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resp conditions Flashcards

1
Q

define Chronic obstructive pulmonary disease (COPD)

what are the 2 main types

A

non-reversible, chronic deterioration in air flow thru. lungs caused by damage 2 tissue

x2 main types- chronic bronchitis, emphysema

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2
Q

list 4 risk factors for COPD

A
  • cigarettes/smoking
  • air pollution
  • genetic- A1AT
  • miners/coal workers
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3
Q

name 2 organisms that cause infective exacerbations of COPD

A
  1. H. influenza
  2. S. pneumonia

Abx= amoxicillin

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4
Q

describe chronic bronchitis + 3 presentations of it

A

daily cough w. sputum for 3+ months in @ least 2 consecutive years

  • hypertrophy + hyperplasia of mucous glands
  • chronic inflammation in bronchi + bronchioles = luminal narrowing
  • mucus hypersecretion, ciliary dysfunction, narrowed lumen
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5
Q

describe emphysema

A

destruction of elastin layer in alveolar ducts/sacs/resp bronchioles
- infammation + scarring= reduction in air flow + reduction in SA of aveoli

panacinar emphysema= A1AT def

centriacinar emphysema= smokers

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6
Q

typical presentation of Px with COPD

A

typically older patient w. chronic cough & purlulent sputum
+ extensive smoking history ( or A1AT)
+ SOB, cough, wheeze, recurrent resp infections
+ barrel chest/hyperinflation

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7
Q

describe ‘blue bloater’

chronic bronchtitis

A

cyanosis
chronic productive cough
purluent sputum
dyspnoea
peripheral oedema
obesity
recurrent chest infections

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8
Q

describe ‘pink puffer’

emphysema

A

minimal cough
pursed lip breathing
dyspnoea
accessory muscle breathing
cachexia (body/musc wasting)
barrel chest + hyperesonat precussion

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9
Q

investigations for COPD

A
  1. spirometry- FEV1/FEV <0.7= obstruction
  2. DLCO- diffuse capacity of CO across lung > COPD= low
  3. CXR- hyperinflation + exclude other causes eg cancer
  4. ABG- may show T2 resp failure
  5. genetic test for A1AT

**GOLD= clinical presentation + spirometry
bronchodilator irreversible (<12%) = COPD

bronchodilator reversible >12% = asthma

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10
Q

what can be used to guage the severity of COPD

A

MRC dyspnoea grading scale 1-5
1=breathless on strenuous excercise
5= cant leave home due 2 breathlessness

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11
Q

managment of COPD

1st,2nd,3rd

A

smoking cessaation + vaccines (pneumococcal vax + annual flu vax)

long term management=
1st. SABA (salbutamol) or SAMA (ipratropium bromide)

2nd. SABA + LABA (salmeterol) + LAMA (tiotropium bromide)

3rd. SABA + LABA + LAMA + ICS

consider long-term O2 therapy if severe sats <88%

maintain O2 88-92%

SABA= short-acting beta antagonist
SAMA= short-acting muscarinic antagonist
LABA= long-acting beta antagonist
LAMA= long-acting muscarinic antagonist

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12
Q

define asthma

A

chronic inflammatory condition caused by episodes of bronchoconstriction and mucus hypersecretion in response to triggers

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13
Q

list 6 things that can trigger asthma

A

cold air
excercise
allergens (cats, dust, pollen)
drugs (BB, ACEi,)
cigarette smoke
air pollution

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14
Q

what type of sensitivity is allergic asthma and what is mediated by

A

allergic (70% of asthma)
IgE mediated,, T1 hpersensitivity due 2 enviromental triggers

non- allergic = 30%- non IgE mediated (intrinsic)

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15
Q

what does IgE mast cell degranulation result in the releasing of

A

histamines
leukotrienes
tryptase
raised EOSINOPHILS

this causes bronchial constriction and mucus hypersecretion

ATPOPIC triad= (allergic rhinitis, atopic eczema and asthma)

chronic remodelling and mucus hypersecretion

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16
Q

presentations of asthma

A

episodes of:
* widespread polyphonic wheeze
* breathlessness
* chest tightness
* DRY cough
* usually worse @ night (diurnal variation)

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17
Q

investigations for asthma

A

PULMONARY FUNCTION TESTS!

