Respiratory, Mhu, Mbbs Iv

- Resp disorder=>RV struc/func change.

- Pulm HTN common path

- Can be 1o (very rare) or 2o

- Defined as MAP >20mmHg at rest of >30mmHg in exercise in pulmonary artery

- Progressive increase in pulm vasc. resistance => RV failure

- Classified in 4 categories same as NYHA HF

5 groups

1- idiopathic (1o)

2 - left-sided heart disease & extrinsic compression of the pulmonary veins (eg, tumors), pulmonary veno-occlusive disease.

3 - Lung path/hypoxia: COPD, ILD, impaired resp (OSA, alveolar hypoventilation disorders), long-term high altitude.

4 - chronic thromboembolic pulmonary hypertension (CTEPH). acute embolism, 0.1%survivors get CTEPH.

5 - unclear or mixed aetiology

eg. Haem eg. myeloproliferative disorders Systemic eg. sarcoidosis, neurofibromatosis, vasculitis. Metabolic, eg. thyroid disorders + others inc. tumor obstruction, mediastinal fibrosis, and chronic renal failure on dialysis

- hx: Dyspnea upon exertion, Fatigue, Lethargy, Syncope with exertion, Chest pain, Anorexia, RUQ pain, less common = Cough, Hemoptysis, Hoarseness (d/t compression of the recurrent laryngeal nerve by the distended pulmonary artery)

- PE: loud P2 fixed or paradoxic splitting. Systolic ejection murmur, left sternal border, louder on insp.

- RV heave.

- Prominent A wave on JVP.

- R side S4 w left parasternal heave.

- Signs of Cor pulmonale.

- Signs of underlying cardiac, pulmonary, hepatic, or collagen-vascular disease are often present.

- pulm HTN=>inc. RV filling pressure=>inc. afterload=>inc. stretch=> RV remodelling

- PE: sudden inc. pulm resistance

- ARDs: d/t mechanical ventilation requires a higher transpulmonary pressure=>RV overload. + other features of condit.

COPD most common cause

other: sarcoidosis, scleroderma, polycythemia vera (inc. blood visc.=>pulm HTN), vasculitis, chronic thromboembolic (repeated PE)

Fatigue, tachypnea, exertional dyspnea, cough. Angina (RV ischemia or pulmonary artery stretching, typically do not respond to nitrates) - s/s dec. cardiac output + hypoxaemia

- Hemoptysis (rupture of a dilated or atherosclerotic pulmonary arteriole)

- (Rare) hoarseness (comp. left recurrent laryngeal nerve by dilated Pulm art)

- (advanced) hepatic congest=>anorexia, RUQ discomf, jaundice.

- syncope on exert = inabil to inc. CO in ex=> dec. systemic BP

- inc. venous + cap pressure=> peripheral oedema. (also dec. GFR and inc ADH contributes)

inc. chest diameter, labored respiratory efforts with retractions of the chest wall, distended neck veins w prominent a or v waves, cyanosis

- palp: RV heave, parastenal or subxiphoid, hepatojugular reflux + pulsatile liver, ascites (systemic venous congestion), pitting oedema (strong assoc. w hypercapnia)

- perc, hyperresonance lungs

- AUSC. wheezes and crackles may be heard as signs of underlying lung disease. Splitting 2nd HS + loud pulm. component (early stage sign). Syst ejection murmur w sharp ejection click over pulm art + diastolic pulm regurg (late sign). tricuspid regurg, RV 3rd+4th HS

Exudate if one of the following true

- Effusion protein:serum > 0.5

- Effusion LDH:serum LDH > 0.6

- Effusion LDH level >2/3 the upper limit of the laboratory's reference range of serum LDH

- Atelectasis: Due to increased negative intrapleural pressure

- Heart failure

- Hepatic hydrothorax

- Hypoalbuminemia

- Nephrotic syndrome

- Peritoneal dialysis

- Urinothorax: Due to obstructive uropathy

- CSF leak into pleural space: Thoracic spine injury, ventriculoperitoneal (VP) shunt dysfunction

