Acute respiratory distress syndrome (ARDS)

D E FI N I T ION 

Syndrome of acute and persistent lung inflammation with increased vascular

permeability. Characterized by:

. acute onset;

. bilateral infiltrates consistent with pulmonary oedema;

. hypoxaemia: PaO2/FiO2
200mmHg regardless of the level of positive end-expiratory

pressure (PEEP);

. no clinical evidence for " left atrial pressure (pulmonary capillary wedge pressure

(PCWP)
18 mmHg).

. ARDS is the severe end of the spectrum of ‘acute lung injury’ (ALI).

AETIOLOGY

Severe insult to the lungs or other organs induces the release of inflammatory

mediators, increased capillary permeability, pulmonary oedema, impaired gas exchange

and # lung compliance. Common causes include: sepsis, aspiration, pneumonia, pancreatitis,

trauma/burns, transfusion (massive, transfusion-related lung injury), transplantation

(bone marrow, lung) and drug overdose/reaction.

Patients progress through three pathologic stages: exudative, proliferative and fibrotic stage.

EPIDEMIOLOGY 

Annual UK incidence1 in 6000.

HISTORY

Rapid deterioration of respiratory function, dyspnoea, respiratory distress,

cough, symptoms of aetiology.

EXAMINATION

Cyanosis, tachypnoea, tachycardia, widespread inspiratory crepitations.

Hypoxia refractory to oxygen treatment.

Signs are usually bilateral but may be asymmetrical in early stages.

INVESTIGATIONS

CXR: 

Bilateral alveolar and interstitial shadowing.

Blood: 

FBC, U&E, LFT, ESR/CRP, amylase, clotting, ABG, blood culture, sputum culture.

Plasma BNP < 100 pg/mL may distinguish ARDS/ALI from heart failure, but higher levels can

neither confirm heart failure nor exclude ARDS/ALI in critically ill patients.

Echocardiography: 

Severe aortic or mitral valve dysfunction or # LVEF favours haemodynamic

oedema over ARDS.

Pulmonary artery catheterization: 

PCWP
18mmHg(however " PCWP does not exclude

ARDS as patients with ARDS may have concomitant left ventricular dysfunction).

Bronchoscopy:

 If the cause cannot be determined from the history, and to exclude

differentials, e.g. diffuse alveolar haemorrhage (frothy blood in all airways, haemosiderin-

laden macrophage from lavage fluid), lavage fluid for microbiology (mycobacteria,

Legionella pneumophila, Pneumocystis, respiratory viruses) and cytology (eosinophils,

viral inclusion bodies and cancer cells).

MANAGEMENT

Respiratory support:

Supplemental oxygen (FiO2: 50–60%). Almost all patients require

intubation and mechanical ventilation.

Fully supported volume limited and pressure limited modes are both acceptable. The tidal

volume, respiratory rate, PEEP and FiO2 are managed according to the strategy of low tidal

volume ventilation (LTVV). The rationale for LTVV is that smaller tidal volumes are less

likely to generate alveolar overdistension and ventilator-associated lung injury. LTVV

frequently requires ‘permissive hypercapnic ventilation’, a ventilatory strategy that

accepts alveolar hypoventilation in order to maintain a low alveolar pressure and minimize

the complications of alveolar overdistension. The lowest plateau airway pressure possible

should be targeted.

Sedation and analgesia:

 To improve tolerance of mechanical ventilation and to # oxygen

consumption. Neuromuscular blockade should be used only when sedation alone is

inadequate.

0 تعليق

PH.Jafar Jassim 2/16/2021 11:55:00 م

تابع القراءه

Idiopathic fibrosing alveolitis

D E FI N I T ION

 Inflammatory condition of the lung resulting in fibrosis of alveoli and

interstitium. Previously known as ‘cryptogenic fibrosing alveolitis’.

AE T IOLOGY

 In a genetically predisposed host (e.g. with telomerase/surfactant protein

mutations), recurrent injury to alveolar epithelial cells may result in secretion of cytokines

and growth factors (e.g. TNF-a, IL-1 and MCP-1) which cause fibroblast activation,

recruitment, proliferation, differentiation into myofibroblasts and " collagen synthesis

and deposition. Profibrogenic molecules, e.g. PDGF and TGF-b, are secreted by inflammatory,

epithelial and endothelial cells.

Certain drugs can produce a similar illness (e.g. bleomycin, methotrexate and amiodarone).

Histological patterns: Usual interstitial pneumonia (UIP: patchy interstitial fibrosis, later:

‘honeycomb’ lung). Desquamative interstitial pneumonia (DIP: diffuse intra-alveolar

accumulation of macrophages, mild thickening of alveolar septa, lymphoid aggregates)

and non-specific interstitial pneumonia (NSIP).

Risk factors: Smoking (in 75%), occupational exposure to metal (steel, brass, lead) or wood

(pine) in 20% cases; chronic microaspiration, animal and vegetable dusts.