Pathway as follows:

Fraction expired nitrous oxide (feNO) = raised (non specific in lung damage)

Then do Spirometry = FEV1:FVC less than 0.7 (obstruction)

Then do bronchodilator reversibility- >12% increase in FEV1 = reversible

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18
Q

how would you manage episodic/chronic asthma

episodic algorithm

A
  1. SABA (salbutamol)
  2. SABA + ICS (budesonide)
  3. SABA + ICS + LTRA (montelukast)
  4. SABA + ICS + LABA (salmeterol) +/- LTRA
  5. increase ICS dose
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19
Q

how would you manage acute exacerbations of asthma

A

OSHITME

Oxygen
SABA
HYDROCORTISONE (ICS)
IPRATROPIUM BROMIDE
THEOPHYLINE
MgSO4
Escalate care (BiPAP)

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20
Q

describe T1 resp failure

associated conditions? O2 and CO2? spirometry?

A

restrictive
-problem getting air in due 2 scarring

causes= (ILDs) pulmonary fibrosis, sarcoidosis, good pasture’s

low O2, normal CO2
FVC <0.8

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21
Q

describe T2 resp failure

associated conditions? O2 and CO2? spirometry?

A

problems getting air out
-more mucus + lumen blockage

causes= COPD, asthma, bronchiectasis

low O2, raised CO2

FEV1:FVC <0.7

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22
Q

what is mesothelioma

common exam presentation

A

lung cancer- plueral malignancy which affects pluera (and peritoneum)

male 40-70 w. ASBESTOS EXPOSURE DECADES AGO (long latent period)

