Flashcards in PT 1 - RESP Deck (19)
1. Q. Name the lobes and fissures of the lung
A. Right lung: superior, middle, inferior – horizontal and inferior fissure
B. Left lung: superior, inferior lobes – oblique lobe
C. Lung (ribs 6,8,10), pleura (8,10,12)
1. Q. What are the three main features of COPD? What is seen on investigation, what are the treatment aims
A. Productive cough + SOB + infection risk
B. SMOKERS, air pollution
C. Obstructive picture on investigation, FEV1/FVC ratio is low < 70% expected
D. Aim for O2 sats 88-92% as hypoxia gives resp drive
E. Tx: smoking cessation, bronchodilation, pulmonary rehab, oral steroids
1. Q. What is bronchiectasis? What can cause it? Name some S&S
A. Permanent dilatation of bronchi/bronchioles
B. Chronic inflammation: asthma, CF, infection
C. Chronic, productive, foul smelling cough
D. Clubbing, SOB, recurrent RT infection
E. Tx: physio, empirical abx, inhaled steroid therapy sometimes (beclomethasone)
1. Q. How is tuberculosis diagnosed?
A. Acid-fast bacilli with Ziehl-neelsen stain on sputum sample
B. Consolidation on CXR
C. Tuberculin skin test
D. Maxtoux test: screens high risk pts for latent TB, tuberculin PPD injected
a. Exposure = immune response
E. Tx: RIPE for 6 months, notifiable disease to PH England
1. Q. What pathogens are responsible for pneumonia? What tx for CAP and HAP?
A. Bacterial: strep pneumoniae, H.influenza, C.pneumoniae
B. Virial: RSV, adenovirus, influenza virus
C. NB. Water cooler/ait conditioner/spain = Legionnaire’s disease, legionella pneumophilia, atypical pneumonia
D. CAP Tx: amoxicillin
E. HAP Tx: taxobactam/piperacillin
1. What is CF? What S&Ss?
A. Autosomally recessive inherited channelopathy resulting in Na/Cl channel dysfunction due to abnormal CFTR gene deletion
B. Results in thick mucus plugs
C. Respiratory secretions
D. Productive cough and mucus plugs, recurrent infection (Pseudomonas aeruginosa), s.o.b
E. Exocrine pancreatic insufficiency
F. Malabsorbtion, steatorrhoea
G. SYMPTOMS, NEONATE: FAILURE TO THIRVE, MECONIUM ILEUS (SMALL INTESTINE BLOCKAGE DUE TO THICKER SECRETIONS), REACTAL PROLAPSE
H. OTHERS: COUGH, WHEEZE, RECURRENT INFECTIONS, BRONCHIECTASIS, PNEUMOTHORAX, HAEMOPTYSIS, RESP FAILURE, COR PULMONALE, GALL STONES, CIRRHOSIS, MALE INFERTILITY, OSTEOPOROSIS, ARTHRITIS, VASCULITIS, NASAP POLYPS/SINUSITIS,
I. SIGNS: CLUBBING, CYANOSIS, BILATERAL COARSE CRACKLES
1. Q. How is CF diagnosed? Managed?
A. Diagnosis: sweat test >60mmol/L Cl-, CXR (bronchiectasis, hyperinflation), genetic testing
B. Mx: resp physio, pancreatic enzyme supplementation, empirical abx
C. CHEST: PHYOI, ABX, MUCOLYTICS, BRONCHODILATORS
D. SEVERE CHEST: OXYGEN, DIURETICS, VENTILATION, TRANSPLANT
E. GI: PANCREATIC ENZYME REPLACEMENT, FAT SOLUBLE VITAMIN REPLACEMENT, URSODEOXYCHOLIC ACID FOR LIVER FUNCTION
F. OTHER: DM, OESTEO, RX ARTHRITIS, FERTILITY COUNSELLING
1. Q. What causes extrinsic allergic alveolitis? What is the most common cause?
A. Inhalation of allergens provokes a hypersensitivity reaction type III. (immune complex formation)
B. Common: farmer’s lung (spores), others: Pigeon fancier’s lung (proteins in bird droppings), Malt worker’s lung (aspergillus clavatus), Bagassosis/sugar worker’s lung (sugar cane fibres)
C. Acute phase- alveoli infiltrated with acute inflam cells i.e. neutrophils
D. Chronic exposure- small granuloma formation
E. Clinical features: 4-6 hrs post exposure- fever, rigors, dry cough, dyspnoea, crackles (no wheeze)
F. Chronic- weight loss, exertional dyspnoea, type 1 respiratory failure, cor pulmonale.
Q. What is seen on investigation of extrinsic allergic alveolitis? What is the tx?
A. CXR- upper zone mottling/consolidation. Honeycomb lung in very advanced cases
B. Treat- Remove allergen, O2, oral prednisolone (steroids)
Q. Describe the basic physiology and histology of the resp system
A. Functional unit of gas exchange = alveolus
B. Conducting airways: 16th generation of bronchi/bronchioles, Ends with terminal bronchioles (columnar or low cuboidal epithelium)
C. Histology of the trachea: Mucosa - columnar ciliated pseudostratified epithelium & goblet cells, Supported by the elastic lamina propria (elastin), Submucosa – sero-mucinous glands.