E P IDEMIOLOGY 

Rare. Prevalence in UK is 6 in 100 000. <:, is 2 : 1. Mean age 67 years.

H ISTORY 

Gradual onset of progressive dyspnoea on exertion.

Dry irritating cough. No wheeze.

Symptoms may be preceded by a viral-type illness.

Fatigue and weight loss are common.

Full occupational and drug history is important.

EXAMINA T I ON 

Finger clubbing (50%).

Bibasal fine late inspiratory crepitations.

Signs of right heart failure in advanced stages (e.g. right ventricular heave, raised JVP,

peripheral oedema).

INVE S T I G A T IONS

Blood: ABG (normal in early disease, but # PO2 on exercise; normal PCO2 which rises in late

disease). One-third have rheumatoid factor or antinuclear antibodies.

CXR: Usually normal at presentation. Early disease may feature small lung fields and ‘ground

glass’ shadowing. Later, there is reticulonodular shadowing (especially at bases), signs of

cor pulmonale and eventually, in advanced disease, honeycombing.

High-resolution CT: More sensitive in early disease than CXR. Affecting mainly lower zones

and subpleural areas, with reticular densities, honeycombing and traction bronchiectasis.

Pulmonary function tests: Restrictive ventilatory defect (# FEV1, # FVC with preserved or

increased ratio), # lung volumes, # lung compliance and # TLCO.

Bronchoalveolar lavage: To exclude infections and malignancy.

Lung biopsy: Gold standard for diagnosis but may not be appropriate.

Echocardiography: To look for pulmonary hypertension.

MANAGEMENT 

No curative treatment available.

Combination of azathioprine, oral glucocorticoids and high-dose acetylcysteine, reassess the

response (symptoms, lung function tests) every 3 months. After 3–6 months of treatment,

if there is no evidence of a response, treatment is discontinued. Immunosuppressant

therapy may not be offered to patients with severe loss of lung function or extensive

fibrosis on high-resolution chest CT.

Supportive care: Home oxygen may be necessary. Pulmonary rehabilitation. Opiates in

terminal stages for relieving distressing breathlessness. Psychosocial support is necessary

because of poor long-term prognosis.

Acute exacerbation: Broad-spectrum antibiotics and high-dose glucocorticoids.

Idiopathic fibrosing alveolitis (continued)

Surgical: Single lung transplantation. Lung transplantation may be an option for patients

with progressive disease and minimal comorbidities.

COMPL I C A T IONS 

Right heart failure. Lung cancer (12%). Pulmonary embolus. Death

from respiratory failure.

P ROGNOSIS

 Poor; mean survival is only about 3 years. Good prognostic factors:

Clinical: Young age, female, response to steroids.

Radiological: Predominantly ‘ground glass’ shadowing.

Histology: DIP and NSIP better response to treatment than UIP.

4 تعليق

PH.Jafar Jassim 10/31/2020 02:03:00 ص

تابع القراءه

Extrinsic allergic alveolitis

D E FI N I T ION

 Interstitial inflammatory disease of the distal gas-exchanging parts of the

lung caused by inhalation of organic dusts. Also known as hypersensitivity pneumonitis.

AE T IOLOGY

 Inhalation of antigenic organic dusts containing microbes (bacteria, fungi or

amoebae) or animal proteins induce a hypersensitivity response (a combination of type III

antigen–antibody complex hypersensitivity reaction and a type IV granulomatous lymphocytic

inflammation) in susceptible individuals. Examples:

Farmer’s lung: Mouldy hay containing thermophilic actinomycetes.

Pigeon/budgerigar fancier’s lung: Bloom on bird feathers and excreta.

Mushroom worker’s lung: Compost containing thermophilic actinomycetes.

Humidifier lung: Water-containing bacteria and Naegleria (amoeba).

Maltworker’s lung: Barley or maltings containing Aspergillus clavatus.

E P IDEMIOLOGY

 Uncommon, 2% of occupational lung diseases, 50% of reported cases

affect farm workers (incidence is about 4–10 in 100 000/year), marked geographical variation

reflecting dependence on occupational causes.

H ISTORY

Acute: Presents 4–12 h post-exposure. Reversible episodes of dry cough, dyspnoea, malaise,

fever, myalgia. Wheeze and productive cough may develop on repeat high-level

exposures.

Chronic: Poorly reversible manifestation in some, slowly " breathlessness and # exercise

tolerance, weight loss. Exposure is usually chronic, low level and there may be no history

of previous acute episodes.

Full occupational history and enquiry into hobbies and pets important.

EXAMINA T I ON

Acute: Rapid shallow breathing, pyrexia, inspiratory crepitations.

Chronic: Fine inspiratory crepitations (see Cryptogenic fibrosing alveolitis). Finger clubbing

is rare.

