resp top tier Flashcards
is primary or secondary lung cancer more common
secondary
gender association with lung cancer
m >f
risk factors for lung cancer
Smoking inc passive Urban areas Asbestos Chromium Arsenic Coal Ionising radiation Genetic risk HIV Pre-existing lung disease
types of lung cancer
non- small cell carcinoma (main)
- squamous
- adenocarcinoma
- large cell
- carcinoid tumour
small cell carcinoma
where is lung cancer located
mainly bronchial , sometimes pleura
squamous non-small cell carcinoma
- how does it present
- spread?
- as obstructive lesion –> infection
- local spread common. metastases widespread but relatively late
adenocarcinoma (non-small cell carcinoma) is strongly associated with what
asbestos
small cell carcinoma
- arises from what
- secretes what
- growth/ prognosis
- endocrine cells - kulchitsky cells
- secrete polypeptides and amines which act as hormones or neurotransmitters
- Grow rapidly , with widespread metastases. Highly malignant – frequently inoperable at presentation (poor prognosis)
presentation of lung cancer
Cough Chest pain Haemoptysis (Red flag) Dyspnoea , breathlessness, wheeze Recurrent infection finger clubbing weight loss anaemia nodes headaches
spread of lung cancer and associated symtpoms
- brachial plexus - shoulder/arm pain
- bone - pain and fractures
- sympathetic ganglion - horner’s syndrome (eyes)
- brain - seizures, neurological deficit, headaches
- abdominal pain
- left recurrent laryngeal nerve - hoarse voice
investigations of lung cancer
CXR
- round fluffy / spiking shadow
- hilar enlargement (medial of each lung)
- Consolidation (= filled with fluid rather than air so is no longer compressible. Appears white)
- lung collapse
- pleural effusion
CT/PET - for staging
Bronchoscopy- Biopsy and assess operability
Sputum biopsy
Pleural fluid biopsy
Bloods - FBC low
non small cell carcinoma management
Surgery- can be curative (if no metastatic spread)
Chemo (downstages tumours to render them operable. Advanced disease. or post op
Radiotherapy (good for localised squamous cancers. Advanced disease. Or post op
Stop smoking
Remove carcinogens
small cell carcinoma management
chemo
Limited disease = Chemo-radio combo
Extensive disease = chemo
what sort of symptom relief / palliative care can you think of that would benefit lung cancer
- corticosteroid (dexamethasone) for superior vena cava obstruction
- Analgesia
- Antiemetics
- Bronchodilators
- Antidepressants
- tracheal stenting
- cryotherapy
treatment for PE- short and long term
Immediate - depends on patient condition/signs
- Oxygen if hypoxic
- Morphine + antiemetic for pain/ distress
- IV LMW heparin - anticoagulant
- IV fluid for hypotension
- Call ICU
- Consider thrombolysis if hemodynamically unstable
Long term
- LMW heparin
- Anticoagulants - DOAC or warfarin
PE investigations
Bloods
- FBC
- U/E
- ** D-dimer = +
- Baseline clotting
- ** Troponin levels = raised due to impact on right heart
ABG (decreased PaCO2 and PaO2)
** CT pulmonary angiography (specific, sensitive)
CXR (may be normal. May have dilated pulmonary artery / oligaemia (decreased blood flow through certain segment)
ECG - normal /tachy / RV strain / RBBB
If no other risk factors, consider underlying malignancy
symptoms of PE
Acute breathlessness Pleuritic chest pain Haemoptysis Dizzy Syncope Calf pain
signs of PE
- Pyrexia (Fever)
- Cyanosis
- Tachypnoea
- Tachycardia
- Hypotension
Raised JVP
Pleural rub
Pleural effusion
Tender hard calf
pathophysiology of PE - the two types
inc cause
cause usually = venous thrombi (DVT)
Big
- Embolus obstructs R ventricular outflow (on way to lungs) - but doesn’t block it i don’t think
- Pulmonary vascular resistance increases suddenly
- Causing acute right sided heart failure
Small embolus
- Blocks terminal peripheral pulmonary vessel
- May not notice unless causes pulmonary infarction
- Lung tissue ventilated but not perfused (V/Q mismatch)- impaired gas exchange
risk factors for PE
- DVT
- Previous PE
- Thrombophilia
- Recent surgery - esp abdominal, pelvic, hip replacement, knee replacement
- Malignancy (If not other risk factors, consider underlying malignancy )
- Pregnancy / post partum
- Immobilisation eg leg fracture
- Combined oestrogen pill / hormone replacement therapy
COPD complications
- Respiratory failure
- Recurrent infections
- Pulmonary hypertension → cor pulmonale - enlargement of R heart (heart failure)
- lung carcinoma
COPD management
Smoking cessation - slows deterioration
Avoid infections
Exercise
Bronchodilators = short/long acting beta agonists /muscarinic antagonists:
- 1st line= SABA/SAMA
- 2nd line= LABA/LAMA
- 3rd line= LABA/LAMA + corticosteroid (inhaled/systemic)
- 4th line= LABA + LAMA + corticosteroid (inhaled/systemic)
- 5th line= long term oxygen therapy – Need to be careful not to remove the hypoxic drive in blue bloaters
Ventilation
Surgery - lung transplant
investigations into COPD
- ECG - RV/RA hypertrophy
- ABG - reduced oxygen
Spirometry
= gold standard.