- Malignancy: Carcinoma, lymphoma, leukemia, mesothelioma, paraproteinemia

- Infectious: Abscess in tissues near lung, bacterial pneumonia, fungal disease, parasites, tuberculosis

- Inflammatory: Acute respiratory distress syndrome (ARDS), asbestosis, pancreatitis, radiation, sarcoidosis, uremia

- Abdominal fluid: Abscess in tissues near lung, ascites, Meigs syndrome, pancreatitis

- Connective-tissue disease: Churg-Strauss disease, lupus, rheumatoid arthritis, Wegener granulomatosis

- Endocrine: Hypothyroidism, ovarian hyperstimulation

- Iatrogenic: Drug-induced, esophageal perforation, feeding tube in lung

- Lymphatic abnormalities: Chylothorax, malignancy, lymphangiectasia

- CHF (transudate)

- Pneumonia (exudate)

- Cancer (exudate)

- Pulmonary embolus (transudate or exudate typically exudate)

- Viral disease (exudate)

- CABG surgery (exudate)

- Cirrhosis with ascites (transudate)

Uncommon, often 2o to infection=>abnormal + permanent distortion of one or more of the conducting bronchi or airways

- Cough + daily mucopurulent sputum (lasting months to years (classic))

- Blood-streaked sputum or hemoptysis from airway damage assoc. w acute infection

- Dyspnea, pleuritic chest pain, wheezing, fever, weakness, fatigue, and weight loss

- Rarely, episodic hemoptysis w little to no sputum (dry bronchiec)

- Inc sputum prod

- Increased viscosity of sputum

- Foul smelling sputum

- Low-grade fever (rare)

- Inc. constitutional symptoms (eg, malaise)

- Inc dyspnoea, wheezing, or pleuritic pain

- Crackles, rhonchi, scattered wheezing + inspiratory squeaks

- Clubbing in ~3%: more severe=more freq

- Cyanosis+plethora with polycythemia from chronic hypoxia (rare)

- Weight loss/wasting

- Nasal polyps/signs chronic sinusitis

- PE of cor pulmonale, in advanced disease

- High Res CT is the standard

- Sometimes CXR enough

- Chronic resp sympts (daily cough)

- Sputum analysis may be done

Most are vit D deficient and this corresponds with severity (more freq exacerbations, lower FEV1 etc)`

- Increased pulmonary markings

- Honeycombing

- Atelectasis

- Pleural changes

- Tram tracking (cylindrical)

- Dilated bronchi in varicose bronchiectasis

- Clustered cysts in cystic bronchiectasis

- tram tracking

- Signet-ring (dilated bronchus + adjacent pulmonary artery being the stone)

- diameter bronchus lumen >1.5xadjacent vessel diam (1-1.5=normal)

- Large cystic spaces & honeycombing in cystic

- Beaded bronchi in varicose

Cystic, Varicose, cylindrical

Tram tracking (Linear lucencies and parallel markings radiating from the hila

- Large cystic spaces + honeycomb appearance; this contrasts with the blebs of emphysema, which have thinner walls and are not accompanied by proximal airway abnormalities

- Clustered cysts

- irregular or beaded bronchi, with alternating areas of dilatation and constriction

- Dilated bronchi

- Antibiotics and chest physio=mainstays

- Bronchodilators - Corticosteroids

- Dietary supps

- O2 (in v severe hypoxemic patients)

- Surgical therapies

- 7-10 days of one of

- Amoxicillin - Tetracycline - Trimethoprim-sulfamethoxazole

- Macrolides (eg, azithromycin or clarithromycin)

- A 2nd gen ceph

- A fluoroquinolone

Chronic, progressive, fibrosing interstitial pneumonia of unknown cause, primarily occurring in older adults

Gradual onset (often >6 mo) of exertional dyspnea +/- nonproductive cough, Weight loss, Low-grade fevers, Fatigue, Arthralgias/Myalgias

- Fine bibasilar inspiratory crackles (v. common)

- Digital clubbing (25-50%)

- Pulm HTN at rest (20-40%)