INVE S T I G A T IONS

Blood: FBC (neutrophilia, lymphopenia), ABG (# PO2, # PCO2).

Serology: Precipitating IgG to fungal or avian antigens in serum; however, these are not

diagnostic as are often found in asymptomatic individuals.

CXR: Often normal in acute episodes, may show ‘ground glass’ appearance with alveolar

shadowing or nodular opacities in the middle and lower zones. In chronic cases, fibrosis is

prominent in the upper zones.

High-resolution CT-thorax: Detects early changes before CXR. Patchy ‘ground glass’

shadowing and nodules.

Pulmonary function tests: Restrictive ventilatory defect (# FEV1, # FVC with preserved or

increased ratio), # TLCO.

Bronchoalveolar lavage: Increased cellularity with " CD8þ suppressor T cells. Lung biopsy

(transbronchial or thorascopic).

MANAGEMENT

Advice: Complete avoidance of exposure to the antigen (e.g. change of work practice or

hobby), if this is problematic, then minimize exposure and encourage use of respiratory

protection masks.

Medical:

Acute flare: Spontaneous recovery usually within 1–2 days, high-dose corticosteroids for 2–4

weeks may accelerate recovery but do not appear to affect long-term outcome.

Chronic disease: Trial of high-dose oral prednisolone for 1 month may be carried out, this is

gradually reduced, or stopped if no objective response demonstrated.

Extrinsic allergic alveolitis (continued)

General: Regular follow-up to monitor lung function. Environmental assessment is necessary

for risk posed to others. In UK, farmer’s lung patients are entitled to compensation,

depending on the degree of disability.

COMPLICATIONS 

Progressive lung fibrosis, pulmonary hypertension, right heart failure.

P ROGNOSIS 

The acute form generally resolves if further exposure is prevented, with

chronic disease some patients will improve while a minority progress to lung fibrosis.

1 تعليق

PH.Jafar Jassim 9/07/2020 03:03:00 ص

تابع القراءه

Cystic fibrosis

D E FI N I T ION

 Autosomal recessive inherited multi-system disease characterized by recurrent

respiratory tract infections, pancreatic insufficiency, malabsorption and male infertility.

AE T IOLOGY 

Caused by a defective CFTR gene on chromosome 7q, which encodes a

cAMP-dependent Cl

channel. This channel regulates Na

þ

and Cl

concentrations in

exocrine secretions, especially in the lung and pancreas. Any loss of function mutations

results in thick viscous secretions. Greater than 800 mutations reported, most common is

DF508 phenylalanine deletion (75% cases in UK).

At birth, the lung is normal histologically but as the lung matures there is mucous gland

hyperplasia, recurrent infection leads to fibrosis, consolidation and bronchiectasis.

E P IDEMIOLOGY 

Most common life-threatening autosomal inherited condition in Caucasians.

Incidence is 1 in 2500 live births. In UK, 1 in 25 are carriers.

H ISTORY

Lung: Recurrent chest infections, chronic cough, wheeze, sputum, haemoptysis.

Gut: Meconium ileus (in neonates), steatorrhoea (caused by " fat in the stool).

Other: Chronic sinusitis, nasal polyps, male infertility, arthritis.

EXAMINA T I ON

Chest: Chest wall deformities, coarse crepitations and wheeze.

Signs of malnutrition: Anaemia, weight loss, signs of vitamin deficiencies, slow growth,

failure to thrive in children, delayed puberty in adolescents.

Other: Clubbing, nasal polyps, signs of diabetes, hepatomegaly.

INVE S T I G A T IONS

Sweat test: Pilocarpine iontophoresis (low electrical current) stimulates sweat secretion

which is collected and analyzed for Na

þ

and ClCl



levels >60 mmol is diagnostic of

cystic fibrosis).

Neonatal screening: Standard day 6 Guthrie heal prick, blood is tested for immunoreactive

trypsin (raised by 2–5 in babies with cystic fibrosis).

CXR: May be normal in mild disease or show increased bronchial markings, ring shadows,

fibrosis (often upper zone). Consolidation or bronchiectasis in more advanced cases.

Pancreatic assessment: Faecal elastase, faecal fat content, GTT, HbA1c.

Genetic analysis: For CFTR mutations. Rarely necessary.

Lung function tests: To assess lung function and for long-term prognosis.

MANAGEMENT

Multidisciplinary specialist care is necessary.

Respiratory:

. Chest physiotherapy (postural drainage, regular exercise), positive expiratory pressure

masks;

. bronchodilator therapy (if responsive);

. nebulized recombinant human deoxyribonuclease (rhDNase) and hypertonic saline can be

used to assist in mucociliary clearance and may reduce pulmonary exarcebations;

. antibiotic prophylaxis and aggressive treatment of infections (especially Pseudomonas);

. influenza vaccination.

