Bronchiectasis, Asthma & Vasculitis Flashcards
(28 cards)
WHAT DO YOU UNDERSTAND BY THE
TERM ASTHMA?
* Inflammatory disorder characterised by —-
[BHR] to various stimuli which results in widespread — of the —
– — airways — , either spontaneously or with
therapy
* Inflammatory response includes:-
– —, – cells & — and is associated with
* Exudation of — , — & smooth muscle – ,
* Deposition of – , — plugging & – damage
* An exaggerated contractile response of the airways to a variety of stimuli.
– NOT a disease with destruction of tissue
bronchial hyper responsive
narrowing
airway
reversible airway obstruction
t lymphocyte , mast cells , estinphils
plasma , oedema , hypertrophy
matrix , mucous , epithelial
ASTHMA – DEFINITION
* — , — —- resulting from
exaggerated — in response to various stimuli
* Recurrent episodes of — , breathlessness, chest — & coughing
* — disease triggered by a wide variety of — agents
episodic , reversible bronchospasm
bronchosocntrictio
wheezing , chest tightness
heterogeneous
inciting
ASTHMA EPIDEMIOLOGY
* Asthma is —
* 300 million people worldwide
* — of children, — of adults
* — commonest; – > —
* — least common, higher frequency in —
* Childhood asthma has a — prognosis
* Newly diagnosed Adult-Onset Asthma – relatively
common
common
10-15%
7-105
young children
boys > girls
adolescents
adults
good
pathogenesis of asthma 1:
* Atopic / Allergic / Extrinsic
– Genetic predisposition to
develop specific —
antibodies directed against
common environmental —
– — identifiable risk
factor for development of
asthma
* — exposure → specific — antibodies.
– IgE production ↑ — type T cell responses relative to the Th1 type
– Genetic & environmental influences
* IgE antibodies synthesized & secreted by—
* Bind to —-affinity receptors on — &—- )
– Subsequent inhalation of allergen causes — allergen-specific IgE antibodies on the — surface
IgE
allergens
strongest
allergen
ige
th2
plasma cells and basophils
cross linking
mast cells
pathogenesis of asthma 2:
* Rapid — of Mast Cells &—- release
– — Phase Histamine, cysteinyl leukotrienes
(LTC4, D4, and E4) & prostaglandin D2 ,
contract airway smooth muscle (ASM)
– — Phase influx of inflammatory cells
monocytes, dendritic cells, neutrophils, T-
lymphocytes, — , and basophils →
ASM —
so basically:
1- acute response: — , bronchial oedema — and increase — production
2- chronic response : bronchial — , chronic bronchial wall — and airway smooth muscle —-
- acute anf chronic response lead to airway —
- increase Mechanical Work of Breathing
Hypoventilation [when Severe]
Hyperinflation
degranulation
mediator
early
late
estiophils
contraction
bronchospasm
oedema
mucous
hyper responsivness
inflammation
hypertrophy
obstruction
PATHOGENESIS OF ASTHMA 3
* Airway —
* Smooth muscle surrounding
airway becomes —
& — airway
* Reduces airflow leading to —
* Airway epithelium becomes — , — & —
* Inflammatory mediators
symptoms :
▪ — Breathlessness
▪ Wheeze
▪ Chest tightness
▪ Cough
▪ +/- sputum production
▪ Generally worse in morning
▪ History: — triggers
inflammation
oedematous
tightens
wheeze
oedematous, erythematous &
inflamed
mediators
episodic
elicit triggers
CONTRIBUTORY FACTORS TO ASTHMA
VARY WITH AGE OF ASTHMA ONSET:
* Atopy:
– ↑ —- levels & immediate —- on skin testing predominates in —-
asthma; — type
* Non-allergic or — asthma
– associated with — age - may be difficult to manage
– Often associated with —-
* Genetics & Family History:
– no single gene but several, in combination with environmental factors, influence
development
* Think of all the inflammatory Mediators and their respective genes
– Younger Maternal Age & Low Maternal Vit D levels & Maternal smoking
* Environment:
– early childhood exposure to allergens and maternal smoking – house dust mite
allergens, cockroach allergy in U.S.A
* Infections:
– Rhinovirus & RSV
* Occupational sensitizers:
– 250 materials in workplace cause occupational asthma, isocyanates, wood dust,
bleaches, allergens from animals
IgE
hypersensitivity
childhood
extrinsic
intrsic
older
COPD
CONTRIBUTORY FACTORS TO ASTHMA -CONTD
VARY WITH AGE OF ASTHMA ONSET:
* Cold Air & Exercise:
– exercise-induced — [EIB]
– 5-20% general population
– Elite Endurance — [ swimming, cycling, triathlon, pentathlon, rowing ]
* Therapeutic Use Exemption
– 90% patients with asthma – have some EIB
* Leukotrienes LTC4 and LTD4; histamine & interleukin (IL)-8 [dictates treatment]
* Atmospheric pollution and irritant dusts:
– many patients with asthma experience worsening of symptoms on exposure to tobacco smoke,
car exhaust fumes, solvents, sulphur dioxide, ozone etc.
