internal medicine-pulmonology Flashcards
obstructive pulmonary/lung disease’s?
asthma, COPD, bronchiectasis and CF.
diseases under COPD + etiology of COPD?
chronic bronchitis and emphysema.
-aetiology: smoking, dust, silica, pollutant + alpha-1 anti-trypsin defiiciency
pathogenesis of Chronic bronchitis (mucus issue)
goblet cells undergo hyperplasia+ HT. excess mucus due to irritant. ciliary dysfunction-less motility, shortening, mucus plug, air trapping of CO2. VQ mismatch ,hypoxemia, hypercapnia. risk of pneumonia: -1. flu, m.cattarhals, strep pneumonia.
pathogenesis of emphysema (structural issues):
-inflammation stimulated-> protease (elastase) since alpha anti-trypsin deficiency-autosomal dominant liver-> air trapping, bernouli principle , alveoli collapse, loss in surface area in alveolar septa exchange gradient. hypoxemia and hypercapnia (later event).- mild
morphology (big balloons in lungs)
centri-acinar emphysema: proximal (closer) airway. affects upper parts of lobes.
pan-acinar (-distal-lower lobes of lungs affected .
distal -acinar emphysema- distal alveoli-spontaneous secondary pneumotrhoax due to bleb rupturing in the pleura.
air in pleural space- pneumothorax.
hypoxemic vasoconstriction- low ventilation and perfusion (V/G mismatch)- back up of blood, pressure -> pulmonary hypertension-> cor pulmonale-< RSHF-
right sided heart failure (Cor -pulmonale) investigations, symptom
increased JVP, hepatomegaly, splenomegaly, peripheral oedema.
investigations: echo- decreased ejection fraction, right ventricular catheterisation for checking pulmonary capil P >18 mmhg (swan-ghonzs) BNP levels
clinical features:
blue bloaters- bronchitis-obesity, cyanosis, productive cough, wheezing on expiration, crackles, increased AP, hyper-rsonance, inspiratory, dyspnoea on exertion.
pink puffers; pursed lips-> prolong expiration, pink- mild hypoxemia (early stage-oxygenation), weight loss (utilize accessory muscles),
clinical diagnosis (history, occupation, fhx)
liver disease (LFT), Fhx,
-chronic bronchitis: 3 months (2years)
x-ray- lucid spots, flat diameter, hyper inflated lungs, best * - pulmo function test- spirometry- FEV1 (lowest), FVC (low).
FEV1/FVC; <75%.
increased TLC, RV & low DLCO
pulse oximetry: <88%
& <90 % (HCT + RSHF)
start supplemental O2.
ABG: low pH, respiratory acidosis hypoxic,
EKG: rule out MI, CHF, multi-focal atrial tachycardia, inverted T wave- RV strain.
high resolution CT & Xray- air trapping, flat diaphragm, AP diameter, emphysema- bolus (air-pocket). possible polycythemia.
treatment & prevention of COPD?
-cessation of smoking, influenza vaccine, pneumococcal vaccine -ppsv 23.
supplemental oxygen-15+ hrs if P02 <55 mmhg or compensated Hct.
P. chemoreceptor sitmulated in hypoxia-> medullary respiratory centre, high flow O2 diminishes-> respiratory failure-> affect vasoconstriction autoregulation to shunt blood.#
-venturi mask (non breather): high flow.
nasal cannula: better controlled.
-corticosteroid+ LAbA.
anticholinergics (M receptor antagonist) and B2 agonist.
SAMA-ipratropium
LAMA- triopratium “tail”
SABA-albuterol
LABA-formeterol, salmeterol.
mild/ intermittent-> SABA+ SAMA MDI/ Nebuliser
moderate+ severe: LAMA+ LABA. MDI
ICS: acute exacerbation -> IV/ PO steroid
inhaled corticosteroid-> LABA.shorterm due to ADE.
azithromycin- anti-inflammatory Ab long term.