GI: Adequate nutritional intake is vital, using high-calorie oral supplements and oral

pancreatic enzyme replacement, vitamin (especially fat-soluble) supplements.

Endocrine: Insulin replacement therapy if diabetes develops.

Surgical: Single lung or heart–lung transplants is an option in end-stage disease (5-year

survival is 55%).

COM P L IC A T I ONS 

Recurrent chest infections, bronchiectasis (particularly Haemophilus,

Staphylococcus and Pseudomonas).

Cystic fibrosis (continued)

Malabsorption, meconium ileus, intussusception, rectal prolapse.

Diabetes mellitus Type I (30% by late teens).

Male infertility (females are fertile but conception may be difficult).

Gallstones.

P ROGNOS I S

 Life expectancy is in the third decade, but steadily improving. Those with

pancreatic insufficiency and those colonized by Pseudomonas have poorer prognosis. Gene

replacement therapy may be possible in the future.

0 تعليق

PH.Jafar Jassim 9/07/2020 02:56:00 ص

تابع القراءه

Chronic obstructive pulmonary disease (COPD)

D E FI N I T ION 

Chronic, progressive lung disorder characterized by airflow obstruction, with

the following.

Chronic bronchitis: Chronic cough and sputum production on most days for at least 3

months per year over 2 consecutive years; and/or

Emphysema: Pathological diagnosis of permanent destructive enlargement of air spaces

distal to the terminal bronchioles.

AE T IOLOGY 

Bronchial and alveolar damage as a result of environmental toxins (e.g.

cigarette smoke). A rare cause is a1-antitrypsin deficiency (<1%) but should be considered

in young patients or in those who have never smoked. Overlaps and may co-present

with asthma.

Chronic bronchitis: Narrowing of the airways resulting from bronchiole inflammation

(bronchiolitis) and bronchi with mucosal oedema, mucous hypersecretion and squamous

metaplasia.

Emphysema: Destruction and enlargement of the alveoli. This results in loss of the elastic

traction that keeps small airways open in expiration. Progressively larger spaces develop,

termed bullae (diameter is >1 cm).

E P IDEMIOLOGY

 Very common (prevalence up to 8%). Presents in middle age or later.

More common in males, but likely to change with " female smokers.

H ISTORY 

Chronic cough and sputum production (see Definition).

Breathlessness, wheeze, # exercise tolerance.

EXAMINA T I ON

Inspection: May have respiratory distress, use of accessory muscles, barrel-shaped overinflated

chest, # cricosternal distance, cyanosis.

Percussion: Hyper-resonant chest, loss of liver and cardiac dullness.

Auscultation: Quiet breath sounds, prolonged expiration, wheeze, rhonchi and crepitations

sometimes present.

Signs of CO2retention: Bounding pulse, warm peripheries, flapping tremor of the hands

(asterixis). In late stages, signs of right heart failure (e.g. right ventricular heave, raised JVP,

ankle oedema).

INVE S T I G A T IONS

Spirometry and pulmonary function tests: Obstructive picture as reflected by # PEFR, #

FEV1: FVC ratio (mild, 60–80%; moderate, 40–60%; severe, <40%), " lung volumes and

carbon monoxide gas transfer coefficient # when significant alveolar destruction.

CXR: May appear normal or show hyperinflation (>6 ribs visible anteriorly, flat hemidiaphragms),

# peripheral lung markings, elongated cardiac silhouette.

Blood: FBC (" Hb and PCV as a result of secondary polycythemia).

ABG: May show hypoxia (# PaO2), normal or " PaCO2.

ECG and echocardiogram: For cor pulmonale (see Cardiac failure).

Sputum and blood cultures: In acute exacerbations for treatment.

Consider a1-antitrypsin levels in young patients or minimal smoking history.

MANAGEMENT1

 Stop smoking.

Bronchodilators: Short-acting b2-agonists (e.g. salbutamol) and anticholinergics (e.g. ipratropium),

delivered by inhalers or nebulizers. Long-acting bronchodilators should be used

if >2 exacerbations per year.

Steroids: Inhaled beclometasone should be considered for all with FEV1 <50% predicted or

those with >2 exacerbations per year. Regular oral steroids should be avoided but may be

necessary for maintenance.

1Refer to http://www.nice.org.uk/nicemedia/pdf/CG012_niceguideline.pdf (NICE 2004 guidelines) for

complete information.

Chronic obstructive pulmonary disease (COPD) (continued)

Pulmonary rehabilitation.

Oxygen therapy (only for those who stop smoking): Long-term home oxygen therapy has

been shown to improve mortality. Indications are:

. PaO2 < 7.3 kPa on air during a period of clinical stability.

. PaO2 7.3–8.0 kPa and signs of secondary polycythaemia, nocturnal hypoxaemia, peripheral

oedema or pulmonary hypertension.

Oxygen concentrators are more economical if being used for >8 h/day.

