA, aerobic gram negative bacilli

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26
Q

What is aspiration pneumonia?

A

occurs in hospitals, in markedly debilitated patients during unconsciousness or vomiting as it can aspirate the stomach with bacteria and can lead to abscess formation in the lungs (normally right lung)

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27
Q

What are lung abscess complications?

A

extension into plural cavity, meningitis, hemorrhage, brain abscess, secondary amyloidosis.

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28
Q

What microorganisms usually cause aspiration pneumonia?

A

streptococcus and staph aureus, gram negative

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29
Q

What is chronic pneumonia caused by?

A

usually by fungus, in immunocompromised eg. histoplasmosis, tuberculosis, aspergillus, nocardia

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30
Q

What are the complications of pneumonia?

A

abscess formation that can cause tissue destruction, emphyema, bacteriaic dissemination which causes bacterimia and sepsis

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31
Q

What investigations should be done for pneumonia?

A 
CXR - consolidation 
sputum testing 
urine antigen testing 
blood testing - WCC up if severe, neurtrophilia if bacteria, haemolytic anaemia, high urea if severe, LFTs are abnormal if its inflamed the liver
blood culture 
gram stain
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32
Q

What would haemolytic anaemia suggest as a causative agent for pneumonia?

A

mycoplasma

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33
Q

What bacteria dose a urine antigen test identify in pneumonia?

A

strepto penumonia, legionella

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34
Q

What does bacteramia lead to in pneumonia?

A

sepsis

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35
Q

What is the treatment of pneumonia?

A 
oxygen
IV fluids - if severe
NSAIDs and opioids 
antibiotics - NARROW SPECTRUM
pneumoncoccal vaccines
smoking cessation
influenza vaccine
protein conjugate vaccine
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36
Q

What are the cardinal signs of pneumonia? (CDEF)

A

chest pain, dyspnoea, exudate, fever

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37
Q

What is a risk of using opioids?

A

respiratory depression

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38
Q

What is needed to be done to find the causative agent in pneumonia?

A

empirical therapy using b lactams or macrolides, once this is done, a more specific causative agent can be found

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39
Q

What is empirical therapy for pneumonia?

A

most likely pathogen
risk factors for antimicrobial resistance
medical co morbidities and allergies

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40
Q

What antibiotics are used in mild, moderate and severe pneumonia?

A

mild - amoxicillin
moderate - amoxicillin and clarithromycin
severe - coamoxiclav and clarithromycin

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41
Q

What is the empirical therapy for gram positive and gram negative bacteria?

A 
positive = penicillins (b lactams)
negative = -mycins (macrolides)
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42
Q

How do B-lactams (amoxicillin and flucoxacillin) treat bacteria (staph)?

A

attack the peptidoglycan cell wall of the bacteria

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43
Q

How do macrolides (clarithromyscin and erythromycin) treat bacteria?

A

inhibit protein synthesis

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44
Q

When would you use IV antibiotics for pneumonia?

A

if it was complicated

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45
Q

What will strep pneumoniae show on CXR?

A

air bronchograms, effusions and collapses due to retenetion of secretions (raised WBC)

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46
Q

What will mycoplasma show on CXR?

A

bilateral or extensive infection of one lobe (normal WBC)

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47
Q

What will legionella show on CXR?

A

multilobar shadowing, pleural effusion and lymphopena

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48
Q

What are the clinical features of a hospital acquired pneumonia?

A

new fever, purulent secretions, radiological infiltrates, leukocytosis, increase in o2 requirements

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49
Q

What is a lung abscess?

A

a localised area of pus in the parenchyma (alveolar tissue)

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50
Q

What causes a lung abscess?

A

aspiration, bacterial pneumoniia, mechanical obstruction of the bronchi, alcoholics, poor dental hygiene, TB, aomebic liver disease

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51
Q

Sign and symptoms of a lung abscess?

A

fever, chills, weight loss, chest pain, productive cough, dull of absent lung sounds

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52
Q

What investigations should be done for a lung abscess?

A

CXR, CT, blood and sputum cultures, thoracentesis

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53
Q

What is the treatment of a lung abscess?

A

postural drainage, antibiotics, lobectomy,

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54
Q

What is empyema?

A

pus in the pleural cavity

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55
Q

What causes empyema?

A

chest trauma, pneumonia, TB

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56
Q

Signs and symptoms of empyema?

A

fever, chest pain, dyspnea, anorexia, malaise, diminished or absent lung sounds

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57
Q

What is the treatment of empyema?

A

thoracentesis to id the pathogen, use antibiotics

thoracotomy and surgical drainage

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58
Q

When does a lung effusion need drainage?

A

pH 1000iu or pH

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59
Q

What is bronchitis?

A

inflammation of the bronchial tubes

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60
Q

symptoms of bronchitis?

A

cough, SOB, wheeze, chest tightness, fever

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61
Q

What causes acute bronchitis?

A

viruses that cause colds, tobacco smoke, air pollution, dusts, vapors, fumes

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62
Q

What is the treatment of acute bronchitis?

A

rest, fluids, analgesic, no antibiotics if viral, amoxicillin if suspected bacterial infection

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63
Q

What is pneumothorax?

A

air in the pleural space

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64
Q

Which lung is more affected in pneumothorax?

A

both are equally affected

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65
Q

In who is primary pneumothorax most common?

A

tall, slim, men (men more common than women)

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66
Q

What are the causes of pneumothorax?

A

ruptured pleural bleb from congenital defects in connective tissue of alveiolar wall, COPD, TB, sarcoidosis, RA, ankylosing spondylitis, lung trauma, idiopathic pulmonary fibrosis, emphysema, asthma, air that cannot be removed on expiration due to a one way valve leading to mediastinal shift and lung collapse

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67
Q

What causes primary pneumothorax?

A

tall young men in 20s, smoking, diving, high altitude flying

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68
Q

What is tension pneumothorax?

A

when air is sucked into pleural space during inspiration but not expelled so interpleural pressure remains positive so lung deflates further

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69
Q

What is the difference of treatment of tension and non tension pneumothorax?

A

tension - medical emergency, immediate needle thoractemy, chest drainage
non tension - observe, aspirate, chest tube drainage

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70
Q

How does a tension pneumothorax present?

A

falling o2 sats, hypotension, tracheal deviation, diagnose clinically with immediate treatment

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71
Q

What are the complications of tension pneumothorax?

A

respiratory and cardiac arrest and death

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72
Q

symptoms of pneumothorax?

A

dyspnea, unilateral pleuritic chest pain, decreased lung sounds on affected side, percussion hyper-resonance,

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73
Q

What is pleuritic chest pain?

A

pain when breathing

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74
Q

How do you diagnose non tension pneumothorax?

A

CXR - pleural line shows tracheal deviation away from lesion, absent vascular markings, air, shrunken lobe of lung, diaphragm hyperexpansion, mediastinal shift
Ct scan
ABG - hypoxia

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75
Q

When should you do drainage in pneumothorax?

A

if ventilated, tension after needle, persistant or recurrent, >2cm secondary spontaenous pneumothorax >50yrs after aspirate

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76
Q

When do you put the needle in needle decompression?

A

the 2nd intercostal space in the midclavicular line?

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77
Q

How can you prevent pneumothorax?

A

advice on flying/diving and pleurectomy and chemical pleurodesis with talc if they cant have surgery, bleb resection

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78
Q

When is pain generalised in pneumothorax?

A

if no pleural adhesions

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79
Q

When is pain localised in pneumothorax?

A

if visceral pleura has previously become adherant to parietal pleura as the negative pressure would be lost once there is communication with the atmospheric pressure so elastic recoil pressure causing lung to partially deflate

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80
Q

What is a chylothorax?

A

accumalation of lymph in pleural space

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81
Q

What cause a chylothorax?

A

due to leakage from thoracic duct post trauma of infiltration by carcinoma

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82
Q

What is a pleural effusion?

A

excessive fluid in pleural space (transudate or exudate)

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83
Q

Which is the outer pleura?

A

the parietal

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84
Q

What are the symptoms of pleural effusion?

A

pleuritic chest pain, dyspnoea, dry cough,

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85
Q

What is the cause of an EXUDATE pleural effusion?

A

parapenumonic, TB, breats cancer, PE, RA, SLE, haemothorax, parasites, fungi, lymphoma, ARDS, hypothyroidism

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86
Q

What is a exudate fluid?

A

protein = >35g/L

lactic dehydrogenase = >200iu/L

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87
Q

What is a transudate fluid?

A

protein is

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88
Q

What is the cause of a TRANSUDATE pleural effusion?

A

ovarian tumours, CCF, cirrhosis, HF, hypoalbuminaemia, nephrotic syndrome, constrictive pericarditis, peritoneal dialysis, unithorax, malignancy, PE

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89
Q

What does pleural effusion fluid contain?

A

proteins and cells

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90
Q

How do you diagnose pleural effusion?

A

pleural aspiration with US guidance

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91
Q

How is a pleural effusion detected and how much fluid is needed to detect it?

A

CXR >300ml

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92
Q

For a pleural effusion to be detected clinically, how much fluid is needed?

A

> 500ml

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93
Q

What is the treatment of pleural effusion?

A

transthorantesis, needle drainage, aspiration to dryness, inhalation of sclerosing agent, treat underlying cause

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94
Q

What is used to prevent a recurrence of a pleural effusion?

A

pleurodesis

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95
Q

How much fluid is produced and reabsorbed by the parietal pleura?

A

15ml/day

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96
Q

How happens when airway and pleural communication is maintained?

A

a bronchopleural fistula results, then air will be rebasorbed once it closes and it will collapse in 40 days

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97
Q

What kind of pleural effusion causes raised hemidiaphram?

A

subpulmonary effusion

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98
Q

how does fluid in the fissures present?

