KEY wk 5 lec 2 Flashcards
types of obstructive vs restrictive lung diease
obstructive:
-bronchial asthma
-COPD (chronic bronchitis and emphysema)
-bronchiectasis
restrictive:
-acute: ARDS (diffuse alveolar damage)
-chronic: idiopathic pulmonary fibrosis
restrictive vs obstructive lung disease
obstructive: cant exhale bc airway narrow or obstructed; trap air in lungs (air trapped in alveoli)
restrictive: cant inhale bc lung expansion reduced from stiff lung tissue or impaired respiratory mechanics
pulmonary function tests (2)
spirometry
bodyplethysmogrpahy
FEV1/FVC in obstructive vs restrictive
obstructive: reduced
restrictive: normal or increase (“physiological”)
TLC (total lung capacity) and RV (residual volume) and FRC (functional residual capacity) in restrictive vs obstructive lung disease
obstructive: increased by air trapped (hyperinflation)
restrictive: low lung volumes; decreased both because lung cant expand
bronchial asthma (obstructive)
pathophysiology
irreversible or reversible?
inflammatory cell involved
episodic airway obstruction, hyper responsiveness and inflammation
reversible
eosinophils
bronchial asthma “trias” definition
chronic inflammation
reversibility of obstructive ventilatory impairment
obstructive ventilatory impairment and bronchial hyperactivity (sx)
risks for bronchial asthma
polygenic inheritance (i.e. Beta receptor) and environment and atopy
sx of atopy and test
Nose: Allergic rhinitis
Eye: Allergic conjunctivitis
Skin: Eczema
Nose: Hey fever
Allergies (food, contact, inhalation)
Positive skin tests (prick tests)
triggers of bronchoconstrictions
allergens
infections in upper airays
inhalatory irritants
anxiety, cold air, GERD, exercise
drugs esp NSAIDS, aspirin
food preservatives (sulphites)
classification of asthma
allergic vs non allergic
- Allergic - Atopic
- Nonallergic – Nonatopic 3. Drug-induced asthma
- Occupational asthma
- Cardiac asthma
allergic asthma
sx
type _ hypersensitivity
causes
kids, hay fever, eczema
type I hypersenstiivity
pollens, dusts, drugs
pathogensis of allergic asthma
ILs? Th_? Ig_?
hyperactive airway constricts to stimuli; increase airway resistance
type 1 hypersensitivity
CD4+ and Th2 release IL-4 and IL-5 which then stimulate eosinophils –> produce IgE
nonallergic asthma
what levels are normal
causes
adults
NOT type 1 hypersensitivity; IgE is normal
Th17 and Th1 drive infalmmation
exercise, cold air, drugs, GERD, viral (rhinovirus, parainfluenza), hormonal, pregnancy
early vs late stage of asthma
early: bronchoconstriction via histamine, prostaglandin, leukotrienes
late: neutrophils release proteases and eosinophils release major basic protein
mechanisms of airway obstruction
hyper responsive, inflammation, collagen deposition, smooth muscle constriction vascular proliferation, edema, goblet cell metaplasia and mucus hypersecretion
2 components of airway hyperresponsiveness
- functional: hyper responsive to direct smooth muscle acting agents like histamine or methacholine
- structural: wall thickness (smooth muscle hypertrophy, collagen deposition, edema, inflammation)
gross vs microscopic morphology of asthma
gross: status asthmatics= hyperinflated lungs, mucus plugging
microscopic: charcot-leyden crystals (from major basic protein), curschmann spirals, eosinophil infiltrate
spirometry in asthma exacerbation (obstructive)
FEV1/FVC
PEF (peak expiratory flow)
residual volume
and reversibility from
FEV1/FVC: reduced
PEF reduced
RV increased
reversible via bronchodilator
spirometry between exacerbations in early vs late asthma
early= normal
late=
low peak expiratory flow (PEF)
reduced FEV1/FVC
increase residual volume