Treatment of acute infective exacerbations:

Provide 24% O2 via non-variable flow Venturi mask.

Increase slowly if no hypercapnia and still hypoxic (measured by ABG).

Corticosteroids (oral or inhaled) are of proven benefit.

Start empirical antibiotic therapy (follow local policy) if evidence of infection.

Respiratory physiotherapy is essential to clear sputum.

Consider non-invasive ventilation in severe cases.

Prevention of infective exacerbations: Pneumococcal and influenza vaccination.

COMPL I C A T IONS

 Acute respiratory failure, infections (particularly Streptococcus pneumoniae,

Haemophilus influenzae), pulmonary hypertension and right heart failure, pneumothorax

(resulting from bullae rupture), secondary polycythaemia.

P ROGNOS I S

 High level of morbidity. Three-year survival rate of 90% if age <60 years and

FEV1 >50% predicted; 75% if >60 years and FEV1 40–49% predicted.

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PH.Jafar Jassim 9/04/2020 02:54:00 ص

تابع القراءه

Bronchiectasis

D E FI N I T ION L

ung airway disease characterized by chronic bronchial dilation, impaired

mucuociliary clearance and frequent bacterial infections.

AE T IOLOGY

 Severe inflammation in the lung causes fibrosis and dilation of the bronchi.

This is followed by pooling of mucus, predisposing to further cycles of infection, damage and

fibrosis to bronchial walls.

. Causes of bronchiectasis.

. Idiopathic in 50% of cases.

. Post-infectious: After severe pneumonia, whooping cough, tuberculosis.

Host defence defects: e.g. Kartagener’s syndrome,1 cystic fibrosis, immunoglobulin deficiency,

yellow-nail syndrome.2

. Obstruction of bronchi: Foreign body, enlarged lymph nodes.

. Gastric reflux disease.

. Inflammatory disorders: e.g. rheumatoid arthritis.

E P IDEMIOLOGY

 Most often arises initially in childhood, incidence has # with use of

antibiotics, approximately 1 in 1000 per year.

H ISTORY

 Productive cough with purulent sputum or haemoptysis.

Breathlessness, chest pain, malaise, fever, weight loss.

Symptoms usually begin after an acute respiratory illness.

EXAMINA T I ON

 Finger clubbing; Coarse creptitations (usually at the bases) which shift

with coughing; Wheeze.

INVE S T I G A T IONS

Sputum: Culture and sensitivity, common organisms in acute exacerbations: Pseudomonas

aeruginosa, Haemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae,

Klebsiella, Moraxella catarrhalis, Mycobacteria.

CXR: Dilated bronchi may be seen as parallel lines radiating from hilum to the diaphragm

(‘tramline shadows’). It may also show fibrosis, atelectasis, pneumonic consolidations, or

it may be normal.

High-resolution CT: Dilated bronchi with thickened walls. Best diagnostic method.

Bronchography (rarely used): To determine extent of disease before surgery (radioopaque

contrast injected through the cricoid ligament or via a bronchoscope).

Other: Sweat electrolytes (see Cystic fibrosis), serum immunoglobulins (10%of adults have

some immune deficiency), sinus X-ray (30% have concomitant rhinosinusitis), mucociliary

clearance study.

MANAGEMENT 

Treat acute exacerbations with two IV antibiotics with efficacy for

Pseudomonas. Prophylactic courses of antibiotics (oral or aerosolized) for those with

frequent (3/year) exacerbations.

Inhaled corticosteroids (e.g. fluticasone) have been shown to reduce inflammation and

volume of sputum, although it does not affect the frequency of exacerbations or lung

function.

Bronchodilators may be considered in patients with responsive disease.

Maintain hydration with adequate oral fluid intake.

1 Kartagener’s syndrome is caused by immotile cilia and is characterized by a combination of chronic

sinusitis, infertility and situs inversus.

2 Yellow-nail syndrome is characterized by pleural effusions, lymphoedema and yellow dystrophic nails.

Approximately 40% will also have bronchiectasis.

Bronchiectasis (continued)

Consider flu vaccination.

Physiotherapy: Cornerstone of management is sputum and mucus clearance techniques (e.g.

postural drainage). Patients are taught to position themselves so the lobe to be drained is

uppermost, 20 min twice daily. Some studies show that these techniques reduce

frequency of acute exacerbations and aids recovery.

Bronchial artery embolization: For life-threatening haemoptysis due to bronchiectasis.

Surgical: Various surgical options include localized resection, lung or heart–lung

transplantation.

COMPL I C A T IONS 

Life-threatening haemoptysis, persistent infections, empyema, respiratory

failure, cor pulmonale, multi-organ abscesses.

P ROGNOS I S

 Most patients continue to have the symptoms after 10 years.