A

intrapulmonary mass

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99
Q

How is drainage of a pleural effusion achieved?

A

lymphatic pump from contractions of lymphatic wall smooth muscle and tissue pressure oscillations related to resp movement

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100
Q

What is the max drainage that can be done from a lymphatic pump?

A

300ml/day

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101
Q

When is a Abrams needle good in pleural effusion?

A

for TB, but there is low malignancy pick up

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102
Q

How does pleurodosis work?

A

insert an irritant into the pleural space to cause tissue damage, then as the tissue heels, it cause scar tissue to develop, so the two pleuras adhere together to remove potential space for pleural effusion

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103
Q

Why is drainage of a pleural effusion done slowly?

A

to prevent pain and shock but it is only a temporary relief

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104
Q

What is the first line of treatment for pleural effusion’?

A

transthorantesis

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105
Q

What is a complication of pleural effusion?

A

empyema which can then harden (organising) making it harder to treat and drain - and can spill over into blood vessels

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106
Q

What is a parapneumonic effusion?

A

a pleural effusion caused by pneumonia, lung abscess of bronciectasis

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107
Q

What are the 3 classifications of parapneumonic effusion?

A

uncomplicated, complicated, empyema thoracis

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108
Q

What is an uncomplicated parapneumonic effusion?

A

exudative, from increasing passage of interstitial fluid from pneumonia inflammation

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109
Q

What is complicated parapneumonic effusion?

A

bacterial invasion into the pleural space, visibly infective, pH

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110
Q

What kind of parapneumonic effusion is cloudy or clear?

A

uncomplicated

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111
Q

What is the treatment of complicated parapneumonic effusion?

A

drainage for resolution and antibiotics, decortication (surgical drainage), intrapleural fibrinolytics

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112
Q

What is empyema thoracis?

A

frank pus accumulating in the pleural space

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113
Q

What are the 3 stages of parapneumonic effusion?

A

exudative, fibrinopurulent, organisation

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114
Q

What are the signs of a pleural effusion?

A

decreased expansion, stony dull percussion, diminished breath sounds on affected side, bronchial breathing above the effusion

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115
Q

How are small effusions seen compared to large effusions on CXR?

A

small - blunt costophrenic angles

large - water dense shadows with concave upper borders

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116
Q

What is a bullae?

A

air space in lung parenchyma

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117
Q

How is bronchitis clinically defined?

A

cough and sputum production on most days for 3 months of two successive years

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118
Q

What is pulmonary hypertension?

A

increased resistance in the lungs so pulmonary artery pressure is 25mmHg at rest

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119
Q

What is the normal pulmonary artery pressure?

A

10-14mmHG

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120
Q

What can pulmonary hypertension lead to?

A

arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries, cor pulmonale

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121
Q

What are the symptoms of pulmonary hypertension?

A

SOB, dyspnoea, fatigue, syncope, exercise intolerance, structural lung damage (scarring), cough, right ventricular hypertrophy, left parasternal heave, loud P2 sound, portal hypertension, abdominal distension

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122
Q

What are the causes of pulmonary hypertension?

A

idiopathic, left heart disease, lung diseases, hypoxia, chronic thromboembolic, haematologic, systemic, metabolic, familial hereditary, drugs, toxins, connective tissue disorder, congential heart disease, portal hypertension, HIV

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123
Q

What are the types of pulmonary hypertension?

A

pulmonary arterial hypertension (PAH)
pulmonary venoocclusive disease
pulmonary hypertension from LHD
pulmonary hypertension due to hypoxia and lung disease
chronic thromboembolic pulmonary hypertension

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124
Q

What will a CXR show in pulmonary hypertension?

A

enlarged RA and RV, prominent pulmonary arteries

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125
Q

What does an ECG show in pulmonary hypertension?

A

p pulmonale, right axis deviation due to RVH

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126
Q

What do blood tests show in pulmonary hypertension?

A

raised Hb, haematocrit, e.g. polycythamia

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127
Q

What is the treatment of pulmonary hypertension?

A

treat the underlying cause, O2, ABG monitor, treat cardiac failure, stop smoking, endothlin antagonists to restrict pulmonary vasculature

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128
Q

What is the diagnostic test for pulmonary hypertension?

A

right heart catheterization to show pressure >30

ECHO estimates pressure and shows ventricular function

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129
Q

What is cor pulmonale?

A

right sided heart failure due to chronic pulmonary hypertension due to RV strain, causing compensatory hypertrophy and eventual failure

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130
Q

What is the most common cause of cor pulmonale?

A

COPD

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131
Q

What are the side effects of cor pulmonale?

A

centrally cyanosed, breathless, ankle oedema, venous overload, progressive hepatic congestion, parasternal heave from RVH, loud P2 sound, fatigue, dyspnea, tachypnea, orthopnea, distended jugular veins

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132
Q

What effect does cor pulmonale have on the valves?

A

The pulmonary valve will become incompetent so will develop a tricuspid incompetence with increase jugular venous pressure, ascites and upper abdominal discomfort from liver swelling

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133
Q

Treatment of cor pulmonale?

A

bed rest, treat underlying cause, stop smoking, treat heart condition, small frequent meals, limit fluid

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134
Q

What is a pulmonary embolism?

A

occlusion of the pulmonary vasculature by a clot

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135
Q

What is the cause of a pulmonary embolism?

A

DVT, air embolus, fat embolus, amniotic fluid embolus, foreign material introduced by an IV drug user, RV thrombus post MI, septic emboli, neoplastic cells, parasites

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136
Q

How is a pulmonary embolism classified?

A

small/medium, multiple or massive

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137
Q

Pathophysiology behind pulmonary embolism?

A

platelet factor is released causing vasoconstriction, meaning decreased alveolar perfusion of the lung so reduced gas exchange leading to decreased surfactant, a ventilation/perfusion mismatch, hypoxaemia and dyspnoea

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138
Q

Risk factors for pulmonary embolism?

A

recent surgery, thrombophilia, pregnancy, leg fracture, prolonged best rest, reduced motility, malignancy, previous PE

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139
Q

What investigations should be done for a pulmonary embolism?

A

D dimer, thrombophilia screening, CXR, ECG, ABG, CT with pulmonary angiography, V/Q scan, Wells score

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140
Q

What will an ECG show in pulmonary embolism?

A

sinus tachycardia, S1Q3T3 pattern, excludes MI

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141
Q

What will an ABG show in pulmonary embolism?

A

hypoxaemia

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142
Q

When should a Thrombophilia screening take place?

A

In pulmonary embolism patients younger than 50

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143
Q

What is the treatment of a pulmonary embolism?

A

oxygen, IV fluids, thrombolysis therapy if indicated, LMW heparin, anticoagulation, IVC filter

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144
Q

When would thrombolysis therapy be indicated?

A

massive pulmonary embolism or haemodynamically unstable

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145
Q

What are the symptoms of a small pulmonary embolism?

A 
pleuritic chest pain
breathless
haemoptysis
tachypoenic
fever
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146
Q

What are the symptoms of a massive pulmonary embolism?

A 
severe chest pain
shocked, pale, sweaty
syncope
tachypoenic
tachycardia
hypotension and peripheral shut down
raised JVP
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147
Q

What are the symptoms of multiple pulmonary embolism?

A

increased breathlessness, weakness, syncope, occasional angina

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148
Q

What causes a pulmonary infarct?

A

a pulmonary embolism with chronic left heart failure, which causes decreased surfactant levels

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149
Q

In how many patients with pulmonary embolism does a pulmonary infarct occur?

A

10-15%

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150
Q

What does a CXR show in a pulmonary infarct?

A

Hamptom hump (wedge shape on pleura without air bronchograms) in lower lobes usually - leaves linear scar on healing

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151
Q

What does a CT show on a pulmonary infarct?

A

Hamptom hump and bubbly consolidation, convex borders

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152
Q

What is extrinsic allergic alveolitis?

A

inhalation of allergens which provoke a hypersensitivity reaction
diffuse granulomatous inflammation of lung tissue and airways in people who are sensitised by repeated inhalation of organic antigens in dusts

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153
Q

What happens in the acute and chronic phase of extrinsic allergic alveolitis?

A

acute - alevoli infiltrated with acute inflammatory cells

chronic exposure - small granuloma formation and obliterative bronchiolitis

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154
Q

What are the acute clinical features of extrinsic allergic alveolitis?

A

fevers, rigors, dry cough, dyspnoea, crackles, SOB

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155
Q

What are the chronic clinical features of extrinsic allergic alveolitis?

A

weight loss, exertional dyspnoea, type 1 respiratory failure, cor pulmonale, inspiratory cackles in lower lung

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156
Q

What is the most common cause of extrinsic allergic alveolitis?

A

farmers lung from mouldy hay

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157
Q

What is causes pigeons fanciers lung?

A

avian protein in bird droppings

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158
Q

What is Malt workers lung?

A

aspergillus clavatus from mouldy malt

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159
Q

What causes Bagassois/sugar workers lung?

A

sugar cane fibres

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160
Q

What is another name for extrinsic allergic alveolitis?

A

occupational lung disease

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161
Q

What is seen in the CXR of extrinsic allergic alveolitis?

A

upper zone mottling/consolidation
ground glass appearance
honeycomb lung in advance, micronodular shadowing

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162
Q

What is the treatment of extrinsic allergic alveolitis?

A

remove allergen, O2, oral prednisolone, compensation if occupational

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163
Q

What organism causes farmers lung?

A

saccharopolyspora rectivigula

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164
Q

What organism causes Hot tub lung?

A

poorly maintained hot tubs - aspergillus clavatus

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165
Q

What organism causes mushroom workers lung?

A

mushroom compost - thermophillic actinomycetes

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166
Q

What causes chemical workers lung?