D. Ventilatory airways = acinus (collection of alveoli)
E. Respiratory bronchioles – ciliated cuboidal epithelium
F. Clara cells (secrete surfactant component) – non-ciliated cells.
G. No cartilage plates or glands/diffuse lymphatic tissue in bronchioles.
1. Q. What is normal V/Q rate?
A. Normal V/Q (4l/min)/(5l/min = CO) ~ 0.8.
B. Postural V/Q mismatch when standing = higher V/Q due to RELATIVE decrease in blood supply due to gravity at APEX. There are regional V/Q changes.
1. Q. Name 5 causes of respiratory failure
B. Low inspired O2 ( decreased PiO2) – e.g at altitude (type 1)
C. Alveolar hypoventilation (=hypoxia and hypercapnia – type 2) e.g. MND, Guillan-Barre, COPD exacerbation, severe asthma, drug toxicity, stroke, reduced GCS
D. Ventilation/perfusion (V/Q) mismatch
E. Impaired diffusion: e.g. ARDS, pulmonary fibrosis, sarcoidosis
F. Shunt e.g. pulmonary AV shunt
Q. What drugs are associated with respiratory depression?
A. OPIODS (pin-point pupils on examination).
1. Q. What is bronchiectasis? What can cause it?
A. ‘Abnormal, permanent dilatation of the airways’
B. Dilatation (‘ectasia’) – pooling of secretions – scarring and inflammation of surrounding tissues.
C. Ciliary dysfunction +/- ulceration
D. Persistent severe inflammation (bronchitis), obstruction and destruction of lung parenchyma.
E. Associated with chest sepsis, septicemia, metastatic abscess formation, R-sided cardiac failure and amyloid deposition.
F. LOCALISED (obstruction, focal severe infection) e.g. measles, staphylococcus aureus, klebsiella infection, streptococcus pneumoniae and pseudomonas aeruginosa (opportunistic, CF?)
G. DIFFUSE (cystic fibrosis, ciliary dyskinesias e.g PCD)
H. Consider underlying primary IMMUNE DEFICIENCY syndromes e.g. Common Variable Immune Deficiency (CVID)!
*post-infectious = commonest identifiable cause of bronchiectasis
1. Q. Name 4 S&S of bronchiectasis, What is the gold standard for imaging? What is seen?
A. Persistent cough, clubbing, purulent sputum, dyspnoea, (no smoking history, young age), haemoptysis +- recurrent infections with long recovery time
B. High res CT
C. Thickened, dilated bronchi and cysts at the end of the bronchioles
D. Airways larger than associated blood vessels = big brochoarterial ratio
E. Signet sign on CT – cylindrical type bronchiectasis
1. Q: What is the mainstay of treatment in BRONCHIECTASIS? Name two complications
A. Antibiotic therapy, physiotherapy (e.g postural drainage) & airway pharmacotherapy (mucolytics, Inhaled corticosteroids (anti-inflammatory agents) (in adults) ect.)
B. Complications: empyema and lung abscess
1. Q. What is seen on investigation of COPD?
A. Emphysema, Bronchitis, small airway involvement, pulmonary vasculature changes
B. Emphysema = destruction of lung parenchyma = enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls
C. Centrilobular (commoner = UPPER LOBE) or panacinar pattern (commoner in A1AT = LOWER LOBE).
D. Lobules are MACROSCOPIC structures. If there are confluent areas of destruction > macroscopic BULLAE > increases AIR TRAPPING.
E. Bronchitis = cough & sputum production on most days for 3 months of 2 successive yrs.
F. Submucosal bronchial gland enlargement
G. Goblet cell metaplasia (abnormal change) & mucus hypersecretion
H. Airway oedema
I. Inflamed bronchial tree
J. Smooth muscle and connective tissue hypertrophy
K. Airway epithelial squamous metaplasia & ciliary dysfunction
L. Small airway involvement (<2mm) = DON’T FORGET THIS
M. Involved in EARLY on in COPD – obstructive bronchiolitis = major site of airway obstruction
N. Pulmonary vasculature changes
O. Intimal thickening + endothelial destruction
P. SM hypertrophy and collagen deposition + breakdown of collagen bed architecture.
Q. Leads to pulmonary hypertension, hypoxia and a decrease in TLCO and KCO
1. Q. How is COPD severity accessed?
A. MEDICAL RESEACH COUNCIL (MRC) dyspnoea scale:
grade 1 = not troubled by breathless except on strenuous exercise,
grade 2 = SOB when hurrying on a level or walking up a slight hill,
grade 3 = walks slower than most people on the levels, stops after a mile or so
grade 4 = stops after 100 yards (few mins)
grade 5 = Too breathless to leave house, breathless when dressing/undressing
B. Classification of airflow limitation on post-bronchodilator FEV1
a. GOLD 1 mild = FEV1<80%
b. Mod 50% < 80%
c. Severe 30% < 50%
d. Very severe < 30%