0 تعليق

PH.Jafar Jassim 9/04/2020 02:46:00 ص

تابع القراءه

Asthma

D E FI N I T ION

 Chronic inflammatory airway disease characterized by variable reversible

airway obstruction, airway hyper-responsiveness and bronchial inflammation.

AE T IOLOGY

Genetic factors: Positive family history, twin studies. Almost all asthmatic patients show

some atopy (tendency of T lymphocyte (Th2) cells to drive production of IgE on exposure to

allergens). Linkages to multiple chromosomal locations point to ‘genetic heterogeneity’.

Environmental factors: House dust mite, pollen, pets (e.g. urinary proteins, furs), cigarette

smoke, viral respiratory tract infection, Aspergillus fumigatus spores, occupational

allergens (isocyanates, epoxy resins).

PATHOLOGY/PATHOGENESI S

Early phase (up to 1 h): Exposure to inhaled allergens in a presensitized individual results in

cross-linking of IgE antibodies on the mast cell surface and release of histamine,

prostaglandin D2, leukotrienes and TNF-a. These mediators induce smooth muscle

contraction (bronchoconstriction), mucous hypersecretion, oedema and airway

obstruction.

Late phase (after 6–12 h): Recruitment of eosinophils, basophils, neutrophil and Th2

lymphocytes and their products results in perpetuation of the inflammation and bronchial

hyper-responsiveness.

Structural cells (bronchial epithelial cells, fibroblasts, smooth muscle and vascular endothelial

cells), may also release cytokines, profibrogenic and proliferative growth factors, and

contribute to the inflammation and altered function and proliferation of smooth muscle

cells and fibroblasts (‘airway remodeling’).

E P IDEMIOLOGY 

Affects 10% of children and 5% of adults. The prevalence of asthma

appears to be increasing. ,¼<. Acute asthma is a very common medical emergency and still

responsible for 1000–2000 deaths/year in the UK.

H ISTORY 

Episodes of wheeze, breathlessness, cough; worse in the morning and at night.

Ask about interference with exercise, sleeping, days off school and work.

In an acute attack it is important to ask whether the patient has been admitted to hospital

because of his/her asthma, or to ITU, as a gauge of potential severity.

Precipitating factors: Cold, viral infection, drugs (b-blockers, NSAIDs), exercise, emotions.

May have a history of allergic rhinitis, urticaria, eczema, nasal polyps, acid reflux and family

history.

EXAMINA T I ON 

Tachypnoea, use of accessory muscles, prolonged expiratory phase,

polyphonic wheeze, hyperinflated chest.

Severe attack: PEFR <50% predicted, pulse > 110/min, respiratory rate > 25/min, inability to

complete sentences.

Life-threatening attack: PEFR < 33%, silent chest, cyanosis, bradycardia, hypotension,

confusion, coma.

INVE S T I G A T IONS

Acute: Peak flow, pulse oximetry, ABG, CXR (to exclude other diagnoses, e.g. pneumothorax,

pneumonia), FBC (" WCC if infective exacerbation), CRP, U&Es, blood and sputum

cultures.

Chronic: PEFR monitoring: There is often a diurnal variation with a morning ‘dip’.

Pulmonary function test: Obstructive defect, with improvement after a trial of a b2-agonist.

Blood: Eosinophilia, IgE level, Aspergillus antibody titres (see allergic Aspergillus lung disease).

Skin prick tests: May help in the identification of allergens

Asthma (continued)

MANAGEMENT

Acute:

. Resuscitate, monitor O2 sats, ABG and PEFR.

. High-flow oxygen.

. Nebulized b2-agonist bronchodilator salbutamol (5 mg, initially continuously, then 2–4

hourly), ipratropium (0.5mg qds).

. Steroid therapy (100–200mg IV hydrocortisone, followed by 40mg oral prednisolone for

5–7 days).

. If no improvement: IV magnesium sulphate. Consider IV aminophylline infusion or IV

salbutamol.

. Summon anaesthetic help if patient is getting exhausted (PCO2 increasing).

Treat any underlying cause (e.g. infection, pneumothorax). Give antibiotics if there is

evidence of chest infection (purulent sputum, abnormal CXR, " WCC, fever). Monitor

electrolytes closely (bronchodilators and aminophyline # K

þ

).

. May need ventilation in severe attacks. If not improving or patient tiring, involve ITU early.

Discharge: When PEF >75% predicted or patient’s best, diurnal variation < 25%, inhaler

technique checked, stable on discharge medication for 24 h, patient owns a PEF meter

and has steroid and bronchodilator therapy. Arrange follow-up.

Chronic ‘stepwise’ therapy: Start on the step appropriate to initial severity and step up or

down to control symptoms. Treatment should be reviewed every 3–6 months.

Step 1: Inhaled short-acting b2-agonist as needed. If used >1/day, move to Step 2.

Step 2: As Step 1 plus regular inhaled low-dose steroids (400 mcg/day).