A

plastics, rubber, foam industry - anhydride, diisocyanate

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167
Q

In chronic extrinsic allergic alveolitis, what happens to symptoms when the antigen is removed?

A

there is only partial improvement - and it eventually leads to chronic hypoxaemia and pulmonary hypertension leading to RH failure

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168
Q

What will bloods show in extrinsic allergic alveolitis?

A

increased CRP and ESR, serum antibodies

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169
Q

What will spirometry show in extrinsic allergic alveolitis?

A

restrictive spirometry

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170
Q

What causes type 1 hypersensitivity?

A

IgE mediated (mast cells and basophils) e.g. anaphylaxis, hayfever, asthma

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171
Q

What is the hypersensitivity classification called?

A

Gell-Coomb

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172
Q

What causes type 2 hypersensitivity?

A

antibody mediated e.g. goodpastures syndrome, haemolytic anaemia, Grave’s disease

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173
Q

What causes type 3 hypersensitivity?

A

immune complex formation which are then deposited around the body, acute and chronic e.g. extrinsic allergic alveolitis, SLE, RA

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174
Q

What causes type 4 hypersensitivity?

A

T lymphocyte mediated, delayed, forms granulomas e.g. TB, sarcoidosis

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175
Q

What is hypersensitivity pneumonitis?

A

inflammation of lung tissue from an inhaled antigen

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176
Q

When type of hypersensitivity is hypersensitivity pneumonitis?

A

mix of type 3 and 4

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177
Q

example of hypersensitivity pneumonitis?

A

farmers lung, cigarette smokers

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178
Q

What can hypersensitivity pneumonitis lead to?

A

recurrent infections, COPD, cor pulmonale, pneumothorax

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179
Q

How does hypersensitivity pneumonitis cause complications?

A

chronic exposure leads to inflammation and fibrosis, decreasing gas exchange, leading to stiff lung from reduced surfactant production, causing respiratory failure and death

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180
Q

symptoms of hypersensitivity pneumonitis?

A

SOB on exertion, dry cough, fever, burning sensationin chest, fatigue, weight loss, improved symptoms on no exposure (e.g. during the week)

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181
Q

DD for hypersensitivity pneumonitis?

A

idiopathic pulmonary fibrosis, infection, sarcoidosis,

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182
Q

What causes berylliosis?

A

inhalation of beryllium from aerospace, nuclear, electrical and manufacturing industries

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183
Q

What does beryylliosis show on histology?

A

granulomatous

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184
Q

What makes up a granuloma?

A

giant cells, macrophages, epithelioid cells

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185
Q

What is the treatment of berylliosis?

A

steroids

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186
Q

How does berylliosis present?

A

progressive dyspnoea and pulmonary fibrosis

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187
Q

What causes silicosis?

A

silica particle inhalation from foundries, sandblasting, mines, quarries and pottery

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188
Q

Why can’t silica be removed by the respiratory defences?

A

macrophages engulf the silica, causing the macrophages to release fibrogenic factors, leading to fibrosis, collagen deposit and COPD

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189
Q

What does silicosis increase the risk of?

A

TB and bronchogenic carcinoma

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190
Q

What does a CXR show in silicosis?

A

eggshell calcification of hilar lymph nodes and nodular lesions in upper lobes

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191
Q

How does silicosis present?

A

progressive dyspnoea and restrictive ventilatory defect

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192
Q

What causes asbestosis?

A

inhalation of asbestos fibres seen in old roofing and plumbing, ship building

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193
Q

What are the three types of asbestosis and which is most fibrogenic?

A

crocidolite (blue) = most
amosite (brown)
chrysotile (white) = least

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194
Q

What are asbestos fibres?

A

they are inconsumable silicate

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195
Q

What can asbestosis lead to?

A

malignant mesothelioma, lung cancer, chest neoplasia, persistant pleural effusion, diffuse pleural fibrosis and diffuse interstitial lung fibrosis

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196
Q

What is malignant mesothelioma?

A

pleural mesothelial cell tumours - mainly from asbestos exposure

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197
Q

What does the CXR show in asbestosis?

A

ivory white, calcified supradiaphramatic and pleural plaques

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198
Q

What are the symptoms of asbestosis?

A

dyspnoea, clubbing, fine and inspiratory cackles, SOB, weight loss, bloody pleural effusions, metastases

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199
Q

What is the treatment of asbestosis?

A

treat the symptoms and stop smoking

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200
Q

What does fibrotic shadowing on CXR in the upper zone suggest?

A

TB, EEA, Berylliosis, coal workers, silicosis, sarcoidosis

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201
Q

What does fibrotic shadowing on CXR in the middle zone suggest?

A

progressive massive fibrosis

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202
Q

What does fibrotic shadowing on CXR in the lower zone suggest?

A

asbestosis, idiopathic pulmonary fibrosis

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203
Q

What causes coal workers lung?

A

coal dust inhalation

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204
Q

How does coal dust inhalation cause pneumoconiosis?

A

it accumulates in the lung parenchyma and engulfed by macrophages, the macrophages then die and release fibrogenic factors causing tissue fibrosis

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205
Q

What are the symptoms of simple pneumoconiosis?

A

asymptomatic or chronic bronchitis

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206
Q

What does the CXR show in acute and chronic pneumoconiosis?

A

acute - round opacities in upper zone

chronic - upper zone fibrotic masses

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207
Q

What is the treatment of pneumoconiosis?

A

avoid exposure, treat chronic bronchitis, stop smoking, claim compensation

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208
Q

What is progressive massive fibrosis?

A

progression of coal workers lung

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209
Q

What are the symptoms of progressive massive fibrosis?

A

progressive dyspnoea on exertion cough with black sputum, fibrosis and cor pulmonale and respiratory failure, shows upper zone fibrotic masses

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210
Q

What is byssinosis?

A

cotton workers lung caused by cotton mills that limits the airway

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211
Q

What are the symptoms of byssinosis?

A

tight chest, cough, breathlessness

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212
Q

What is Caplans syndrome?

A

the association between RA, pneumoconiosis and pulmonary rheumatoid nodules

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213
Q

Which occupational diseases have RhF present?

A

Caplans, Progressive massive fibrosis, asbestosis, silicosis

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214
Q

What is Bauxite fibrosis?

A

shavers disease cuased by bauxite fibres

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215
Q

What is siderosis?

A

inhalation of iron particles - but no resp symptoms of altered lung function

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216
Q

Which cancer is closely related to asbestos exposure?

A

malignant mesothelioma

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217
Q

Where does malignant mesothelioma usually occur?

A

in pleura (rarely peritoneum or other organs)

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218
Q

What can the latent period between asbestos exposure and malignant mesothelioma be?

A

45 years

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219
Q

How does malignant mesothelioma present?

A

chest pain, weight loss, SOB, finger clubbing, recurrent pleural effusions

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220
Q

What are the signs of malignant mesothelioma metastases?

A

lymphadenopathy, hepatomegaly, bone pain, abdo pain

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221
Q

What will investigations show in malignant mesothelioma?

A

pleural thickening and blood in pleural fluid (these pleural plaques can also increase bronchial adenocarcinoma)

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222
Q

What is the treatment of malignant mesothelioma?

A

chemo - but poor prognosis

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223
Q

What is sarcoidosis?

A

a multisystem chronic inflammatory condition with NON-CASEATING granulomas at various sites in the body

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224
Q

What is a granuloma?

A

a collection of epithelioid histiocytes

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225
Q

Who who is sarcoidosis commonly seen?

A

adults over 50, normally sporadic, more common in females

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226
Q

Where is sarcoidosis usually seen?

A

thorax > skin > eyes > liver > heart > nervous system

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227
Q

What are the symptoms of sarcoidosis?

A

fever, fatigue, cachexia, decreased exercise tolerance, chest pain
lung - interstitial lung disease, dry cough, fever, SOB, chest tight
skin - erythema nodosum on legs, lupus pernio on nose and cheeks
eyes - granulomatous uveitis (worse on posterior)
hepatomegaly, hypercalcaemia

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228
Q

What does a CXR show in sarcoidosis?

A

bilateral hilar/para tracheal lymphadenopayhy, pulmonary infiltration

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229
Q

What will investigations show in sarcoidosis?

A 
increase in eosinophils, calcium and ESR
INCREASED SERUM ACE
interstitial lung disease 
increase CD4:CD8 ratio 
transbronchial biopsy and histology
staging
increased Igs
restrictive ventilatory defect 
non caseating granuloma biopsy
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230
Q

What is the management of sarcoidosis?

A

symptomatic relief, oral corticosteroids, surgery, stop smokiing, osteoporosis prophylaxis, influenza vaccination, bed rest, NSAIDs

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231
Q

What are the complications of sarcoidosis?

A

lung infections, PE, increased fibrotic disease,, pulmonary hypertension, respiratory failure

232
Q

What is idiopathic pulmonary fibrosis?

A

idiopathic interstitial pneumonia, inflammatory cell infiltrate, unknown cause of fibrosis

233
Q

What is the main cause of interstitial lung disease?

A

idiopathic pulmonary fibrosis

234
Q

What are the complications of idiopathic pulmonary fibrosis?

A

respiratory failure and increased risk of lung cancer

235
Q

What are the signs and symptoms of idiopathic pulmonary fibrosis?

A

dry cough, dyspnoea on exertion, weight loss, malaise, cyanosis, finger clubbing, fine late inspiratory crackles

236
Q

What does the CXR show in idiopathic pulmonary fibrosis?

A

bilateral lower lung reticulonodular shadows and honeycombing, decreased lung volume

237
Q

What is the treatment of idiopathic pulmonary fibrosis?

A

supportive care with oxygen and pulmonary rehabilitation, lung transplant, opiates

238
Q

What does idiopathic pulmonary fibrosis show on biopsy?