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23
Q

presentation of mesothelioma

A

lung Sx= SOB, chest pain, constant cough + haemoptysis

recurrent laryngeal nerve compression= hoarse voice
bone pain

systemic Sxs=TATT, night sweats, wt.loss, rigors

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24
Q

investigations and managemnt for mesothelioma

A

1st= imaging (CXR then CT)= pluerall thickening +/- effusion

GOLD= biopsy

CA-125 may be raised non specifically

Tx= v. aggresive tumour- purely palliative

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25
where does small cell lung cancer occur and who is affected
central resp system (bronchi) -small cells w. minimal cytoplasm on biopsy **SMOKERS** exclusively affected
26
presentation of small cell lung cancers
lung Sx= cough w. haemoptysis, SOB, recurrent chest pain systemic (constitutional Sxs) compression Sx | **paraneoplastic syndromes**
27
investigations and management of small cell lung cancers
1st= imaging (CXR then CT GOLD= bronchoscopy then biopsy v, early - can try chemo/radio - often just palliative
28
describe 5 neoplastic syndromes caused by small cell caricinomas
1. SIADH= hyponatraemia 2. raised ACTH= cushing's 3. carcinoid= flushing + diarrhoea 4. lamberton eaton syndrome 5. SVC syndrome (pemberton's sign)
29
list 3 non-small cell lung cancers
squamous cell carcinoma adenocarcinoma carcinoid tumour
30
where do squamous cell carcinomas arise from, how does it present and who is most commonly affected
lung epithelium mainly affects **smokers** Lung Sx constitutional Sx compression Sx PARANEOPLASTIC SYNDROME = **PTHrP** metastises late
31
investigations and management of squamous cell carcinomas
1st= imaging (CXR then CT) GOLD= bronchoscopy + biopsy TNM staging surgical excision, mets= chemo/radio less aggresive than SCLC
32
where do adenocarcinomas arise from and what is a major risk facotr
arise from mucous secreting glandular epithelium RF= ASBESTOS EXPOSURE
33
presentation of NSCLC adenocarcinomas + what are they closely related to
Lung Sx; Constitutional Sx, Compression Sx, Metastasises common Adenocarcinoma NSCLC is also closely related to HYPERTROPHIC PULMONARY OSTEOARTHROPATHY → Triad of clubbing, arthritis and long bone swelling
34
investigations and managment for NSCLC adenocarcinomas
1st = Imaging (CXR then CT) GS = Bronchoscopy + biopsy TNM staging surgical excision, if mets- radio/chemo relatively treatable
35
what can compression of the sympathetic chain (T1-L2)in resp tumours cause
ipsilateral **horner's syndrome** * miosis * ptosis * anhidrosis * right arm weakness
36
what does pembertons sign look like and what does it indicate
raise arms above head + facial flushing = pemberton's sign -shows SVC obstruction due to compression
37
what is mean pulmonary arterial pressure above in pulmonary HTN + give 4 causes
resting mPAP= >25mmHg severe= 55+ causes= * precapillary=primary pulmonary HTN, PE * capillary= COPD, asthma * post capillary= LV failure * chronic hypoxemia= COPD, high altitude
38
presentation of pulmonary HTN | what happens
reactive pulmonary vasoconstriction responding to hypoxemia= RVH + resp failure * exertional dyspnoea + fatigue 1st then * RV failure= raised JVP, periphera oedema
39
investigations for pulmonary HTN
DIAGNOSTIC= RH catheter (directly measure pressure) CXR= RVH ECG= evidence of RA dilation (peaked p waves)
40
management of pulmonary HTN + a comp
phosphodiesterase 5 inhibitor- sildenafil (viagra) CCB- amilodipdine prostaglandin analogues comp= COR PULMONALE
41
define goodpasture's + common presentation | 3 rfs
T2 hypersensitivity response resulting in pulmonary + renal pathology EXAM= HAEMOPTYSIS + HAEMATURIA (aka coughing and pissing blood simultaneously) | HLA DR15, smoking, asbestos
42
name antibodies in goodpasture's + what they do
**ANTI-GBM antibodies**- attack basement membranes of alveoli + glomeruli- nephritic syndrome & alveolar haemorrhage
43
presentation+ investigationm + managment for good pasture's
lung= cough, haemoptysis, chest pain renal= haematuria, HTN, oedema Dx= serology: **anti-GBM antibodies positive** lung + kidney biopsy= Ig complex formation | Tx= prednisolone + plasma exchange
44
describe how TB is spread