Step 3: As Step 2 plus inhaled long-acting b2-agonist (LABA). If inadequate control with LABA,

" steroid dose (800 mcg/day). If no response to LABA, stop and " steroid dose (800 mcg/

day).

Step 4: " Inhaled steroid dose (2000 mcg/day), add a fourth drug, e.g. leukotriene receptor

antagonist, SR theophylline or b2-agonist tablet.

Step 5: Addition of regular oral steroids. Maintain high-dose inhaled steroid. Consider other

treatments to minimize the use of oral steroids. Refer for specialist care.

Advice: Educate on proper inhaler technique and routine monitoring of peak flow. Develop

an individualized management plan, with emphasis on avoidance of provoking factors.

COMPL I C A T IONS

 Growth retardation, chest wall deformity (e.g. pigeon chest), recurrent

infections, pneumothorax, respiratory failure, death.

P ROGNOS I S

 Many children improve as they grow older. Adult-onset asthma is usually

chronic.

0 تعليق

PH.Jafar Jassim 8/31/2020 03:05:00 ص

تابع القراءه

Aspergillus lung disease

D E FI N I T ION 

Lung disease associated with Aspergillus fungal infection.

AE T IOLOGY 

Inhalation of the ubiquitous Aspergillus (usually Aspergillus fumigates) spores

can produce three different clinical pictures:

1. Aspergilloma: Growth of an A. fumigatus mycetoma ball in a preexisting lung cavity (e.g.

post-TB, old infarct or abscess).

2. Allergic bronchopulmonary aspergillosis (ABPA): Aspergillus colonization of the

airways (usually in asthmatics) leads to IgE- and IgG-mediated immune responses.

Proteolytic enzymes and mycotoxins released by fungi, CD4/Th2 cells producing IL-4 and

IL-5 and mediating eosinophilic inflammation, and IL-8 mediated neutrophilic inflammation

result in airway damage and central bronchiectasis.

Invasive aspergillosis: Invasion of Aspergillus into lung tissue and fungal dissemination.

Secondary to immunosuppression (e.g. neutropaenia, steroids, haematopoietic stem cell/

solid organ transplantation, AIDS).

E P IDEMIOLOGY

 Uncommon. Most common in elderly and immunocompromised.

H ISTORY

Aspergilloma: Asymptomatic, haemoptysis, which may be massive.

ABPA: Difficult to control asthma, recurrent episodes of pneumonia with wheeze, cough,

fever and malaise.

Invasive aspergillosis: Dyspnoea, rapid deterioration, septic picture.

EXAMINA T I ON

 Tracheal deviation in large aspergillomas.

Dullness in affected lung, # breath sounds, wheeze (in ABPA).

Cyanosis may develop in invasive aspergillosis.

INVE S T I G A T IONS

Aspergilloma: CXR: Round opacity may be seen with a crescent of air around it (usually in the

upper lobes).

CT or MR imaging if CXR does not clearly delineate a cavity.

Cultures of the sputum may be negative if there is no communication between the cavity and

the bronchial tree. Also Aspergillus is a common colonizer of an abnormal respiratory

tract.

ABPA:

Immediate skin test reactivity to Aspergillus antigens.

Eosinophilia.

" Serum total IgE.

" Serum specific IgE and IgG to A. fumigatus or precipitating serum antibodies to A.

fumigates.

CXR: Transient patchy shadows, collapse, distended mucus-filled bronchi producing tubular

shadows (‘gloved fingers’ appearance). Signs of complications: Fibrosis in upper lobes

(similar to tuberculosis), parallel-line shadows and rings (bronchiectasis).

CT: Lung infiltrates, central bronchiectasis.

Lung function tests: Reversible airflow limitation, # lung volumes/gas transfer in progressive

cases.

Invasive aspergillosis: Detection of Aspergillus in cultures or by histologic examination

(septated hyphae with acute angle branching). Diagnosis may be made in patients with

risk factors, suggestive clinical findings and microscopic evidence of septate hyphae on

examination of either bronchoalveolar lavage fluid or sputum or a positive serum

galactomannan or beta-D-glucan assay (constituents of Aspergillus cell walls).

Chest CT scan may show nodules surrounded by a ground-glass appearance (halo sign) in

invasive pulmonary aspergillosis (haemorrhage into the tissue surrounding the area of

.fungal invasion)

Aspergillus lung disease (continued)

MANAGEMENT

Aspergilloma: Surgical resection for large aspergillomas if uncontrolled or symptomatic

(recurrent haemoptysis). Adjunctive itraconazole or voriconazole, if there is concern for

residual disease following surgery, or tissue invasion beyond the confines of the cavity.

ABPA: Combination of steroids and itraconazole. Monitor LFTs. The usual duration of therapy

is 3–6 months. Inhaled steroids and broncholdilators may help control symptoms of

asthma. The response is monitored with serial measurement of the serum total IgE level.