A

usual interstitial pneumonia

239
Q

What is the prognosis like for idiopathic pulmonary fibrosis?

A

poor due to the resp fialure and lung cancer risk
50% 5 year survival
3000 deaths per year

240
Q

What is a secondary cause of pulmonary fibrosis?

A

infarction, TB and pneumonia

241
Q

Risk factors for idiopathic pulmonary fibrosis?

A

cigarettes, infectious agents, dust exposure, antidepressant, chronic aspiration, genetics

242
Q

What is an interstitial lung disease?

A

distinct cellular infiltrates and extracellular matirx deposition in the lung distal to the terminal bronchiole

243
Q

What will histology show in most interstitial lung disease?

A

hyperplasia of type 2 pneumocytes

244
Q

What are the common symptoms in interstitial lung disease?

A

dyspnoea on exertion, dry cough, restrictive spirometry, decreased gas transfer

245
Q

What are the causes of interstitial lung disease?

A

hypersensitivity pneumonitis, industrial dusts, drugs, infections, GORD, sarcoidosis, RA, connective tissue disorders e.g. SLE, idiopathic pulmonary fibrosis

246
Q

What is Langerhans cell histiocytosis?

A

rare, multisystem disease of histocyte proliferation

247
Q

What are the clinical features of Langerhans cell histiocytosis?

A

unifocal bone lesions in older children, multifocal in young children , pulmonary Langerhand cell hisiocyte in smokers, honeycomb lung, fibrosis, nodular shadows

248
Q

What is Lymphangiolyomyomatosis?

A

benign proliferation of lymphatic smooth muscle cells

249
Q

How does lymphangiolyomyoatosis present?

A

dyspnoea, chylous pleural effusions, haemoptysis, pneumothorax

250
Q

What is pulmonary alveolar proteinosis?

A

accumulation of lipoproteinaceous material in alveoli caused by a defect in the GM-CSF stimulation of alveolar macrophages

251
Q

How does pulmonary alevolar proteinosis present?

A

bronchial lavage with milky appearance, large, foamy macrophages from lack of maturation, causing proteinaceous fluid accumulation

252
Q

what does neutrophils with a linear and reticular morphological appearance with lower and peripheral distirbution suggest?

A

idiopathic pulmonary fibrosis

253
Q

What does a nodular morphological appearance with central distribution and lymphocytes suggest?

A

sarcoid

254
Q

What do eosinophils in a BAL suggest?

A

eosinophilic pneumonia

255
Q

How does cryptogenic organising pneumonia present?

A

malaise, cough, breathlessness, fever, pleuritic chest pain, bilateral parenchymal shadowing, normal/restrictive lung function, normal WBC, increased ESR, buds of connective tissue in bronchioles, ground glass appearance

256
Q

Treatment of interstitial lung disease?

A

corticosteroids, immunosuppresants, lung transplant

257
Q

Risk factors for interstitial lung disease?

A

RA, RhF, male, age, anti CCP, smoking, DMARDS

258
Q

What is bronchiectasis?

A

chronic infection of bronchi and bronchioles leading to permanent dilation of these airways, leading to increased infection risk

259
Q

What organisms cause bronchiectasis?

A

H.influenzae, Strep.pneumoniae, Staph.aureus, Pseudomonas aeruginosa

260
Q

What are the causes of bronchiectasis?

A

CF, post infection of measles/pertussis/bronchiolitis/penumonia/TB/HIV, bronchial obstruction, allergic bronchopulmonary aspergillosis, hypogammaglobulinaemia, IBD, tumours, a1trypsin deficiency

261
Q

signs and symptoms of bronchiectasis?

A

persistent cough, copious purulent foul smelling (yellow/green) sputum, intermittent haemoptysis, clubbing, coarse inspiratory creps, wheeze, increased fungal infection risk, febrile episodes, weight loss, recurrent exacerbations

262
Q

What is clubbing?

A

distorted angle of nail bed

263
Q

What will a CXR show in bronchiectasis?

A

thickened bronchial walls, dilated bronchi, tram track opacities of bronchi and bronchioles

264
Q

What is the sputum like in bronchiectasis?

A

foul smelling, green/yellow, purulent, lots of

265
Q

What will investigations show in bronchiectasis?

A

thickened dilated bronchioles and cysts, serum Igs, IgA deficiency, sweat electrolytes, mucociliary clearance, obstructive spirometry, aspergillus screen

266
Q

What is the treatment of bronchiectasis? (ABCDS)

A

postural drainage, chest physio to aid mucus clearance, antibiotics, bronchodilators e.g. salbutamol, corticosteroids for ABPA, surgery,

267
Q

pathophysiology behing bronchiectasis?

A

chronic infection causes chronic inflammation, destroys elastic and muscular tissue, airways dilate permanently, poor mucus clearance, impaired airflow and drainage, accumulation of mucus in lungs, mucus colonises bacteria so frequent and severe lower RTIs, worsening of bronchiectasis

268
Q

complications of bronchiectasis?

A

empyea, lung abscess, pneumothorax, resp failure, reduced QoL, pleural effusion, metastatic abscess formation, septicaemia,

269
Q

What organism is common in bronchiectasis and CF?

A

pseudomonas aeruginosa

270
Q

What is the macroscopic appearance of bronchiectasis?

A

cylindrical, varicose, cystic

271
Q

What is the pathophysiology of cystic fibrosis?

A

a mutation in the CF transmembrane conductance regulator gene (CFTR) Ch7 which codes for Cl- channel, this leads to defective cl- secretion and increased Na+ absorption across the airway epithelium so there is thick mucus leading to the inability to clear pathogens so increased infections and bronchiectasis

272
Q

In who is cystic fibrosis most common?

A

1/2000 caucasian births, increasing prevalence,

273
Q

What genetic pattern in cystic fibrosis?

A

autosomal recessive

274
Q

What is the mean survival of cystic fibrosis?

A

around 40 years

275
Q

What are the symptoms of a neonate with cystic fibrosis?

A

failure to thrive, meconium ileus (SI blockage due to thicker secretions), rectal prolapse

276
Q

What are the general symptoms of a child/adult with cystic fibrosis?

A

cough, wheeze, recurrent, brochiectasis, pneumothorax, haemoptysis, respiratory failure, cor pulmonale

277
Q

What are the signs of cystic fibrosis?

A

clubbing, cyanosis, bilateral coarse crackles

278
Q

How does cystic fibrosis affect fertility?

A

men - 98% infertile due to blocked ducts, but no reduced libido
women - normal fertility

279
Q

What GI symptoms are seen in cystic fibrosis?

A

pancreatic insufficiency (DM, steatorrhoea), distal intestinal obstruction syndrome, gallstones, cirrhosis

280
Q

What other symptoms are associated with cystic fibrosis?

A

osteoporosis, arthritis, vasculitis, nasal polyps, sinusitis, neuropathy, right blindness, salty sweat, bone loss

281
Q

What are the diagnostic tests of cystic fibrosis?

A

sweat test - shows high chloride and sodium content (salty) >60mml/L sodium
faecal elastatse - shows pancreatic dysfunction
screening of CF mutation
Guthnes test in neonatal showing increased serum immunoreactive trypsinogen
may show bronchiestasis

282
Q

What is the used for prevention of cystic fibrosis?

A

hygiene, vaccination, flu vaccine, penumovax, pseudomonal vaccine, segregation in and out of hospital, prophylactic antibiotics (flucoxacillin for s.aureus and amoxyl for h.influenzae)

283
Q

What is the treatment of cystic fibrosis?

A

postural drainage, chest physio, antibiotics for acute severe exacerbations, mucolytics, bronchodialators, oxygen, diuretics, ventilation, transplant, pancreatic enzyme replacement, fat soluble vitamin replacement, ursodeoxycholic acid, treat complications, screening and counselling, gene therapy transfer,

284
Q

What are the 3 main organisms that cause cystic fibrosis?

A

psuedomonas aeruginosa, burkholderia cepecia complex, mycobacteria abscessus

285
Q

What is the treatment of pseudomonas aeruginosa cystic fibrosis?

A

nebulised recombinant human DNAase
nebulised tobramycin
oral azithromycin
decrease exacerbations once chronic colonisation

286
Q

Why is pseudomonas aeruginosa so resistant?

A

has unique strains with a flagella, and improving antibiotics sensitivity
the loss of the flagella and biofilm formation is associated with chronicity, antibiotic resistance and epidermic strains

287
Q

How will symptoms differ in those with a multiresistant strain of pseudomonas aeruginosa cystic fibrosis?

A

lower fev1, consume more rescources, poor outcomes

288
Q

What are the 3 types of Burkholderia cepecia complex?

A

Bcc genomovars
Non Bcc CF pathogens
Cepacia syndrome

289
Q

What is Wegners granulomatosis?

A

a granulomatosis with polyangitis (GPA) with unknown cause - necrotising granulomatous inflammation and vasculitis of small and medium vessels, endobronchial involvement and caviating nodules

290
Q

What are the clinical features of Wegners granulomatosis?

A

nasal obstruction, ulcers, nasal septum destruction, progressibe glomerulonephritis, cough, haemoptysis, purpura, nodules, peripheral neuropathy

291
Q

What will investigations show in Wegners granulomatosis?

A

raised cANCA, antibodies against pr3
proteinuria, haematuria
cxr - nodules and fluffy infiltrates of pulmonary haemorrhage
Ct show diffuse alveolar haemorrhage

292
Q

What is the treatment of Wegners granulomatosis?

A

corticosteroids and cyclophosphamide to cause remission
azathioprine and methotrexate for maintenance
plasma exchange in severe renal disease

293
Q

What is the prognosis like for Wegners granulomatosis?

A

poor

294
Q

What causes Goodpastures syndrome?