arterial blood gases in asthma during exacerbation vs in between exacerbations
during: CO2 low; hyperventilate (compensatory), CO2 rises if respiratory failure (later stages)
between: PaO2 and PaCO2 are normal;
classic triad of symptoms in asthma
when are they worse and because of what hormone
wheeze, cough, dyspnea
worse or only present at night becasue of cortisol drop
status asthmaticus= prolonged attacks
face findings in asthma
Dark rings under the eyes
(“allergic shiners”)
Dark transverse crease on the nose (“allergic salute”)
2 types of COPD
- chronic bronchitis
- emphysema
airflow limitation that’s not reversible; progressive and inflammatory
risk factors for COPD
genes (alpha-1-antitrypsin deficiency)
tobacco smoke *** BIGGEST
occupational dusts
air pollution
4 evens of COPD
- inflammatory and immune cell recruitment to airways
- proteinase damage ECM in airways
- cell death via oxidant induced damage
- disordered repair of elastin (emphysema)
cellular mechanisms in COPD
chronic bronchitis: larger airways, airway remodelling, mucus secretion
emphysema: terminal airways, loss of alveoli, loss of elastin
both from apoptosis, inflammation, immune response, oxidants
chronic bronchitis
time line
causes
types
productive cough for > 3 months
cigarettes irritate airway and increase and hyperplasia of mucus glands, metaplasia of goblet cells, thicken submucosal layer
simple, obstructive and asthmatic
pathology in chronic bronchitis
airway obstruction
air trapping- hyperinflation
emphysema
what changes to lungs
lose pulmonary parenchyma –> lose elastic recoil –> exhalation; airway collapse –> air trapping
lose alveolar septa and airway walls and dilate terminal airways
morphology of emphysema
dilation of airspaces
bull form in pleural space
2 types of emphysema and their causes and what area of lungs are effected
centriacinar emphysema from smoking affect respiratory bronchioles in upper lobes
panacinar emphysema from alpha1-antitrypsin deficiency affect alveoli, alveolar ducts, respiratory bronchioles in lower lobes
CT patterns of emphysema
- centrilobular (upper lobe; smoking)
- pan lobular (diffuse loss, lower lobe; A1 antitrypsin deficiency)
- paraseptal (smoking)
blue bloater vs pink puffer
blue (chronic bronchitis): peripheral edema (fat), RV heart fail, cyanosis, hypercapnia
pink (emphysema): hypercapnia, hypoxemia, minimal cyanosis, muscle wasting (skinny)
obstructive bronchitis vs emphysema
obstructive bronchitis:
-chronic productive cough
-hypercapnia
-right ventricular failure
-peripheral edema
emphysema:
- dyspnea
-hypoxemia
-hypercapnia
-hyperventilation
spirometry on obstructive ventilatory impairment
FEV1 is reduced
FVC is normal of slightly reduced
FEV1/FVC is reduced to < 0.7
complications of COPD
pulmonary hypertension (from hypoxia induced vasospasm)
cor pulmonale (right sided heart failure bc of pulmonary hypertension)
mismatched ventilation-perfusion (shunt blood to areas of poor ventilation)
respiratory failure
bronchiectasis (obstructive lung disease)
what forms and which is most common
irreversible airway dilation
focal or diffuse
cylindrical or tubular (most common), varicose or cystic
2 compoennts/ causes of bronchiectasis
infection and obstruction
infection destroys smooth muscle and elastic fibers of airway wall
non infectious vs infectious bronchiectasis and what type of presentation
non-infectious (obstruction of airway) causes focal bronchiectasis
1. extrinsic (compressed by adjacent lymphadenopathy or parenchymal tumor mass)
2. intrinsic (airway tumor or aspirated foreign body)
infectious disease or systemic causes diffuse bronchiectasis (I.e HIV immunodeficiniey, mycobacterial, antitrypsin genes, autoimmune, IBD, rheumatoid arthritis, idiopathic)