TB spread via resp droplets (airborne infection) 1. alveolar macrophages ingest bacteria- BUT resistant bacteria resist being killed > granuloma forms 2. T cells cause necrosis to central part of granuloma= **caseating granuloma (primary ghon focus)** 3. ghon focus spreads to nearby lymph nodes= **ghon complex** 4. if TB spreads systemically= miliary TB 5. most often contained within granuloma= latent TB
45
describe the bacteria involved in Tuberculosis
mycobacterium infection aerobic, non-motile, non-sporing slow growing bacilli w. thick waxy capsule acid-fast bacilli- turns r**ed/pink Ziehl- neelsen stain** **resitant to phagolysosomal killing** Africa/S. asia
46
systemic + pulmonary presentations of TB
systemic= wt. loss, low grade fever, night sweats, malaise pulmonary= productive cough, haemoptysis, cough 3weeks +, SOB
47
investigations for TB | + Ix for latent TB
CXR sputum culture for acid-fast bacili= Ziehl-Neelsen stain turns red/pink biopsy= caseating granuloma | latent= tuberculin skin test 'mantoux' interferon gamma release assay
48
describe the 3 kinds of pneumonia
* community acquired= outside hospital enviroment * hospital acquired= after @ least 48hrs in hosptial + not intubated on admission * atypical= caused by atypical organisms not detectable by gram stain | pnuemonia= inflammation of air sacs in lungs caused by infection
49
managment of TB
RIPE Rifampicin x6months Isoniazid x6months Pyrazinamide x2 months Ethambutol x2 months ## Footnote SE= rifampicin- haematuria isoniazid- peripheral neuropathy pyrazinamide- hepatitis, gout ethambutol- optic neuritis
50
list 4 organisms causing community accquired pnuemonia
streptococcus s.pneumoniae H.influenzae haemophilius
51
list 4 organisms causing hospital acquired pneumonia
psuedomonas aeruginosa E.coli S.aureus klebsiella
52
which organism causes pnuemonia in immunocompromised/HIV
(pneumocystis jirovecii) PCP
53
name 2 organisms that cause atypical pneumonia
mycoplasma pneumoniae legionella pneumophila
54
a. which organism is likely to cause pneumonia associated with water cooler/air conditioner
legionella
55
presentations of pneumonia
symptoms= cough, SOB, fever, pluertic chest pain signs= raised RR + HR low BP + O2 sats dull to precuss ## Footnote auscultation= wheezing, coarse crackles, bronchial breath sounds, increased vocal resonance
56
investigations for pneumonia
FBC= elevated WCC sputum culture 2 ID organism CXR= **localised/widespread consolidation** effusion
57
describe the scoring system used for pneumonia
CURB-65 Confusion Urea >7mmol/L resp >30 BP= <90 systolic, <60 diastolic | 1 point for each ## Footnote 0-1= home treatment 2= short stay inpatient/closely monitored outpatient 3+ =hospital inpatient
58
management of pneumonia
using CURB-65 0-1= oral amoxicillin 2= amoxicillin + clarithromycin 3+ = IV co-amoxiclav + clarithromycin | maintain O2 sats btwn 94-98% analgesia= paracetamol/NSAIDs IV fluids
59
what is plueral effusion and describe the 2 causes
plueral effusion= collection of fluid btwn. parietal and visceral pluera of plueral cavity **transudative**= fluid shift due to increase in hydrostatic/oncotic pressure (fluid overload, hypoalbuminemia, nephrotic syndrome) **LOW PROTEIN COUNT** **exudative**= inflammation causes fluid + protein to leak into plueral space **HIGH PROTEIN COUNT**
60
presentations of plueral effusion
* SOB + cough * dull precussion over effusion * tracheal deviation away from effusion
61
investigations for plueral effusion
1st= CXR> blunting of costophrenic angles plueral USS thoracocentesis ID + Dx underlying cause
62
managent of plueral effusion
usually dependent on cause * heart failure- loop diuretics * infective- Abxs * malignant- therapeutic thoracentesis * large effusions= chest drain @ 5th intercostal space
63
define a pneumothorax | list types
air in plueral space causing lungs to collapse - plueral space= normally vaccum (negative intraplueral pressure) | spontaneous, tension ## Footnote also: traumatic, latrogenic, lung pathology
64
what is the typical patient with a pneumothorax
tall, thin male with connective tissue disorder, smoker and has some kind of trauma
65
presentation of a pneumothorax
symptoms= SOB, one sided sharp plueritic chest pain signs= **hyperresonant percussion note ipsilaterally** + reduced breathing sounds
66
investigations for a pneumothorax