A

a type 2 cytotoxic reaction driven by antibodies, directed against the basement membrane of kidney and lung (antiglomerular basement membrane antibodies)

295
Q

What are the symptoms of Goodpastures syndrome?

A

acute glomerulonephritis, lung symptoms, haemoptysis, diffuse pulmonary haemorrhage, upper RTI, cough, tiredness, anaemia, massive bleeding

296
Q

What does the CXR show in Goodpastures syndrome?

A

infiltrates due to pulmonary haemorrhage in the lower zones

297
Q

What does a kidney biopsy show in Goodpastures syndrome?

A

crescentric glomerulonephritis

298
Q

What is the treatment of Goodpastures syndrome?

A

treat shock, vigorous immunosuppressive treatment and plasmapheresis to remove autoantiboeds against the basement membrance
can improve spontaneously or lead to renal failure

299
Q

What is Churg Strauss syndrome?

A

a triad of asthma, eosinophilia and vasculitis that affects lungs, nerves, heart and skin

300
Q

What can Churg Strauss syndrome lead to?

A

septic shock, systemic inflammatory response syndrome, glomerulonephritis, renal failure

301
Q

What do investigations show in Churg Strauss syndrome?

A

eosinophilic infiltration and increased eosinophils in blood count, vasculitis of small arteries and veins, extravascular granulomas, ANCA positive, ground glass consolidation and bronchial wall thickening, anti MPO positive

302
Q

What is vasculitis?

A

inflammatory disorder of blood vessels causing destruction or stenosis, primary or secondary

303
Q

What is vasculitis of large vessels called?

A

Giant cell arteritis or Takayasus arteritis

304
Q

What is vasculitis of medium vessels called?

A

polyarteritus nodoas, kawasaki disease

305
Q

What is vasculitis of small vessels called?

A

ANCA positive vasculities e.g. Churg Straus, Wegeners granulomatosis, microscopic polyangiitis, glomerunephritis
ANCA negative vasculities e.g. Henoch Schoelein purpura, good pastures syndrome and cryoglobuliemia

306
Q

What are the symptoms of vasculitis?

A

depends on which organ is affected, fatigue and raised inflammatory markers , proteinuria, haematuria

307
Q

What is the treatment of vasculitis?

A

steroids and immunosuppressants

308
Q

What are the 4 x-ray stages of sacoidosis?

A

1-BHL only
2-BHL and infiltrates
3-infiltrates only
4-advanced parenchymal disease (fibrosis, bullae, bronchiectasis)

309
Q

What is the main lung malignancy?

A

carcinoma of the bronchus

310
Q

Risk factors for carcinoma of the bronchus?

A

smoking, asbestos, chromium, arsenic, iron oxides, radon gas

311
Q

Symptoms of carcinoma of the bronchus?

A

cough, haemoptysis, weight loss, anorexia, lethargy, sypnoea, chest pain

312
Q

Signs of carcinoma of the bronchus?

A

cachexia, clubbing, anaemia, lymph nodes, metastases sign e.g. bone tenderness (particularly vertebral and hepatomegaly)

313
Q

What is the most common histology in carcinoma of the bronchus in smokers?

A

squamous

314
Q

What is the most common histology in carcinoma of the bronchus in non smokers?

A

adenocarcinoma

315
Q

What are the 5 histologys seen in carcinoma of the bronchus?

A

squamous, adenocarcinoma, small cell, large cell, alveolar cell carcinoma

316
Q

Management of NSCLC?

A

mainly pallitative - surgical resection and radiotherapy w/wo adjuvant chemo

317
Q

Management of SCLC

A

chemotherapy and radiotherapy

318
Q

How can lung cancer be prevented?

A

quit smoking, reduce exposure to carcinogens

319
Q

Management of lung cancer?

A

palliative, radiotherapy, SVC stent, endobronchial therapy, pleural drainage for symptomatic pleural effusions, analgesics, steroids, anti emetics, bronchodilators

320
Q

Types of lung malignancy?

A

carcinoma of the bronchus, slow growing bronchial adenoma, benign hamartoma, malignant mesothelioma

321
Q

Where in the UK smoke the most?

A

Yorkshire and Humber and North West

322
Q

What does a PET scan do?

A

a functional non anatomical image that characterizes extent of mediastinal nodal involvement and highlights distant metastases - good for detecting asymptomatic metastases

323
Q

Positive and negative of PET scans?

A

high negative predicted value but low positive predicated value

324
Q

What causes false negatives in a PET scan?

A

BAC, carcinoid small lesions

325
Q

What causes false positives in a PET scan?

A

inflammation and infection

326
Q

What chemical is used in a PET scan?

A

fluro 2 deoxyglucose (FDG) is taken up by rapidly dividing cells, with a half life of 110mins

327
Q

Is NSCLC or SCLC more common?

A

80% NSCLC

328
Q

What is the 10yr survival for NSCLC?

A
329
Q

Symptoms of lung cancer metastatic disease?

A

bone pain, headache, siezures, neurological deficit, hepatic pain, abdominal pain

330
Q

At what stage is NSCLC mainly diagnosed?

A

stage 4

331
Q

What investigations help identify lung cancer type?

A

CXR, Ct scan, bronchoscopy, percutaenous needle biopsy, US guided aspirate, surgical biopsy

332
Q

What investigations help stage a lung cancer?

A

bloods, CT thorax and abdo, PET scan, CT head, medistinoscopy, pleural aspiration

333
Q

What investigations are used to determine how fit a lung cancer patient is?

A

ECG, lung function, exercise test with ECHO, exercise capacity, perfromance status, risk of pre op morbidity

334
Q

What are the stages of a performance status for lung cancer?

A

0-normal activity without restriction
1-restricted in strenuous work but can do light work
2-self caring but no work
3-limited self care, in bed/chair >50% of day
4-no self care, bed/chair bound

335
Q

What is the function of surgery and chemo in cancer?

A

surgery controls primary tumour

chemo eradicated micro metastases

336
Q

How to 60-70% of SCLC present?

A

as a perihilar mass (5% as a peripheral coin lesion)

337
Q

What is a pleural fibroma?

A

soft tissue neoplasm of pleura, mainly benign, can grow and compress lung tissue

338
Q

What does a pleural fibroma occasionally secrete and what does this cause?

A

insulin related factors that can produce hypoglycaemic symptoms

339
Q

What makes up a pleural neoplasma?

A

a pleural fibroma and malignant mesothelioma

340
Q

What is a BALTOMA?

A

a bronchus associated tissue lymphoma

341
Q

What are hamartomas?

A

irregular proliferations of benign or normal tissue, most commonly condroid hamartoma which incorporates cartilage, glandular tissue, fat, fibrous tissue and blood vessels

342
Q

What is the difference between radical and palliative radiotherapy?

A

radical is treatment 5x/week, it is curative

palliative is minimum number of visits needed for symptom control - normally not curative

343
Q

What is conformal radiotherapy?

A

conformation of target volume more accurately to shape of tumour and then the reduced tumour is irradiated, there is an escalation of radiation dose and then toxicity is reduced

344
Q

What is sterotactic ablative radiotherapy?

A

conformal radiotherapy with allowance for breathing motion and dose escalation, for those with peripheral tumours who are inoperable from co morbidity etc, it allows high rates of local control with low morbidity

345
Q

Side effects of palliative radiotherapy?

A

fatigue, anorexia, oesophagitis, systemic symptoms, skin reactions, nausea, alopecia if it is cranial

346
Q

Side effects of chemotherapy?

A

alopecia, nausea, vomiting, peripheral neuropathy, constipation, diarrhea, mucositis, rash, bone marrow suppression, fatigue, anaphylaxis

347
Q

Symptoms of a paraneoplastic lung cancer?

A

secretion of PTH, SIADH, ACTH secretion, hypertrophic pulmonary osteo arthropathy, myasthenic syndrome, finger clubbing, migratory thrombophebitis, non infective endocarditis, DIC

348
Q

What is TB?

A

a granulomatous disease that can affect any organ, mainly the lungs, caused by Mycobacterium tuberculosis or M.bovis (acid fast bacillus)

349
Q

How is TB transmitted?

A

aerosal droplets

350
Q

Is TB organisms aerobic or anaerobic?

A

aerobic, slow growing and immpermeable due to high lipid in cells wall, non spore forming, non mobile

351
Q

How does TB cause infection?

A

droplets inhaled, bacteria colonise alveoli, bacteria engulfed by macropahegs, multiplication of bacteria within macrophages, granulomas form about M.tuberculosis (caseous necrosis)

352
Q

What are the two types of granulomas that form in TB?

A

immunocopetent and non immunocompetent

353
Q

What happens in immunocompetent TB?

A

caseous necrosis produces conditions that decrease growth of bacteria e.g. decrease o2 and ph levels

354
Q

What does immunocompetent TB lead to?

A

latency

355
Q

What happens in non immunocompetent TB?

A

granuloma formation does not contain bacteria, leading to liquification of necrotic tissue, drained into the bronchus which is then coughed up

356
Q

What are the primary symptoms of TB?

A

cough, chest pain, haemoptysis, weight loss, anorexia, night sweats, fever, malaise, dyspnoea

357
Q

What is progressive TB?

A

when TB progresses or causes miliary disease

358
Q

What is post progressive TB?

A

asymptomatic with nodules, fibrosis or cavity, systemic haemoptysis, pneumonic, pleurisy

359
Q

What are the different forms of TB?

A

primary, latent reactivation, secondary, lymph node, bone, abdominal, genitourinary, miliary, meningitis

360
Q

How does lymph node TB present?

A

node swelling and is centrally necrotic

361
Q

How does bone TB present?

A

joint pain and swelling, Potts disease of the spine

362
Q

How does abdominal TB present?

A

ascites, abdominal lymph nodes

363
Q

How does GU TB present?

A

epidymitis, dysuria

364
Q

How does miliary TB present?