– FEV1/FVC<70%,
– FEV1<80% of predicted
CXR
- > 6 ribs visible
- Hyperinflation
- flattened diaphragm
- -Large central pulmonary arteries
- Decreased peripheral vascular markings
CT
- Bronchial wall thickening
- Scarring
- Air space enlargement (dark areas)
symptoms of COPD
Increased sputum production Chronic cough Shortness of breath, dyspnoea Low moor, tired, lethargic Weight loss
Signs of COPD
Barrel shaped chest - hyperinflation Ankle swelling Tachypnoea Expiratory wheeze Use of accessory muscles of respiration eg may lean forward Decreased expansion Expiration through pursed lips (prevents alveolar and airway collapse) Quiet breathing sounds Cyanosis (if chronic bronchitis)
two appearances of COPD
BLUE BLOATER
- chronic bronchitis
- capillary bed not damaged
- compensatory increase in CO and decrease in ventilation leads to hypoxia (blue). Obstruction causes increasing residual lung volume (bloating)
PINK PUFFER
- emphysema
- damages capillary bed
- compensatory hyperventilation (puffing) prevents hypoxia. Lack of cyanosis (pink)
two types of COPD (diseases)
CHRONIC BRONCHITIS
- Airway narrows due to:
- – Hypertrophy and hyperplasia of mucus secreting glands in bronchial tree
- –Bronchial wall inflammation
- –Mucosal oedema - increase in mucus in airway lumen
- Blue bloaters → compensatory increase in CO and decrease in ventilation leads to hypoxia (blue). Obstruction causes increasing residual lung volume (bloating). (no capillary bed damage)
EMPHYSEMA
- Lung tissues distal to terminal bronchioles (alveoli) is destroyed : smoking → inflammatory factors released that break collagen and elastin down→ loss of elastic recoil → these collapse following expiration - air trapped.
- This also causes damage to capillary bed → inability to oxygenate → hyperventilation
- Pink puffers → compensatory hyperventilation (puffing) prevents hypoxia. Lack of cyanosis (pink)
what type of respiratory failure is associated with COPD
Air cannot leave lungs due to obstruction → type 2 respiratory failure (CO2 high, O2 low)
describe COPD nature
Usually progressive, poorly reversible
Persistent inflammatory response
obstructive disease - limits airflow
causes of COPD
Inflammation caused by
- -Smoking
- -Previous infection
- -Environmental dust
- -Fumes , pollution
Alpha 1 anti-trypsin deficiency - (more common cause in younger people)
what is Alpha 1 anti-trypsin deficiency
- AAT is a protease inhibitor
- It protects tissues from inflammatory enzymes (break elastase down causing elastic recoil loss in emphysema)
- Deficiency = more susceptible to damage from smoke
- Liver also affected
COPD
- age
- gender
- lifestyle
Rare under 35
Smokers
m>f
what put you at higher risk of asthma death
- > 3 classes of treatment
- Recent admission to hospital / frequent attender
- Previous near fatal attack
- Brittle asthma disease (type 1, chronic and sever, type 2 , sudden dips)
- Psychosocial factors
complications of asthma
Pneumonia
Pneumothorax - collapsed lung
Asthma death
immediate treatment of asthma attack
- oxygen
- salbutamol nebuliser
- steroids
- ABG, CXR
- Monitor response to treatment
- if deterioration, ITU
- discharge with asthma action plan, prednisolone, nurse/GP follow up soon and education to prevent readmission
asthma
non pharmacological management
possible surgical treatments
- Avoid triggers and allergens inc occupationally
- Quit smoking
- Weight loss
- Record PEF twice a day
- Education on self management
Bronchial thermoplasty
Lung transplant
asthma pharmacological treatment
Bronchodilators
- treats symptoms, not disease
- Mainly for non-eosinophilic
- Short acting used before long acting (depends on disease severity)
- –Beta agonists - salbutamol
- –Theophyllines
- –Long acting beta agonists - salmeterol
