Bronchial syndrome Flashcards
(42 cards)
1
Q
Acute bronchitis
A
- nonproductive or midly productive cough
2
Q
Bronchial syndrome
A
Permanent = COPD Transient = asthma attack
3
Q
Asthma
A
- airflow obstruction
- bronchial hyperresponsiveness
- underlying inflammation
4
Q
Asthma involves
A
- Bronchoconstriction
- Airway edema + inflammation
- Airway hyperreactivity
- Airway remodeling
5
Q
Bronchoconstriction
A
- dominant physiological event
- bronchial smooth muscle contraction - occurs quickly + narrows the airways in response to exposure to stimuli
- stimulus -> IgE mediated activation of mast cells -> released mediatiors ( histamiine , tryptase , leukotrienes , prostagladins ) -> bronchoconstriction
6
Q
Airway inflamation / mucus hypersecretion
A
- narrows the airways
- cell migration / activation -> inflammatory infiltration epithelia -> release of mediators - > epithelial edema
- increase in number of GOBLET CELLS ; increase of mucus production
7
Q
Airway remodelation
A
- diminishing the response to drugs + increasing hyperresponsiveness
1. thickening of the sub- basement membrane
2. subepithelial fibrosis
3. airway smooth muscle hypertrophy + hyperplasia
4. blood vessel proliferation + dilation
5. mucous gland hyperplasia + hypersecretion
8
Q
Hyperresponsiveness
A
= An exaggerated bronchoconstrictor response to a wide variety of stimuli that do not necessarily determine clinical expressed bronchoconstriction to
a healthy person
- Major but not unique response of asthma
- MECHANISMS : inflammation , dysfunctional neuroregulation , structural changes
- Not equivalent to asthma ; normally present in the covalesence of the viral respiratory infection
9
Q
Pathogenesis of asthma
A
- Multifactorial ; depends on interactions of multiple susceptibility genes + environmental factors
- Host : innate imbalance of immune response ; cytokines response profile - determining capability of smooth muscle activation + fibroblast production
- Environment : allergens + respiratory infections
- onset :childhood ( earlier in boys ; girls after puberty)
10
Q
Diagnosis of asthma
A
the clinicial should determine :
- Episodic symptoms : of airflow obstruction or airway hyperresponsiveness are present
- Airflow obstruction : at least partially reversible
- Alternative diagnosis are exluded
11
Q
Methods of diagnosis
A
- Medical history
- Physical exam on upper respiratory tract , chest , skin
- Spirometry : to demonstrate obstruction + assess reversibility , including in childern 5 y or older .
Reversibility is determined by an increase in FEV1 of >= 12 of a short acting bronchodilator
12
Q
Triggers of asthma
A
- Environmental + occupational allergens ( numerous ) = pollens
- Viral infections
- Exercise , rapid changes in environmental temperature
- Inhaled irritants ( perfumes , cleaning products ) tobacco smoke
- stress
- Aspirin /NSAID / β - blockers
13
Q
Domestic trigger of asthma
A
- Home - related Allergens :
> House dust - mite ( dermatophagoides sp )
> Crockroach
> Pets
14
Q
Symptoms of asthma attack
A
- Dyspnea + wheezing
- Cough
- Chest tightness
15
Q
Dyspnea ( asthma )
A
- Starts : brupt
- During nighttime ( 4 am - vagal predominance ) / temporal relationship to the exposure to trigger
- EXPIRATORY
> classic : bradipnea
> wheezing , predominanlty during expiration
16
Q
Cough
A
- Dry at the beginning , becomes productive
Sputum : PEARL appearance - mucus , clear , adherent
MICROSCOPIC EXAM : - Curshman spirals
- Charcot Leyden crystals
17
Q
Cough - variant asthma
A
No dyspnea
18
Q
Physical examination
A
- Anti - dispneic decubitus
- Anxiety
- Tahicardia , mild hypertension , pulsus paradoxus
- Diaphoresis
- No cianosis
19
Q
Respiratory examination
A
- INSPECTION :
- tahipnea
- hyperinflation
- barrel chest
- effort of breathing : use of neck , suprasternal muscles ; pursed lips ,inability to speak - PALPATION :
- diminished chest expansion
- diminished elasticity
- diminished tactile fremitus - PRECAUSSION :
- diffuse hyperrresonance
20
Q
Auscultation
A
- important prolongation of expiration ( usually > 1:3 )
- Diminished vesicular sounds , diffuse
- Rales : bronchial , wheezes predominate , plus ronchi , coarse crackes
- Wheezes persistent after the end of the attack
21
Q
Paraclinical examination
A
- Chest X-ray not mandatory, shows hyperinflation
- Lab: mild leucocitosis with eosinofilia (> 400 cells/μL),
elevated IgE (>150 IU)
-Allergy testing may be indicated for children whose
history suggests allergic triggers . It should be
considered for adults whose history indicates relief of
symptoms with allergen avoidance.. - Sputum microscopic examination
- Pulmonary function tests- spirometry, PEF
22
Q
Status asthmaticus
A
- Very severe asthma attack, symptoms lasting > 24 h
- Loud wheeze slowly diminishes and disappears;
auscultatory silentium - Agitation, from severe, stops- confusion and
drowsiness intervenes - Complete inability to speak
- Bradicardia
- Cold, moist extremities
- PO2 decreases=cyanosis- under 60 mmHg=imminent
respiratory arrest
23
Q
Chronic Obstructive Pulmonary
Disease (COPD)
A
- Is a preventable and treatable disease that is characterized by persistent respiratory symptoms and
airflow limitations that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases. - The chronic airflow limitation is caused by a mixture of small airways disease (bronchitis) and parenchymal destruction (emphysema) the relative contribution of which vary from person to person
24
Q
Pulmonary Emphysema
A
destruction of lung parenchyma leading to loss of elastic recoil and loss of alveolar septa and radial airway traction, which increases the tendency for airway collapse.