A

systemic upset from spread of bacili

365
Q

How does meningitis TB present?

A

bacilli in CSF, meningitis and raised ICP

366
Q

What is the treatment of TB?

A

rifampicin, isoniazid, pyrazinamide, ethambutol, educate for compliance, surgery depends on location

367
Q

Side effects of rifampcin?

A

fever, hepatitis, rash, blood dyscrasia

368
Q

Side effects of isoniazid?

A

hepatisis, peripheral neuropathy, psychosis, haemolytic anaemia

369
Q

Side effects of pyrazinamide?

A

hepatisism hyperuricaemia

370
Q

Sife effects of ethambutol?

A

optic neuritis

371
Q

What tests should be done for TB?

A

sputum culture, sputum stain, transbronchial biopsy, pleural fluid analysis, xray for infiltrates and cavitations, tuberculin skin test

372
Q

What does a transbronchial biopsy show in TB?

A

granulomas

373
Q

What are the two stains you do in a TB invetsigation?

A

Ziehl Neelsen stain for acid fast bacilli

Auramine rhodamine staining is more sensitive

374
Q

What does an x-ray show in TB?

A

Millet seed lesions in miliary TB

375
Q

What medium is used in a TB sputum culture?

A

Ogawa/Lowenstein Jensen medium

376
Q

How long does a liquid and solid sputum culture take in TB?

A

liquid is 1-3 weeks growth

solid = 3-8 weeks growth

377
Q

What is used to detect TB in a culture?

A

automated systems BACTEC M.gorwth indicator tube (MGIT) fleurometric detection in liquid media

378
Q

What happens in a TB skin test?

A

protein derived from the TB organism is injected intradermally and stimulates type 4 delayed hypersensitivity reaction, causing a positive result 48-72 hours post injection
causes increased indurated lesion of >6mm in non BCG vaccinated and >15mm in vaccinated
wont distinguish injection and disease

379
Q

Risk factors for TB?

A

previous treatment, contact with drug resistant patient, originates of travelled to place of high incidence, HIV, non adherance history, substance abuse, homeless,

380
Q

Prevention of TB?

A

skin test and IGRA if susceptible
BCG jab
contact tracing
remove risk factors

381
Q

What does IGRA do in TB?

A

detects the IFN-y production from T cells in TB exposure but does not differentiate between active and latent disease, but it is more sensitive than TST

382
Q

Pathogenesis behind TB?

A

pathogen is ingeted by macrophage and survives in phagosome, preventing acidification, inhibiting ROS and limits antigen presentation

3-9 weeks after, CD4+ T cells via IFN-y prime macrophages to kill bacilli and release tissue dmaging enzymes and CD8+ T cells lyse infected cells so infection is quescent but can cause reactivation

controlled by activated macrophaes to form a granulomata and Langerhan giant cells in an organised reaction

383
Q

When do caseous necrosis and cavitation necrosis occur in TB?

A

caseous - 10^2-10^4 bacilli

cavitation - 10^7-10^9bacilli

384
Q

Where is the most common site of infection?

A

respiratory tract

385
Q

are children or adults most likely to get an RTI?

A

children

386
Q

What kind of viruses can cause RTI?

A

rhinovirus, coronavirus, adenoovirus, respiratory syncytial virus, parainfluenza, influenza A

387
Q

What virus is responsible for the common cold, bronchitis and sinusitis?

A

Rhinovirus

388
Q

What virus is responsible for upper RTI, pharyngitis, bronchitis, and occasionally pneumonia?

A

Adenoviruses

389
Q

What virus is responsible for colds and severe respiratory illness?

A

coronavirus

390
Q

What virus causes pharyngitis?

A

adenovirus (B hemolytic streptococci in 10-30% of cases)

391
Q

How does pharyngitis present?

A

sore throat, tender neck glands, larger tonsils, raised temp and tender anterior cervical LN

392
Q

What virus causes glandular fever?

A

Epstein Barr virus

393
Q

What is persistent and severe tonsilities treated with?

A

phenoxymethylpenecillin (amoxicillin in serious cases)

394
Q

How does sinusitis present?

A

dull constant pain over frontal and maxiallary sinuses with tenderness and posy nasal drip, fever, punilent nasal discharge, ear and tooth pain but no dental problems, recent cold, pain worse on bending over

395
Q

What organisms mainly cause sinusitis?

A

streptococcus pneumoniae and H.influenzae, fungal

396
Q

What complications can sinusitus lead to?

A

brain abscess, sinus vein thrombosis, orbital cellulitis

397
Q

What is the treatment of sinusitis?

A

nasal decongestants, broad spectrum antibiotics, anti inflammatory therapy, topical corticosteroids

398
Q

How does acute epiglottis present?

A

sore throat, pain on wallowing, febrile, wheezing noise on breathing in, fatigue, weight loss, diarrhoea, oral thrush, fever, severe air flow obstruction

399
Q

What organism mainly causes acute epiglottis?

A

haemophilus influenzae type B

400
Q

How do children present with acute epiglottis ?

A

dysphagia, drooling, stridor

401
Q

Treatment of acute epiglottis?

A

life threatening, need endotracheal intubation and Iv antibiotics

402
Q

How does bordetella pertussis present?

A

whooping cough, chronic cough, occasional vomiting, afebrile, vitals stable

403
Q

What is the trasmission of bordetella pertussis?

A

droplet

404
Q

How long is the incubation of bordetella pertussis?

A

7-10days

405
Q

What are the 3 phases of bordetella pertussis?

A

catarrhal stage, paroxysm stage, convalescent phase

406
Q

At what stage of bordetella pertussis are you highly infectious?

A

cararrhal stage (1-2 weeks)

407
Q

How is bordetella pertussis diagnosed?

A

nasopharyngel swab early in infection, PCR asaay, serology ELISA for IgG against PT

408
Q

What is the treatment of bordetella pertussis?

A

antimicrobials (clarithromycin) and vaccination with acellular pertussis at 2,3, 4 months and 3 years

409
Q

How does croup present?

A

barking cough in children and inspiratory stridor

acute laryngo-tracheobrnchitis due to parainfluenza virus

410
Q

complications of bordetella pertussis?

A

pneumonia, encephalopathy, subconjucntival haemorrhage

411
Q

What medium is used for nasopharyngeal aspriate and swab medium?

A

Bordet Gengou medium (15-80% sensitivity)

412
Q

What is asthma?

A

a common chronic relapsing episodic inflammatory condition of the lung airways

413
Q

What are the main 3 characteristics of asthma?

A

airflow limitation, airway hyperresponsiveness, inflammation on bronchi

414
Q

What is atopy?

A

increased responsiveness of the airways of the lung to stimuli, type 1 hypersensitivity reaction, increased IgE antibodies, runs in the family and linked to other atopic diseases

415
Q

What enviromental factors can affect atopy?

A

hygiene hypothesis, childhood exposure to allergens, maternal smoking, RSV infection

416
Q

pathogensis of asthma?

A

narrowing of the airway due to smooth muscle contraction and thickening of the airway wall by cellular infiltration and inflammation, increased secretions within airway lumen

417
Q

What are the 4 stages of asthma?

A

inflammation, bronchoconstriction, mucus and oedema, and remodelling

418
Q

What is the process of inflammation in asthma?

A

allergen exposure, T helper cells release IL-4, produces IgE, mast cell activation, release histamine causes mucus production, validations and bronchoconstriction

419
Q

What is involved in sustained inflammation in asthma?

A

eosinophils

420
Q

What causes bronchoconstriction in asthma?

A

IgE and histmaine blocks B adrenorectors in the smooth muscles surrounding the airways, causing bronchoconstriction

421
Q

What causes oedema in asthma?

A

increased vascular permeability

422
Q

What causes mucus plugs in asthma?

A

increased bronchial secretions of mucus

423
Q

What 3 things are remodelled in asthma and how?

A

smooth muscle - hypertrophy and hyperplasia
basement membrane - collagen and matrix proteins deposited causing thickening
epithelieum - loss of ciliated columnar cells causes mucus secreting goblet cells

424
Q

Symptoms of asthma?

A

intermittent dyspnoea, wheeze, nocurnal cough, sputum, chest tightness

425
Q

Signs of asthma?

A

tachypnoea, audible wheeze, hyprinflated chest, hyperresonant percussion note, decreased air entry, widespread polyphonic wheeze

426
Q

What will respiratory function tests show in asthma?

A

spirometry - decreased FEV1/FVC (20% on 3 days/week for 2 weeks
exercise test
skin prick tests - identify allergens

427
Q

What are the Royal College of Physicians 3 questions for asthma?

A

have you had difficulty sleeping because of your asthma symptoms?
have you had your usual asthma symptoms during the day?
has your asthma interfered with your usual activities?

428
Q

What are the 5 steps of asthma treatment?

A

1 - occasional SA inhaled B2 agonists (salbutamol) as required for symptoms (move to step 2 if >1/day)
2 - add inhaled corticosteroid (beclomethasone)
3 - add LA B2 agonist (salmeterol)
4 - high dose corticosteroid and leukotriene receptor anatagonist (monteleukast)
5 - add daily oral corticosteroid and continue with inhaled steroids, refer to asthma clinic (prednisolone)

429
Q

When would you move back a step of treatment in asthma?

A

when control is good for >3months

430
Q

What is the long term management of asthma?

A

stop smoking, avoid precipitants, educate on good inhaler technique, PEFR monitoring and self management

431
Q

What is the classification of acute severe asthma?

A

33,92,CHEST

432
Q

What does 33,92 CHEST stand for in asthma management?

A

PEFR

433
Q

What is each severity in asthma based on PEFR%?

A 
mild = >75%
moderate = 25, PR>110)
434
Q

Management for acute severe asthma?