- –Anticholinergics (antimuscarinic bronchodilators) - ipratropium, tiotropium
- –Leukotriene receptor antagonists = montelukast
Anti-inflammatory
- reduce airway inflammation
- decreases mortality
- Steroids - beclomethasone
Biologics
- Anti IgE - omalizumab - for atopic disease
- Anti IL5 - mepolizumab - IL5 needed to make eosinophils
steroids for asthma
- route that is best
- how to stop and why
- name 4 side effects
- inhaled
- need to wean off due to adrenal suppression
- Diabetes, cataracts, osteoporosis, hypertension, skin thinning, easy bruising, growth retardation, osteonecrosis of femoral head, hoarse voice, oral candida
bronchodilators
- treats symptoms or disease
- what type are they for mainly
- which are used for less severity?
- name 3 examples of types
- treats symptoms, not disease
- Mainly for non-eosinophilic
- Short acting used before long acting (depends on disease severity)
- short/ long acting beta agonists, theophyllines, anticholinergics, antimuscarinics, leukotriene receptor antagonists
asthma lung tests
Spirometry / peak flow
- Reduced FEV1
- FEV1/FVC <70%
- PEFR (peak expiratory flow rate) reduced more than expected
- Variability (>20% change 3/7 days)
Exhaled nitric oxide
- FENO (fraction of exhaled nitric oxide) - gives information about eosinophils in lung
Reversibility testing
- Before and after medication taken
Peak flow meter taken home
- Keep diary of PEFR
- Diurnal variation!
non- lung tests for asthma investigation
examination -- may be normal as it is episodic -- wheeze -- no crackles/sputum -- hyperinflated barrel chest Blood count (eosinophils) Culture Sputum culture Atopy and allergy test CXR
asthma presentation
- Episodic audible wheeze
- Cough
- SOB, intermittent dyspnoea
- Chest tightness
- Diurnal variation (during day)– worse in morning
- Symptoms relieve after aspirin / beta blocker
- Hyperinflated chest (‘barrel’)
- Tachypnoea
how do you grade severe asthma
1 major + 2 minor
Major
Treatment with continuous / near continous oral steroids / requirement for high dose inhaled steroids
Minor Additional daily reliever medication Beta agonists, theophylline, LTRA Symptoms needing reliever medication on daily / near daily basis Persistent airway obstruction (FEV1=20%) >1 emergency visit per annum >3 steroid courses per annum Prompt deterioration with 25% reduction in oral / inhaled steroid dose Near fatal event in the past§
types of asthma
eosinophilic / non eosinophilic
also
atopic (Extrinsic) / nonatopic (intrinsic)
eosinophilic vs non eosinophilic
eosinophilic
- associated with allergy
- Triggers cause inflammatory cascade in bronchial tree
- T cells recruit eosinophils which then cause damage to the epithelium
- Mast cells, eosinophils, T lymphocytes and dendritic cells increase in the bronchial wall and membranes
non eosinophilic
- later onset
- related to smoking and obesity
- neutrophils rather than eosinophils
- less understood
asthma pathophysiology
- Airflow limitation (reversible but may be chronic - due to remodelling and mucus impaction)- due to obstruction
- IgE causes mast cells to degranulate and release histamine –> Narrowed due to smooth muscle contraction- bronchospasm as a result
- Excessive secretions into lumen also obstruct
- Deposition of collagen and matrix proteins (as a result of inflammation) causes remodelling of airways inc an increased number of goblet cells
- Airway hyperresponsiveness to range of stimuli
- Hypersensitivity type 1 reaction
- IgE produced against stimuli
- Inflammation of bronchi
- Inflammation and cellular infiltration causes airway wall thickening
- -Secretions into lumen as a result
what differentiates asthma from COPD
COPD has less diurnal variation More progresseive SOB (Has wheeze) Sputum production Winter symptoms
what does fibrosis have that differentiates it from other stuff like asthma