Lung hyperinflation, airflow limitation, and air trapping follow.
Airspaces enlarge and may eventually develop bullae.
25
Chronic bronchitis
- Is a chronic inflammation of the lower airways,
characterized by chronic productive cough, as a result
of low-grade exposure to respiratory irritants of a
person without hyperresponsiveness of bronchias
- Mandatory symptoms: cough with mucous
expectoration for repeated days, more then 3
months/year in at least 2 consecutive years (if
bronchiectasias and tb are excluded)
26
Etiology of chronic bronchitis
1. SMOKING(the leading risk factor)
2. Indoor air pollution: biomass cooking and heating:(wood,coal burned in open fires or poorly functioning stoves)
3. Genetic: severe hereditary deficiency for α-1 antitrypsin
4. Occupational: mineral dust, cotton dust
5. High level of urban air pollution
27
α-1 antitrypsin deficiency
= congenital lack of α-1 antitrypsin, a neutrophil
elastase inhibitor
- Clinically manifest: homozygotes ZZ
- Emphysema develop before age 45 (rarely before 25); or in non-smokers, no occupational risk;
- Associated: liver impairment (cirrhosis in childhood or
early in adulthood)
28
Chronic bronchitis= pathological changes
1. Inflammatory infiltrate
2. Hyperplasia of mucous glands
3. Localized area of scuamous metaplasia
4. Smooth muscle hypertrophia
5. Peribronchial fibrosis
6. Distruction of elastin fibers
29
Emphysema- pathological changes
1. Centro-lobular: common, in smokers- modifications starts and are more pronounced in the central
portion of the lobule
2. Pan-lobular: common in α-1 antitrypsin def.
3. Distal lobular: peripheral, can associate with giant
bullae
30
Pulmonary symptoms
- Productive cough, mucous sputum
| - Shortness of breath
31
Dispneea ( chronic bronchitis + emphysema )
1. Progressive
2. Persistent
3. Exertional
4. Expiratory
5. With polipneea
6. With wheezing
7. Worsens during respiratory infections
32
Exacerbation
worsening of symptoms, determining
factors not always identified, but infections presumed,
in severe cases > 3/year
33
Type A: emphysema,
| “pink puffer”
- Age: 50-70
- Dispneea is the predominant symptom
- Long thorax
- Cyanosis develop lately
- Weight loss, muscle wasting
- Marked impairment of diffusing capacity
34
Type B: chronic bronchitis,
| “blue bloater”
- Age: 40-60
- Cough and sputum production are the
predominant symptoms
- Pycnic thorax
- Cyanotic from early stages
- Any nutritional status, can be obese
- Marked obstruction
35
Extra-pulmonary manifestations
- Cachexia, loss of fat-free mass
- Muscle wasting: apoptosis, diffuse atrophy
- Osteoporosis
- Apoptosis
- Depression
36
Complications
1. Pulmonary hypertension
2. Cor pulmonale
3. Respiratory failure: symptoms
- Morning headaches
- Cynosis, central
- Chemosis
- Flapping tremor
37
Pulmonary hypertension
1. Consequence of:
- hypoxemia- arterial smooth muscle constriction, in time hypertrophies and vasoconstriction becomes permanent
- Destruction of pulmonary vasculature
2. Right-sided heart failure= cor pulmonale
- systemic congestion
- ECG: clockwise rotation, RA enlargement (P pulmonale),
eventually RBBB
- right A and V dilation, tricuspid regurgitation
38
Clinical examination :Inspection
1. Static : Barrel chest
- short neck
- filled supraclavicular fossae
- Horizontal ribs , large intercostal spaces
- A-P diameter larger than the lateral one
2. Dinamic :
- small amplitude inflations ; retraction of inferior intercostal spaces in inspiration ( Hoover's sign )
- Prolonged expiration
- Eventually , usage of accessory respiratory muscles
39
Palpation
1. Static :
- confirms modification observed before
- reduced passive mobility
2. Dynamic :
- Reduced excursion of apices and bases
- Slightly reduced tactile fremitus
40
Precussion
- Resonance extended to the lateral third of clavicle
- Diffuse hyperresonance
- Tympanic sounds over bullae
- Hirtz maneuver can be negative if hyperinflation is extreme
41
Auscultation
- Prolonged expiration
- Diffuse diminishing of vesicular sounds
- Wheezes, ronchi, crackles- symmetrical
- Asymmetrical auscultation= into exacerbations can signal condensation/effusions/pneumothorax
42
Spirometry
Criteria for diagnosis: FEV1/FVC: < 70%
FEV1: classifies the severity
- mild: >80%
- moderate: <80%
- severe: 30