Invasive aspergillosis: # Immunosuppression if possible. Voriconazole (initially IV, when

stabilized orally). Monitor serum voriconazole trough concentrations. If intolerant of

voriconazole, use liposomal amphotericin B. Add caspofungin in patients who do not

respond. Continue antifungal therapy until all signs, symptoms and radiographic evidence

of the infection have resolved for at least 2 weeks. Debridement is essential in the

treatment of Aspergillus sinusitis.

COMPL I C A T IONS

Aspergilloma: Secondary bacterial infection, massive haemoptysis or haemorrhage.

ABPA: Worsening of asthma, bronchiectasis, lobar collapse, lung fibrosis or respiratory

failure.

Invasive aspergillosis: Septic shock, respiratory failure.

P ROGNOS I S

 Grave prognosis for invasive aspergillosis. Good prognosis for ABPA and

aspergillomas but bronchospasm and haemoptysis can still lead to death.

0 تعليق

PH.Jafar Jassim 8/19/2020 06:20:00 ص

تابع القراءه

يجب أن يتمتع بالثقافة الطبية حتى وإن لم يكن يكن طبيباً  ، والتي تعتبر الثقافة والمعرفة تعتبر عصباً لحياة الإنسان ، وصحة المجتمع الذي يعيش فيه ، وفي هذا المقال سوف تتذكر مجموعة معلومات عامة تختص في مجال الطب.

 من أهمّ الغدد في جسم الإنسان: الغدة الجنبدرقية ، والنخامية ، والدرقية ، والجنسية ، والمعدة ، والكظرية ، والعرقية ، والبنكرياس ، 

واللعابية. 

ينقل القمل للإنسان مرض اسمه التيفوس. 

الغدد الليمفاوية تعمل على تصفية الدم وتطهيره. يطلق عملية غسيل الكلى. 

يعدّ الكبد العضو الوحيد في جسم الإنسان الذي يعود للنمو بعد اقتطاع جزء منه. 

في العام 1989 م تمتت عملية زراعة الكبد في شيكاغو الأمريكية. 

مرض انفصام الشخصية اسمه مرض الشيزوفرينيا. فصيلة الدم

 o + تسمّى باسم فصيلة الدم الكريمة. 

تعرف الذبحة الصدرية بأنّها عبارة عن ألم حاد وقصير الوقت يحدث في الصدر وذلك بسبب إصابة الشريان التاجي. 

فيتامين الوحيد الذي يكسبه الجسم من أشعة الشمس هو فيتامين د. 

يبلغ وزن مخضر الإنسان البالغ من 3 إلى 2 كغم. 

الغدة التي تصبّ جميع محتوياتها بشكل مباشر في الدم هي الغدد الصماء. 

يؤدي نقص فيتامين أ للإصابة بمرض العشى الليليّ. 

من أعراض مرض البلاجرا: الغثيان ، والاكتئاب ، والصداع ، والإسهال ، والتهاب الجلد. 

يعتبر الطبيب العربي مجدي يعقوب من أشهر جراحي القلب على مستوى العالم ، وفردريك بانتينج مكتشف الإنسولين ، والطبيب العربي ابن زهر مكتشف جرثومة الجرب ، وسالك مكتشف مصل شلل الأطفال. يقصد بمرض السرطان الانقسام غير العادي لخلايا الجسم دون توقّف. 

وظيفة كريات الدم البيضاء هي الدفاع عن الجسم ضد الأمراض والجراثيم. 

تقع الغدة الدرقية في الرقبة. 

مادة الميلانين هي المسؤولة عن تلوين جسم الإنسان. 

تعدّ العضلات أثقل من العظام. 

يبلغ عدد فقرات العمود الفقري ثلاثاً وثلاثين فقرة. 

يعتبر مخ ّالمرأة أقل وزناً من مخّ الرجل. يبلغ عدد عظام الجمجمة اثنتين وعشرين عظمة. 

يبلغ حجم الهواء الذي يستنشقه الإنسان في كل عام خمسة ملايين لتر.

يبلغ عدد ضربات قلب الحوت ضربة واحدة في الدقيقة الواحدة. 

يبلغ عدد خلايا الجسم في الإنسان ستين ترليون خلية. 

يبلغ عدد الخلايا العصبية الذي يملكها الإنسان ثمانية وعشرين بليون خلية. 

المسؤول عن التذوق هي الحليمات الذوقية في اللسان. 

تعتبر عضلة الفخذ أكبر عضلة في الجسم ، وعضلة الركاب في الأذن الوسطى أصغر عضلة ، وعضلة الفكين أقوى عضلة. 

ضم المعدة تتكون من المخاط ، ولو لم تكن كذلك له ضمت نفسها .

1 تعليق

PH.Jafar Jassim 7/29/2020 12:19:00 ص

تابع القراءه