A

O SHIT ME
oxygen, salbutamol nebulised, hydrocortisone IV or oral prednisolone, ipratropium 4-6 hourly

theophylline in ICU, magnesium sulphate one off, escalate care to intubation and ventilation

435
Q

Triggers of asthma?

A

cold air, exercise, allergens, infection, smoking, pollution, NSAIDS, BBs, car fumes, smokes, strong perfume, dusts, stress, emotions, occupational, dust mites

436
Q

examples of obstructive lung disease?

A

COPD, asthma, bronchietasis, cystic fibrosis

437
Q

Examples of restrictive lung diseases?

A

pulmonary fibrosis, pleural effusion, interstitial pneumonias

438
Q

What do respiratory function tests show in restrictive lung diseases?

A

FVC reduced more than FEV1 (though it is still reduced)

FEV1/FVC is normal or >80%

439
Q

How many people in the UK have asthma?

A

5.5 million

440
Q

How many children in the UK have asthma?

A

1/11

441
Q

At what age does asthma commonly present in children?

A

3-5 years

442
Q

After a bronchodilator in asthma, how much improvement is seen in an FEV1 or PEFR?

A

> 15%

443
Q

What is PEFR?

A

peak expiratory flow rate

444
Q

DD of asthma?

A

lower RTI, LVHF, PE, bronchial cancer

445
Q

What questions should be asked in a asthma diagnosis?

A

duration, relieving factors, triggers, blood in sputum, colour of sputum,

446
Q

At what time in the day are asthma symptoms worst?

A

morning and night

447
Q

Risk factors for asthma?

A

FH, atopic conditon, previous bronchiolitis, exposure to smoke, mother smokes in pregnancy, premature birth, low birth weight due to underdeveloped lungs

448
Q

Is a PEFR diagnosis of asthma better for children or adults?

A

adults, children use mainly symptoms for diagnosis

449
Q

What is classed as complete control in asthma?

A

no daytime symptoms, no night time awakening due to asthma, no need for resuce medication, no asthma attack, no exacerbations, no limitations on activities, normal lung function, minimal medication side effects

450
Q

How often should asthma treatment be reviewed?

A

every 6 months

451
Q

Prevention of asthma?

A

smoking cessation, weight loss, breathing exercises, reduce dust levels, breast feeding

452
Q

What is the difference between extrinsic and intrinsic asthma?

A

extrinsic in atopic individuals (type 1 hypersensitivity)

intrinsic starts in middle age from sensitization to occupational agents (type 3 hypersensitivity)

453
Q

What genes are involved in developing asthma?

A

genes that produce IL-3/4/5 as they increase mast cell and eosinophil development and IgE production
polymorphic varitation in IL4-13 proteins
ADAM 33 links to hyperresponsivness and tissue remodelling
CD14, TLRZ, TLR4

454
Q

Where are eosinophils found?

A

bronchial walls and in secretions of asthmatics

455
Q

Is asthma reversible or irreversible?

A

reversible

456
Q

Describe the eicosanoid pathway

A

phospholipid -> arachidonic acid -> prostagladins or leukotrienes

457
Q

what enzyme converts phospholipids to arachidonic acid?

A

phospholipase A2

458
Q

What enzyme converts arachidonic acid to prostagladins?

A

cyclo oxygenase

459
Q

What enzyme converts arachidonic acid to leukotrienes?

A

5-lipoxygenase

460
Q

How long does it take histamine, eicosanoids and cytokines to take effect?

A

histamine = seconds
eicosanoids (lipid derived) = minute
cytokines (protein derived) = hours

461
Q

What happens to the bronchioles in 30mins, 3 hours and 6 hours of asthma?

A

30 mins - bronchoconstriction and inflammation
3 hours - vasodilation, increased vascular permeability, WBC recruitment, less bronchoconstriction
6 hours - worsening inflammation, second wave of bronchoconstriction, eosinophil recruitment, basophils and neutrophils

462
Q

How to B agonists treat asthma?

A

cause bronchodilation, increase cAMP, relax smooth muscle, mast cell stabilization, inhibit histamine release,

463
Q

What kind of protein is a B2 adrenoreceptor?

A

G coupled protein

464
Q

Example of non selective muscuranic antagonist?

A

short acting - ipratropium bromide

long acting - tiotropium

465
Q

How do muscuranic antagonists treat asthma?

A

block ACh binding sites so it can’t activate smooth muscle, preventing bronchoconstriction

466
Q

Where are muscurinic receptors found?

A

resp tract
large airways = M3
peripheral lung tissue = M3 and M1

467
Q

What is COPD?

A

an irreversible airway disease that is progressive and has airway obstruction

468
Q

What do respiratory tests show in COPD?

A

decreased FEV1

469
Q

What is COPD made up of?

A

chronic bronchitis and emphysema

470
Q

What is chronic bronchitis clinically defined as?

A

cough and sputum production on most days for 3 months of 2 successive years

471
Q

What is emphysema histologically defined as?

A

enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls

472
Q

Causes of COPD?

A

genetics - a1 antitrypsin deficiency causing loss of protection against proteases causing alveolar desturction

air pollution

smoking (90%)

exposure through occupation

second hand gas exposure

473
Q

What is the pathophysiology behind COPD?

A

infiltration of the bronchi/bronchiole walls with inflammatory cells, neutrophils and CD8+ lymphocytes or inactivation of a1 antitrypsin by cigarette smoke cuases granulocyte release, elastases and proteases causes ulceration, scarring and columnar cells are replaced by squamous cells. squamous cell metaplasia, fibrosis of bronchial wall and mucus gland hypertrophy, leads to air flow limitation

474
Q

What is chronic bronchitis?

A

hypersecretion of mucus due to marked hypertrophy of mucus secreting glands and hyperplasia of goblet cells.

if small airways are affected its reversible but becomes irreversible as the larger ones become affected

epithelial layer become ulcerated and squamous epithelium may be replaced by coloumnar cells, resulting in increased gas diffusion distance

475
Q

What is emphysema?

A

abnormal dilation of air spaces with destruction of alveolar walls, inflammation and scarring, reducing size of lumen of airways and reducing lung elasticity, hypersecretion of mucus reduces lumen size and increases gas exchange distance

476
Q

symptoms of COPD?

A

cough, sputum, dyspnoea, wheeze

477
Q

signs of COPD?

A

tachypnoea, use of accessory muscles of respiration, hyperinflation, decreased cricosternal disatnce

478
Q

What will imaging show in COPD?

A

normal, or hyperinflated lungs, reduced peripheral lung markings and emphysematous bullae

479
Q

What will Hb be in COPD?

A

may be high due to persistent hypoxaemia and secondary polycythaemia

hypoxia, and hypercapnia if advanced

480
Q

Management of COPD?

A

stop smoking, exercise, weight loss, vaccinations, cardiopulmonary rehlabilitation, broncho pulmonary exercise, caution of flying, steroid trial

481
Q

What are the 5 steps of COPD treatment?

A

1 - pulmonary rehab programme (physio and bronchopulmonary exercises, SABA or antimuscarinics
2 - add LABA and cardiopulmonary rehab
3 - inhale glucocorticoid
4 - anticholinergics and LABA and inhaled steroid
5 - add LTOT and lung surgery

482
Q

Is corticosteroid repsonse better in COPD or asthma?

A

asthma

483
Q

Are night time symptoms more common in asthma or COPD?

A

asthma

484
Q

Does asthma or COPD have a better bronchodilator response?

A

asthma

485
Q

Is asthma or COPD caused by smoking mostly?

A

COPD

486
Q

complications of COPD?

A

cor pulmonale, lung cancer, infection, pneumothorax, polycythaemia, respiratory failure

487
Q

How does smoking cause COPD?

A

it increases neutrophil granulocytes that realease elasteses and proteases causing emphysema, then inactivates a1 antitrypsin and causes mucous gland hypertrophy

488
Q

How does the predicted FEV1 value change from mild to very severe COPD?

A

mild - >80%

moderate -

489
Q

What are the 3 types of emphysema and the difference between them?

A

centri-acinar - damage of lung tissue around the respiratory bronchioles
pan acinar - affects whole acinus, so just becomes a collection bullae - associated with a1-antitrypsin deficiency
irregular - affects lung parenchyma patchily, independent of acinar

490
Q

What does a bullous emphysema cause?

A

gas trapping

491
Q

What questionnaire is used to assess impact of COPD on a patients life?

A

CAT

492
Q

What is the difference between blue bloaters and pink puffers in COPD patients?

A

blue - become insensitive to co2, odematous and cyanosed, not particularly breathless, rely on hypoxic drive

pink - remain responsive to co2 and are breathless but rarely cyanosed

493
Q

Is steroid response better in eosinophil or non eosinophil asthma and why?

A

better in eosinophil as they induce eosinophil death with anti IL-5 which reduces exacerbation and anti Il-3 and anti IgE

494
Q

Where are eosinophils produced?

A

in bone marrow (IL-5)

495
Q

What does an airway biopsy show in non eosinophil asthma?

A

eosinophil abscence and neutrophil prescence

496
Q

What is the best treatment for non eosinophil asthma?

A

bronchodialators and bronchial thermoplasty

497
Q

What are the two types of eosinophil asthma?

A

atopic and non atopic

498
Q

What are the 3 types of non eosiophil asthma?

A

smoking associated, obesity related, non smoking

499
Q

What is reversibility testing in asthma?

A

when there is an increase in lung capacity with bronchodialators or anti inflammatory treatment (20%% improvement in PEFR or 15% in FEV1)

500
Q

What is exhaled NO a marker of?

A

eosinophillic inflammation

501
Q

What are results in moderate asthma?

A

PEFR >50%, RR

502
Q

What are the results in severe asthma?

A

PEFR 33-50%, RR>25, HR >110, cant complete sentences

503
Q

What are the results of life threatening asthma?