fibrosis has crackles (v distinctive of fibrosis)
non -allergic asthma (intrinsic) causes
Stress
Cold air
infection
provoking factors of asthma attack
Allergens Infections Menstrual cycle Exercise Cold air Laughter / emotion Trauma Stress Some medications - NSAIDs, B blockers
pneumonia treatment
O2 maintained Analgesia Smoking cessation Antibiotics - Empirically then MC+S guided - CAP --- Mild = amoxicillin --- Moderate/severe = amoxicillin + clarithromycin --- Legionella = fluoroquinolone + clarithromycin (Do not respond to penicillin as they lack cell wall) -HAP = aminoglycoside + penicillin
pneumonia investigations
Culture
- Sputum
- Blood
- Urine - inc antigen test
- Pleural fluid – thoracentesis
Blood - FBC - elevated WCC - ESR/CRP raised - ABG, U/E, LFT for severity serology
CXR
- Consolidation = filled with fluid, rather than air
- Extent, severity
- Listen to chest
CURB65
- Asseses pneumonia severity – monitor/hospitalise
- Confusion, urea, RR, BP, age
pneumonia symptoms
Common Pain Chest Pleuritic Cough Rusty / green coloured sputum = strep pneumonia May be purulent sputum Breathlessness Fatigue
Also - if these symptoms predominate = ‘atypical pneumonia’ Myalgia Arthralgia Headache Night sweats Rigors Malaise Anorexia
pneumonia signs
Fever Consolidation -dullness to percussion -Bronchial breathing Drop in BP Increased RR Raised HR Cyanosis Confusion
pneumonia types
CAP (Community)
- No underlying immunosuppression/ malignancy
- May be primary or secondary to underlying disease
- Local or diffuse infection
- may be atypical (different causative organisms and more prominent extra-pulmonary presentation)
HAP (hospital)
- Purulent sputum
- Post admission 48h - 3months
pneumonia pathophysiology
Spread by respiratory droplets Bacteria multiplies in lungs Acute inflammation Intense infiltration of neutrophils in and around alveoli and terminal bronchioles Fluid collects in the lungs
pneumonia causes
CAP = community acquired - Most common ---Main = strep pneumoniae --- Haemophilus influenzae --- Staph aureus --- Klebsiella pneumoniae - Atypical --- Slower onset --- More prominent extra-pulmonary symptoms and complications --- Legionella pneumophila Mycoplasma pneumoniae Chlamydophila pneumonia
HAP= hospital acquired
- Early onset = same as CAP
- Late onset
- –MRSA
- –Klebsiella pneumoniae
- –Pseudomonas aeruginosa
Aspiration
- inhaled foreign objects that can bring bacteria into the airways
- Gastric contents inhaled
Can be from virus/ fungi but this is rarer
pneumonia risk factors
- Infants
- Eldely
- Smoking
- Existing conditions
- – COPD and other chronic lung conditions- CF
- – CV disease, congestive heart disease
- – Immunocompromised inc HIV
- –Diabetics
- Nursing home residents
- Impaired swallowing
- Alcoholics and IV drug users
prevention of TB
Active case finding of patient contacts - reduce infectivity
Vaccination - BCG (variable efficacy so not offered routinely)
treatment of TB
Notify public health Contact tracing 6 months of treatment. 9 if spread to bone. 12 if spread to CNS - Rifampicin 6months - Isoniazid 6 months - Pyrazinamide first 2 months - Ethambutol first 2 months (RIPE)
TB investigations
CXR
- pleural effusion,
- typical / patchy/ nodular shadow,
- Gohn complex (small calcified nodule)
- Consolidation
- Fibrosis
Blood/sputum serology
- Bronchoscopy lavage if no sputum available
- Ziehl neelsen stain for acid fast bacilli
- Used for mycobacteria . goes RED/PINK
- Caseating granuloma*
Nucleic acid amplification – distinguishes causative mycobacteria
- Miliary – lumbar puncture due to high rate spreading to meninges
- Latent
- – tuberculin skin test (mantoux)- wont pick up miliary/ immunosuppressed
- –Interferon gamma release assays - more accurate (picks up exposure, not active infection)