- Loud P2 component of the second heart sound, a fixed split S2, a holosystolic tricuspid regurgitation murmur, pedal edema

- High res CT is essential: patchy, peripheral, subpleural, and bibasilar reticular opacities + honeycombing (coarse reticular pattern), and lower lobe volume loss

- TTE for pulm HTN

- Bronchoscopy: excludes other diagnoses. Fluid analysis (increased neutrophils [70-90% of patients] and eosinophils [40-60% of all patients])

- lung biopsy

Lots to rule out other differentials:

- Antinuclear ab/ rheumatoid fact pos in 30%, usually low titre (high titre= ?CT disease)

- CRP and ESR Elevated

- Polycythemia (rarely)

- ABGs show chronic hypoxaemia

- PFTs: Restrictive ventilatory defect + reduced diffusion capacity for carbon monoxide (DLCO)

- 6min walk test (measure desat)

- Treat comorbs

- Lifestyle (stop smoking etc)

- Vaccinate

- 02 if [SpO 2] < 88% goal >90% always

- Lung transplant

- Drugs: Systemic prednisalone, Immunosupp (eg, azathioprine), Tyrosine kinase inhibs (eg, nintedanib), Antifibrotic agents (eg, pirfenidone)

- Asbestos

- Beryllium

- Cobalt

- Amiodarone

- Radiation

- Dust

- Cigarettes

- Increased inflammatory cell content

- infection, chronic interstitial disease and acute alveolar disease

- Can also be caused by: normal expiration, partial filling of air spaces, partial collapse of alveoli, interstitial thickening

- Measures partial press diff b/w insp+exp CO. Since Hb has high affinity for CO DCLO shows gas uptake by capillaries in a way less dependent on cardiac output.

- Affected by atmospheric pressure

- Polycythaemia

- Asthma (can also have normal DLCO)

- Inc pulm. blood volume as occurs in exercise.

- Left to right intracardiac shunting

- Alveolar hemorrhage

- Anything that affects the effective alveolar surface area. e.g. fibrosis, alveolitis, vasculitis

- Decrease of total lung area, e.g. Restrictive lung disease

- COPD d/t dec SA alveoli + damaged capillary bed

- Uneven spread of air in lungs, e.g. emphysema, PE, Cardiac insufficiency, Pulmonary HTN,

- Dec. blood vol eg. anaemia

- Drugs: Bleomycin, amiodarone high cumulative dose

Obstructive: Low FEV1:FVC (<70% in adults <85% in people 5-18y/o)

- COPD if non reversible, asthma if reversible (inc. of >12%)

Restrictive: Low FVC

Mixed pathology: Both low FEV1 and low FVC

Type I: PaO2 <60mmHg

Type II: PaCO2 >50 mm Hg.

- FEV1/FVC <0.7

- FEV1 <80% of predicted

Pus in the pleural space.

- Typically comp of pneumonia

- Other: penetrating chest trauma, oesophageal rupture, comp lung surgery, inoculation of the pleural cavity after thoracentesis/chest tube placement.

- Extension of a subdiaphragmatic or paravertebral abscess.

0-2—low risk of needing intensive respiratory or vasopressor support (IRVS)

3-4—moderate risk (1 in 8) of needing IRVS

5-6—high risk (1 in 3) of needing IRVS

7+ —very high risk (2 in 3) of needing IRVS

Severe CAP = a SMART-COP score of 5 or more points.

Used in px with CXR confirmed CAP to assess severity

Pulmonary fibrosis, PE, Heart failure, pneumonia

COPD, resp depression (drugs etc), heart failure

Syndrome of clubbing of the digits, periostitis of the long (tubular) bones, and arthritis

- Bat wing

- Air bronchograms

- Consolidation

- Cotton wool appearance

- Effusion

Right middle lobe pneumonia

right lower lobe pneumonia

- Must have chronic hypoxaemia w proven improvement on 02

- Must be assessed a month after ceasing smoking and acute disease, no reversible factors (anaemia)

- PaO2 must be persistently <55mmHg when awake, at rest, on RA. Or sats <88%

- Polycythaemia or corpulmonale need PaO2<60mmHg

- COPD PaCO2 >45mmHg indic

Pneumoconiosis caused by inhalation asbestos

Malignant mesothelioma, upper respiratory tract, oesophagus, kidney, ovarian and biliary system.