A

PEFR

504
Q

In life threatening asthma, what does a raised CO2 mean?

A

fatal

505
Q

When can you discharge a life threatening asthma?

A

PEFR is >75% and

506
Q

How do glucocortisoids treat asthma?

A

intefere with gene transcription, reduce MC activity and improve anti-inflammatory effect

507
Q

What is the effect of GRE?

A

suppression of cytokines and increase lipocortin

508
Q

Side effects of GRE?

A

susceptibility to infection, osteoporosis, muscle wasting

509
Q

How does anti IgE therpy (monoclonal antibodies) treat asthma?

A

binds to free IgE on the Fc region so it cant bind to receptors , can be free or bound e.g. omalizumab - neutralises free IgE and reduces mast cell sensitisation

510
Q

What are anti histamines treatment for?

A

hayfever not asthma

511
Q

What is the best way to give anti histamines?

A

inhaled as straight to the needed place and has reduced side effects

512
Q

At what step in asthma treatment are oral corticosteroids given?

A

step 5

513
Q

When are inhaled corticosteroids given in asthma treatment?

A

step 2

514
Q

How does an oral cysteinyl leukotriene receptor antagonist treat asthma?

A

inhibits cysteinyl LT which is an asthma mediator, used if not controlled by inhaled steroids in step 2

515
Q

When is oral cysteinyl leukotriene receptor antagonist beneficial in asthma treatment?

A

if aspirin intolerant asthma, asthmatic smokers or those who need a higher dose of corticosteroids or have asthma combine rhinitis

516
Q

Management of catastrophic sudden severe asthma?

A

optimise standard therapy, emergency supplies everywhere, 02 resusciatation at home and work, nebulised B2 adrenorecptors agoists, self injectable adrenaline, prednisolone tablets, medic alert bracelet

517
Q

Example of off target immune responses?

A

goodpastures syndrome, myaesthania gravis

518
Q

Example of excessive immune response?

A

ARDS, EAA, asthma

519
Q

Example of failure to control immune activation?

A

a1-antitrypsin deficiency

520
Q

Example of ontarget immune response?

A

bronchiolitis obliterans

521
Q

Example of bystander damage?

A

COPD

522
Q

Example of immunity gone wrong?

A

unclear mechanisms e.g. connective tissue associated ILDs e.g. organizing pneumonia and complications of RA

523
Q

What clues suggest primary immunodeficiency (PID)?

A 
>4 new ear infections/year
>2 serious sinus infections/year
>2 bouts of pneumonia/year
>2 month on antimicrobials/year
growth retardation in children
recurrent deep skin or organ abscesses
persistent mu oral thrush or fungal infection of skin
>2 deep seated infections or septicaemia
family history
524
Q

examples of recurrent respiratory infections?

A

smoking, copd, asthma, bronchietasis, cf, foriegn body, ciliary dysfunction, HIV, immunocompromised, hypogammaglobulinemia

525
Q

What influences the risk of infection in immunodeficient?

A

defect in neutrophil numbers e.g.chemo, duration of neutropenia e.g. in haematological malignancy not solid tumours, duration is long in AML, malignancy e.g. hodgkins lymphoma, steroids or HSCT

526
Q

treatment for fungal infection?

A

targeted and general, fever based, HRCT, galctomannan, salvage therapy

527
Q

What does a focal infiltrate on CXR suggest?

A

bacterial agents of CAP and s.pneumoniae or PCP, Mycobacterial disease, fungal and cancer

528
Q

What does a diffuse infiltrate on CXR suggest?

A

pneumocystis, TB, fungal, viral, CMV

529
Q

What does a cavity on CXR suggest?

A

MTB, bacteria, pseudomonas, s.aureus, dimorphic fungi, malignancy and IVDA

530
Q

What does a nodule and mass on CXR suggest?

A

mainly infectious, mycobacterial, dimorphic fungi, cryptococcomas, KS, granulomata associated with PCP, lymphoma, cancer and septic emboli, s.aureus, aspergillus

531
Q

What microorgansism are in the lower respiratory tract but don’t cause inflammatory damage so are thought to be protective?

A

prevotella, fusobacteria, velonella

532
Q

What is used in the innate immune system of the resp tract?

A

mucosal defences, macrophages, neutrophils

533
Q

What is in the adaptive immune system of the resp tract?

A

B cell antibodies and T cell cytotoxicity

534
Q

What can cause a granulocyte defect and what does this lead to a risk of?

A

chemo and HSCT - risk of invasive infection of gram bacteria, fungal infection and mycobacteria

535
Q

What can cause a B cell defect and what does this increase the risk of?

A

rituximab, haemotological malignancy and CVID - increased risk of encapsulated bacteria and oto-sino-pulmonary infection

536
Q

What can cause a T cell defect and what does this increase the risk of?

A

immunosuppressin, HIV and SCID - increased risk of viral infection, fungal, mucobacteria, pneumocytosis jinovecu pneumonia

537
Q

What can cause a neutrophil defect?

A

chemo, drugs, granulomatous disease

538
Q

What can cause secondary immunodeficiency?

A

immunosuppressant treatment, haemotological malignancies, HIV infection, malnutriton, alcohol, sepsis

539
Q

What organism cause pneumocystic pneumonia?

A

pneumocytis jirovecii

540
Q

How does pneumocystic pneumonia present?

A

6 week progrssive breathlessness and dry cough

lymphopenia (CD4

541
Q

What investigations would you do for pneumocystic pneumonia?

A

induced sputum or BAL for PCR

542
Q

What is the treatment of pneumocystic pneumonia?

A

high dose co-trimoxazole and pentamidine 2nd line, prednisolone if severe, secondary prophylaxis

543
Q

In who is CMV commonly seen?

A

transplant recipients and HIV

544
Q

Treatment of invasive aspergillosis?

A

vonconzole, caspofungin, amphotencin, liposomal amphotencin

545
Q

What causes invasive aspergillosis?

A

fever in neutropaenic patient caused by borad spectrum antibiotics

546
Q

What is Cheyer stokes respiration?

A

alternatin hyper/hypoventilation every 60seconds, severe cariac disease, secondary to slow perfusion of peripheral chemoreceptors

547
Q

What is agonal breathing?

A

pre terminal patients or from opiate poisoning, 4-8 breaths alternate with complete apnoea

548
Q

Causes of hypoventilation?

A

OHS, hypothyroidism, respiratory muscle weakness, post sedation, REM sleep, loop diuretics

549
Q

Causes of hyperventilation?

A

hyperthyroidism, post cortical CVA, liver cirrhosis, metabolic acidosis, anxiety, stress

550
Q

Type 1 respiratory failure symptoms?

A

cyanosis, increased RR (tachypnoea), accesory muscle use, tachycardia, hypotension, signs of underlying disease and confusion

551
Q

Type 2 respiratory failure symptoms?

A

confusion, drowsiness, warm peripheris, flapping tremor, bounding pulses, myoclonic jerks, papilloedema, frequent chest infection due to impaired cough reflex

552
Q

Treatment of respiratory control disturbance?

A

ABC, treat cause, o2 therapy, CPAP, NIVm IPPV

553
Q

When is continuous positive airways pressure used?

A

positive pressure applied throughout respiratory cycle to a spontaneously breathing patient, used in type 1 hypoxic resp failure, to imporve oxygenation, ventilation and V/Q ratios

554
Q

What is used for type 2 resp failure treatment?

A

non invasive ventilation

555
Q

What is transfer factor?

A

the extent to which 02 passes from air sacs to lungs in blood

556
Q

What resp diseases cause a reduction in transfer factor?

A

IPF, PH, anaemia, COPD

557
Q

What is seen radiologically in lobar collapse?

A

triangular opacity with apex at hilum
sickle sign of air around aortic knuckle
loss of right hemidiaphragm
sail sign

558
Q

What is seen in sarcoidosis?

A

heart block, lymph node enlargement, skin nodules, nephrocalcinosis

559
Q

Criteria for home o2 in COPD?

A

pao2

560
Q

What percentage of asthma is thought to be caused by occupation?

A

10%

561
Q

How long is treatment for idiopathic PE?

A

6 months

562
Q

What does antigentic drift cause?

A

epidemic flu

563
Q

Is it strong or weak ions and acids that completely dissociate in water?

A

strong

564
Q

Do strong or weak ions and acids make good buffers and why?

A

weak as they incompletely dissociate in water, but can dissolve so are good buffers

565
Q

What is a buffer?

A

a weak acid or base that can donate or accept H+ ions to allow changes in H+ ion content with little change in free ionised H+ concentration

566
Q

Examples of extracellular buffers?

A

bicarbonate system, phosphates, proteins

567
Q

Example of intracellular buffer?

A

Hb

568
Q

What is base excess?

A

the amount of acid or base required to return 1 litre of blood to normal mean standard bicarbonate of 22.9ntq/L

569
Q

What should the base excess value be?

A

should be in the range of -2 to +2, any more or less is metbolic acidosis or metabolic alkaliosis, averga eis 1.2

570
Q

Where are chemoreceptors found in the body?

A

aortic arch and carotid sinus and ventral surface of medulla

571
Q

how does the respiratory compensatory mechanism work?

A

detect change in CSF pH, a lower pH stimulates respiration

572
Q

How does the metabolic compensatory mechanism work?

A

control of SID by removal of Cl- from extracellular fluid from transcellular pumps and urinary loss in response to acidosis

573
Q

How does an increase in CO2 affect pH?

A

reduces pH

574
Q

How does an increase in HCO3 affect pH?

A

increase pH

575
Q

What is the lass of mass action?

A

the velocity of a reaction is proportional to the product on the concentrations of the reactants

576
Q

Are cations positive or negative?

A

positive (cat purr positive)

Phase 2a (15 decks)

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