-riboflumlast
-theophylline
treatment & prevention of asthma
intermittent- SABA (prn)
mild: SABA & low dose ICS
moderate: up the iCS + SABA or low dose ICS+ LABA
severe: PO CS+ LABA+ SABA or high dose ICS.
oral /IV CS: methyprednisolone/ prednisone * short term* systemic ADE.
mast cell stabiliser: cromolyn sodium.
alternative to atopic patients (intrinsic asthma)
-LTRA: montelukast
monovlonal
-Ab against IgE- omalizumab
methylxanthie *theophylline ) usually for COPD.
indication : severe allergic asthma.
emergency (acute exacerbation): peak expiratory flow rate based no age, height, gender >70% post SABA
low CO2 in ABG if severe tachypnea
no wheezing in exacerbation means bad- normal PC02- complete obstruction
treatment protocol:
- non-rebreather supplemental O2 >92%.
- SABA+ ipratropium bromide (N,I).
- IV/PO steroids.
- . IV MgSO4: reduce Ca2+ SM.
- positive pressure ventilation (ICU)
- intubation (endotracheal).
definition of bronchiectasis
irreversible airway dilution of middle sized bronchus-> weak wall-> collapse , inflamed, plugged w/ mucus.
irreversible.
pathogenesis of bronchiectasis?
- destruction-chronic inflammation.
CT disorder: SLE, sarcoidiosis, IBS, marfans. - impairement- ability to clear mucus fails, ciliary dysfunction.
CF, ciliary dyskinesia (congential- kartageners syndrome, monoculary dystrophy)
obstruction- malacia, stenosis, foreign body, mucus plug
3. infection- chronic.
-pathogens: pertussis, measles, adenovirus, TB, MAC, allergic aspergillus. risk factor: immunodeficiency - di-George syndrome, HIV etc. 4. recurrent cycle. upper airway- CF, sarcoidosis. middle: primary ciliart dyskinesia. lower- pneumonia. central- ABPA. increased thickness wall, widened, mucus
focal obstruction-carcinoma
toxic inhalation- chemical fumes,
traction bronchiectasis, anti-trypsinogen deficiency.
clinical features?
- crhonic daily cough
- sputum production
- CT finding
episodic exacerbation- fever, dyspnoea, chest pain.
later: fatigue-> correlated with lower fev1.
haemoptysis- erosion of airway near vessels
cyanosis- children (severe hypoxemia, V/W mismatch, pulmonary HTN-> cor pulmonale.
physical- crackles (72%) wheezing (22%)
clubbing
Xray: thickened airwat wall- tram tracking feature.
cystic dilation extending to periphery.
high resolution CT-imaging of choice- enlarged alveoli, signet ring wall thickening.
lab- CBC w/ differential to rule out infection.
IgE, IgA, IgM low in immunodeficiency.
CFTR mutation analysis- underlying CF.
sputum culture and smear- microbio
PFT- obstructive pattern. FVC- normal/ low# FEV1- v. low ratio- very low. sweat chloride test- CF HIV/aid test. hypoglobulinemia aspergillus antigen skin prick test- abpa.
cupful of pus - purulent, foul smelling.
complication-> empyema-> pyemia-> organs (brain abscess).
chronic inflammation- 2nd amyloidosis.
treatment:
control infection
treat underlying situation.
TB- chemo
immuno- IV Ig
ABPA- PO steroids. antifungals itraconazole
autoimmune steroid suppression.
CF- DNase and others.
massive blood– intubation & vascular embolization
1. prevent exacerbation- macrolide, reduce film of pseudomonas.
2.inhaled Ab- aerosolid, ADE- bronchospasm- supervised 1st time.
albuterol prescribed with.
prophylaxis Ab-> create resistance long term.
3.bronchial hygiene- airway hydration, mucolytic- guaifenesin, nebulised saline hypertonic solution.
never give anti-tussive together with mucolytics.
4, vaccination- pneumoccoal PCV.
5.chest physiotherapy-postural drainage.directed forced expiration, oscillatory PEP.
treatment of exacerbation:
antibiotic- culture guided-> H. flu M. cattaralis, S.aureus/ s.pneumonia, P.auerginosa.
outpatient-afebrile, stable.
floroquinolones-> culture and adapt Ab.
inpatient-high RR, >25 , febrile, hypoxemia, hypotension.
antipseudomonas**> guided.
surgery- entire transplant, focal resection, severe haemoptysis-> occlude vessel.
associated abscess should be drained.
cystic fibrosis definition
-umbrella term- obstructive and bronchiectasis form of disease.
autosomal recessive disorder, pancreas insufficiency resulting in cyst and fibroids in pancreas, childhood onset, obstruction of secretary glands in lungs, pancreas, and GIT.
northern european.