pathogenesis of infectious diffuse bronchiectasis; “vicious cycle hypothesis”
infection susceptibility- poor mucocilliary clearance
microbial colonization (p. aeruginosa)
severe infection (pneumonia from Bordetella pertussis or Mycoplasma pneumoniae)
chronic inflmamtion
mediators released from bacteria
gross and microscopic morphology in bronchiectasis
gross: dilate away, esp. lower right lobe, airways extend into pleural space
microscopic: inflammatory infiltrate and tissue destruction
sx and signs of bronchiectasis
dyspnea, chronić cough with sputum, hemoptysis
finger clubbing (pulmonary osteoarthropathy), hypoxemia, hypercapnia, chest radiograph shows parallel lines= thickened bronchial walls
complications of bronchiectasis
recurrent infections (i.e. antibiotics)
hemoptysis –> hemorrhage
rare: pulmonary hypertension, abscess formation, amyloidosis
restrictive lung disease spirometry findings
reduction of all volumes
FEV1/FVC is normal
2 categories of restrictive lung disease
extra pulmonary (obesity, chest deformity, kyphoscoliosis)
intrapulmonary (primary or secondary, acute ARDS or chronic)
intrapulmonary restrictive lung disease cause a reduction in
diffusion capacity
pathogenesis of intrapulmonary restrictive lung diseases
initial to late phase
environmental, idiopathic, genetic
initial phase: inflammation: alveolitis (lymphocytes, neutrophils)
late phase: fibrosis: alveoli’s (lymphocytes, neutrophils)
ACUTE: ARDS (acute restrictive lung disease) - AKA Diffuse Alveolar Damage
secondary too
findings
short time period (mins to days)
second to major systemic insult (i.e. sepsis, shock)
diffuse pulmonary infiltrates and hypoxemic respiratory failure)
increased vascular permeability
necrosis of cells
redution in diffusion capacity
3 stages of diffuse alveolar damage (ARDS)
- exudative stage (protein and necrotic cells on alveolar septae form hyaline membranes)
- proliferative (type II pneumocytes undergo hyperplasia)
- fibrosis
4 main causes of diffuse alveolar damage (ARDS)
- sever pulmonary infetion
- aspiration
- sepsis
- severe trauma with shock
other: viral, acute pancreatitis, acute interstitial pneumonitis….
sx and signs of diffuse alveolar damage (ARDS)
dyspnea, pink frothy sputum
signs: crackles, hypoxemia, diffuse alveolar infiltrates
high mortality
-develop fibrosis –> chronic restrictive lung disease - pulmonary hypertension
chronic restrictive lung disease
inflam, fibrosis, impaired gas exchange (low diffusing capacity from carbon monoxide), obstructive ventilation impairments (decreased and normal FEV1/FVC)
causes of interstitial lung disease
autoimmune (i.e. lupus)
idipathic
work (asbestosis, silica, coal)
drugs
chronic idiopathic pulmonary fibrosis (restrictive)
findings on x ray (initial and late)
initial: ground-glass (exudates in alveoli)
later: honeycomb lung (fibrosis of alveolar septal, parenchyma, and cobblestone pleural surface)
7 histological categories of idiopathic interstitial pneumonia
Usual interstitial pneumonia (UIP) Nonspecific interstitial pneumonia (NSIP) Organising pneumonia (OP)*
Diffuse alveolar damage (DAD) Desquamative interstitial pneumonia (DIP)** Respiratory bronchiolitis (RB)
Lymphocytic interstitial pneumonia (LIP)
sx of idiopathic interstitial pneumonia
dyspnea on exertion
dry cough
tachypnea
signs: bibasilar end-inspiratory crackles, finger clubbing, right sided heart failure, diminished lung volume
pathogenetic implications for therapy for idiopathic interstitial pneumonia
immunosuppressive therapy (corticosteroids etc)
biological therapy (monoclonal antibodies- RTK inhibitors)
long term home oxygen therapy
lung transplant