- lung carcinoma 6-fold inc. risk

- Smoking + asbestos = synergistic carcinogenicity

- Latent period ~20 yrs from exposure (less if intense exposure)

- Progressive SOB on exertion, dry cough, chest discomfort

- Fine crackles, beginning posterioinferiorly, in the inferiorlateral areas and at the end of inspiration

- Clubbing

- Reduced chest expansion

- Signs of Cor pulmonale

Bilateral pleural thickening, pleural plaques (look on diaphragm and 6-9th ribs), diffuse infiltrates particularly in lower zones causing "shaggy heart border", reticulonodular infiltrates in the lower zones.

- early stage=>inc interstitial markings (mostly linear)

- Late stage: honeycombing (w cystic spaces surrounded by coarse interstitial infiltrates + small lung fields)

- ABCDEs, transfer to ICU,

- IV Frusemide, (repeat 20 minuteslater if necessary)

- GTN (if BP >100 syst).

- if non-responsive=>CPAP with 100% O2 + GTN infusion, increasing rate every 5mins while no clin improv. or BP <90

- Morphine IV to dec. anxiety

- digoxin if in AF

Subpleural linear opacities parallel to the pleura; basilar lung fibrosis and peribronchiolar, intralobular, and interlobular septal fibrosis; honeycombing; pleural plaques.

- DCLO goes down first + exertional hypoxemia

- dec. TLC

- VC dec. without FEV1:FVC reduction

- Dec. Small-airway flow rates (eg, midexpiratory forced expiratory flow [FEF25-75])

Oximetry, CXR, HRCT, PFTs

Quit smoking, pall care, surveillance for carcinoma,

• SOB, especially on exertion

• nonproductive cough

• crackles (dry, fine, end-inspiratory)

• clubbing (especially in IPF and asbestosis)

• features of cor pulmonale

• s/s vary with underlying disease process e.g. sarcoidosis is seldom associated with crackles and clubbing

- Inflammatory and/or fibrosing process in the alveolar walls =>􏰀distortion and destruction ofnormal alveoli+microvasculature=>

- lung restriction (decrease in TLC and VC)

- decreased lung compliance (increased or normal FEV1/FVC)

- impaired diffusion (decreased DLCO)

- hypoxemia due to V/Q mismatch (usually without hypercapnia until end stage)

- pulmonary HTN+cor pulmonale occur with advanced disease secondary to hypoxemia and blood vessel destruction

- Antineoplastics: methotrxate, cyclophosphamide, chlorambucil, bleomycin

- Antibiotics: penicillin, sulfonamide

- CV drugs: amiodarone

- illicits: heroin + methadone

- Anti-TNFs: rituximab, infliximab, etanercept

Radition

Typical: Strep. pneumoniae, moraxella catarrhalis, haemophillus influ, s. aureus

Atypical: Mycoplasma pneumoniae, chlamydophila pneumoniae, legionella pneumophila

Viral: flu, adenovirus

Alcoholic: klebsiella, e.coli, s.aureus

1. Latent TB: asymptomatic infection contained by host immune defences (95% of infected px)

2. Primary TB: symptomatic, active disease (5% infected px)

3. Secondary TB: symptomatic reactivation of previously dormant TB (represents 5-10% of those with latent TB, most often within the first 2-3 yr of initial infection) at a pulmonaryor extrapulmonary site

- Resistance to ioniazid + rifampicin

- Extensively drug resistant = the above + fluoroquinalone + more than one injectable

- Dry cough, fever, myalgia/arthralgia, often WBC in normal range

- px 15-30 y/o

- Mild hepatitis +/- haemolytic anaemia

- 10% get, Haemolytic anaemia, Renal failure, Hepatitis, Myocarditis, meningitis, Transverse myelitis, or Cerebellar ataxia.