TB main symptoms
primary = milder/ asymptomatic
Anorexia Fatigue Weight loss Fever Night sweats Cough Haemoptysis Breathlessness
extrapulmonary TB symptoms (spread)
Bone pain/ swelling Ascites Lymph node swelling frequency/ haematuria, dysuria Meningeal inflammation - raised ICP May be hoarse voice/ pleuritic pain depending on involvement of laryngeal / pleura
TB pathophysiology
- Organisms inhaled
- Majority of bacteria killed- engulfed by macrophages and stored in granulomas (local granuloma formation). - Macrophages present antigen to T lymphocyte
- Delayed hypersensitivity reaction occurs
- Occasionally in GI tract
- Caseation= diseased, necrosed tissue forms firm dry mass (cheese-like)
- Cavitation= vapour filled cavities (low presh)
- Fibrosis
types of TB
primary = first infection.. usually mild/asymptomatic
miliary TB = initial infection not successfully controlled by caseating granulomas. bacteria multiply. this is more common in infants, immunocomprimised
latent TB = bacteria present but not problematic. in the majority of infected people, the immune system contains the infections and develops cell mediated immunity memory to the bacteria
secondary TB =Dormant organisms reactivate years later due to host immune system reducing - Age - Alcohol abuse - Malignancy - HIV - Treatment - Illness this is the majority of patient cases
based on features, TB can be pulmonary or extra-pulmonary (Spread)
TB causes
Mycobacterium tuberculosis
Mycobacterium bovis
(mycobacterium africanum)
(Mycobacterium microti)
TB risk factors
High incidence country Immunosuppression (HIV, chemo) Diabetes IV drug user Ageing Poverty Prisons Smoking Alcohol
influenza treatment
Symptomatic - paracetamol, fluids, tamiflu
Bed rest
influenza symptoms
Abrupt fever
Aching in limbs
Sore throat
Dry cough
influenza cause
Influenza = virus
Types = A (most), B, C (mild)
Droplet or direct nasal/eye contact with hands
Antigenic drift – only partial immunity from previous infections. Influenza A can do major and rapid shifts (pandemics)
common cold
- infections and cause
Rhinitis Sinusitis - Usually viral - Bacterial ---strep pneumoniae ---haemophilus influenzae
pharyngitis/ tonsilitis causes
Viral
- Rhinovirus
- Adenovirus
- EBV
- HIV acute
Bacteria
- Lancefield group A - strep pyogenes
- Neisseria gonorrhoeae
- Mycoplasma pneumoniae
diphtheria cause
Corynebacterium diphtheriae
epiglotitis cause
Haemophilus influenzae unless immunocompromised
whooping cough cause + virulence factors
Bordetella pertussis
- ACT toxin - inhibits phagocyte chemotaxis and T cell activation
- Pertussis toxin - inhibits alveolar macrophage defense
- Fimbriae - adherence
- Cytotoxin - causes epithelial necrosis
Bordetella parapertussis and bordetella bronchiseptica (milder)
croup cause
Parainfluenza virus
measles
what causes psuedomembrane (thick, grey ) in tonsils
diphtheria
what causes pain in ear and into teeth, facial pain and purulent discharge
sinusitis
what upper resp infection can cause conjunctivitis
whooping cough
what causes barking cough and crying
what other symptoms are caused by it
croup
also cyanosis increased RR intercostal recessions inspiratory stridor (high pitched wheeze)
diphtheria treatment
erythromycin and anti-toxin
most common cause of COPD exacerbation
haemophilius influenza (then strep pneumonia)
is pulmonary fibrosis productive
non productive
what occupation supports pulmonary fibrosis
miner
tension pneumothorax tracheal deviation goes which way
pleural effusion tracheal deviation goes which way
both causes mediastinum shifts away from the side of the pneumothorax/ pleural effusion
what sign would you see on pleural effusion Xray
meniscus
pink frothy sputum
pulmonary oedema
caused by HF
orthopnea indicates
pulmonary oedema
caused by HF