1st + GOLD= CXR * absent lung markings * affected area darker than normal * tracheal deviation to opposite side
67
managment of a pneumothorax
Small PTX with no SOB = consider discharge and follow up CXR Larger PTX and/or SOB = **needle aspiration** or **chest drain** (more of a longer term Tx) Recurrent = surgical management - pleurodesis
68
describe a tension pneumothorax
one way valve mechanism- air can flow into plueral space but can't leave -pressure increases w. each breath
69
presentation and treatment of a tension pneumothorax
* hypotension * resp distress * low sats * tachycardia * shock * severe chest pain Tx= insert large bore cannula into plueral space @ 2nd intercostal space, midcalvicular line
70
describe the mutation that occurs in cystic fibrosis
autorecessive mutation on chromosome 7- codes for **CFTR protein** | RFs= FHx + white
71
describe the normal function of CFTR and what a defecit of it causes
CFTR normally secretes Cl- & Na + into ductal secretions > makes them thin and watery defect= ductal secretions are thicker w. Na + & Cl - retention >impared mucocillary clearance = stagnation of mucus= increased infection risk + difficulty breathing
72
presentations of cystic fibrosis | resp, neonates, GI, other
* Resp= recurrent infections, bronchiectasis * Neonates= jaundice, failure to thrive, bowel obstruction (meconium ileus) * GI= bowel obstruction, steatorrhea * other= male infertility, DM
73
investigations for cystic fibrosis
newborn= heel prick test older= sweat test > high chloride (+60) reduced elastase FHx + genetic testing
74
management of cystic fibrosis
MDT approach: chest physio & postural drainage, high calorie, high fat diet, minimise contact with ill people + others with CF, pancreatic supplmentation | comp= bronchiectasis
75
define bronchiectasis | including causes
permanent dilation of the airways -irreversible dilation, loss of cilia, mucus hypersecretion | causes= CF, lung cancer
76
presentation and investigations for bronchiectasis
Sx= dyspnoea, cough, haemoptysis, recurrent chest infections Dx= CXR= **kerley B lines, SIGNET RING SIGN** (bronchioles dilated + appear thicker than adjacent pulmonary artery sputum culture- H. influenzae mc. GOLD= **HRCT= dilated thickened bronchi** spirometry= FEV1: FVC <0.7 | Tx= non-curative chest physio + bronchodilators + prohylactic Abxs
77
name 5 different types of interstitilal lung disease
1. idiopathic pulmonary fibrosis 2. sarcoidosis 3. hypersensitivity pneumitis 4. good pastures 5. wegner's granulomatis | ILD= umbrella term for lung pathology that causes lung fibrosis
78
describe idiopathic pulmonary fibrosis
formation of scar tissue with no known cause -seen in older men who **smoke** | Rfs= smoking, occupational (dust), drugs (methotrexate), EBV, CMV ## Footnote progressive scarring = T1 resp failure
79
presentation and investigations for idiopathic pulmonary fibrosis
dyspnoea, dry cough, bibasal crackles Pulmonary Fibrosis: 3 C’s = Cynosis, Cough, Clubbing Dx= spirometry= restrictive lung disease **FVC <0.8** GOLD= HRCT > **GROUND GLASS appearance of lungs**
80
management of interstitial lung disease
pirfenidone, nintedanib non-pharm= smoking cessation, physio, vax | last resort= lung transplant
81
describe sarcoidosis | who does it noramlly affect
idiopathic autoimmune granulomatous disease | 20-40 y/o black women
82
presentation of sarcoidosis
**LUPUS PERNIO- purple rash/nodules on cheeks and shins** * fever * fatigue * dry cough * dyspnoea * uveitis | early= self resolving sympto= corticosteroids
83
describe hypersensitivity pneumonitis | type of hypersensitivity + rfs
T3 hypersensitivity (ab-ag complex deposition)= causes alveolar + bronchial inflammation after exposure to inhaled antigen | Rfs= farming keeping **BIRDS**
84
presentation + investigations + management of hypersensitivity pneumonitits
dyspnoea, cough, fever, malaise, wt. loss Dx= Hx + examination serum IgG positive -CXR= patchy nodular infiltrates CT= ground glass shadowing | Tx= remove allergen + prednisolone
85
what are the ABCDEF respiratory causes of clubbing
Respiratory Causes of Clubbing: ABCDEF Lung Abscess Bronchiectasis Cystic Fibrosis / Cancer Decreased oxygen (hypoxia) Empyema Pulmonary Fibrosis

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