- Erythema multiforme rash

- Look for cold agglutinins (present in 50%),

anti-mycoplasma antibodies

99% are bronchogenic carcinoma (epithelial lung tumours)

Acute exac remains unresponsive to initial bronchodilators=> bronchospasm, airway inflammation, + mucus plugging=>difficulty breathing, carbon dioxide retention, hypoxemia, and respiratory failure.

- Treat like asthma attack

* 85-90%

* squamous cell carcinoma: arise from the proximal respiratory epithelium

* adenocarcinoma: incidence is increasing; most common subtype in nonsmokers - bronchoalveolar carcinoma: grows along the alveolar wall in the periphery; may arise at sites of previous lung scarring

- obstruction of SVC=>neck + facial swelling, dyspnea, cough, hoarseness, tongue swelling, epistaxis, and hemoptysis

- PE: dilated neck veins, increased number of collateral veins covering the anterior chest wall, cyanosis, edema of the face, arms, and chest, Pemberton’s sign (facial flushing, cyanosis, and distension of neck veins upon raising both arms above head)

- milder symptoms if obstruction is above the azygos vein

Causes: Horner’s syndrome (ptosis, miosis, anhydrosis), brachial plexus palsy (most commonly C8and T1 nerve roots)

- Cough

- Haemoptysis

- Dyspnoea

- Chest pain

- Recurrent pneumonia

- Systemic cancer s/s

- Supraclavicular or axillary adenopathy

Small cell

- Often metastasised at presentation

- Weak assoc w smoking

- Usually located peripherally

- Histology glandular, produces mucin

- Metastasises early to distant sites

- 12% 5 yr survival, except for bronchoalveolar subtype, which is resectable and has 60% 5 yr survival)

- Most common type of bronchogenic cancer

- Strong assoc. w smoking

- Usually central (the two ones with S&C in the name are central)

- Histology: keratin, intracellular bridging

- Invades locally and spreads, may cavitate

- 25% survival at 5 yrs

- Strong assoc w smoking

- Peripheral

- Histology is anaplastic, undifferentiated

- Metastasis is early, distant

- 13% survival at 5 yrs

- Severe resp distress

- Hypoxaemia

- Non cardiogenic pulmonary oedema

- Acute onset w/i 7 days of a defined event

*sepsis

*pneumonia

*px noticing a worsening of pulm sx

*usually w/i 72 hours of trigger

- Direct lung injury

*aspiration, pneumonia, inhalation injury, toxicity, nitrogen dioxide, smoke

*Sepsis/shock, trauma, blood transfusion, pancreatitis

*head trauma, intracranial haemorrhage, drug overdose (narcotics, sedatives, TCAs)

- Disruption alveolar capillary membrane=>leaky capillaries=>interstitial and alveolar pulm oedema=>reduced compliance, V/Q mismatch, shunt, hypoxaemia, pulm HTN

Two phases exudative and fibroproliferative

- Exudative:

*first 7d of illness after precipitant

*Alveolar capillary endothelial cells and type I pneumocytes injured=>loss of normal tight alveolar barrier

*dyspnoea, tachypnoea, inc WOB=>respiratory fatigue and failure

- Fibroproliferative phase

*after day 7

*may still experience dyspnoea, tachypnoea, fatigue, hypoxaemia

*most patients clinically improve and are able to wean off mechanical ventilation

*some px develop fibrotic lung changes=>long term support on supp 02 or mechanical vent=>assoc w increased mortality

- 30-40% mortality

- Residual pulmonary impairment, severe debilitation

- Polyneuropathy

- Psychologic probs

- Gradually improve over time more regain near-normal lung fcn w mildly reduce DCLO

- Gram negative rod

- Get it from air-cons, hot tubs (aerosolised water droplets (not person to person)

- Watery diarrhoea, bilateral infiltrates (pneumonia -dry cough etc), neuro symptoms (confusion), hyponatraemia, bradycardia

- Incubation 2-10d

- Pontiac fever is a milder, self limiting manifestation

- Notifiable