* Diet:
– increased intake of fresh fruit & vegetables shown to be protective
– Vit — , patients with sufficient Vit – levels have less severe asthma
* Emotion:
– emotional factors influence asthma both acutely and chronically
* Drugs:
– — , — , — are implemented in triggering asthma - 5% of patients (particularly prevalent in patients with nasal polyps and asthma)
– Beta blockers – direct — innervation that tends to produce —
bronchocontriction
etheletes
vit d
vit d
nsaids aspirin and ibuprofen
parasympathetic
bronchosoction
PATHOLOGY
* — lungs
* — of bronchial lumen by —
* Airway infiltration by — & —
* Mast cell —
* Basement membrane —
* Loss of epithelial —
* — & — of
bronchial smooth muscle and
goblet cells
overinflated
occlusion
mucus
neutrophils and eosinophils
degranulation
thickening
integrity
hyperplasia and hypertrophy
NATURAL HISTORY OF ASTHMA
NOT PRECISELY DEFINED:
* For majority of patients Asthma is not —
– contrasts with chronic bronchitis, cystic fibrosis, bronchiectasis
– Some (minority) patients do develop irreversible changes in—
– Rate of loss of lung function is greater
–>* among adults with asthma
–>* those with more severe asthma symptoms
—>* those with newly diagnosed asthma
* Clinical course is characterised by — & —
* Children
– Wheezing before the age of — years will improve or resolve in a few years in most
– 30 -70% of children with asthma — or become — by early
adulthood
* Adults
– Wheezing adults are likely to experience — asthma
– Older adults (≥65 years) have more impaired lung function than younger adults
* Management of Asthma
– Complex !!
not progressive
lung function
remission and exacerbation
six
improve or symptomatic
presistent
BIOLOGIC TREATMENTS OF ASTHMA
* Severe asthma, high —
* Block – (omalizumab) Block —
(mepolizumab)
* — hospital visits
* Reduced need for —
estinphils
IgE
IL-5
reduce
oral conticosteriods
BRONCHIECTASIS
INCREASING RECOGNITION – — RESOLUTION CT
* Abnormal — , — of the —
caused by — of the — & —
* Classified as an — lung disease
* Disease involves a vicious circle of— & — with mediator release
* Prognosis depends on underlying – &— of lung involved [localised – generalised]
* Inflammation mediated dysfunction of smooth
muscle & elastic tissue in bronchi causing loss of function leading to —
high
abornmal irreversible dilation
bronchi
destructive
muscle and elastic tissue
obstructive
transmural infection n inflammation
cause and extent
dilation
BRONCHIECTASIS INCREASING RECOGNITION – HIGH RESOLUTION CT:
is —-
– —- obstruction
* (eg, foreign body, mucus plug,
tumour)
– — abnormality
* (intralobar bronchopulmonary
sequestration, bronchial stenosis,
bronchomalacia, tracheal bronchus)
– — compression
* (lymphadenopathy [eg, tuberculosis],
vascular compression, or cardiomegaly)
– Past severe —
– Chronic localized –
or infection
* (eg, chronic — — lobe syndrome, — plugging)
localised
intraluminal
congenital
extralumenal
local pneumonia
atelstasis
right middle , mucus plugging
INFECTION:
* Sequel to — and — in — which has imperfectly resolved
* Pneumonia complicating — or –
▪ Incidence reduced due to effective childhood —
strategies
* Allergic Bronchopulmonary —- (ABPA)
* Chronic —- cavities
* Primary Mycobacterium— complex infection
bronchopneumonia and bronchiolitis
meslease and whooping cough
immunisation
aspergillosis
tb
avius
CONGENITAL:
* Primary ciliary dyskinesia:
–> Poorly functioning — contribute to — of secretions and —
* Alpha-1-antitrypsin deficiency
* Cystic Fibrosis
* Young’s syndrome:
–> o Chronic sinopulmonary infections
–> o Male infertility
* Marfan syndrome (very rarely)
* Kartageners Syndrome
o Characterised by a triad of — , — and severe — .
o Autosomal — inherited condition
o Affects ciliary —
cilia
retention
recurrent infection
dextrocardia, bronchiectasis and severe sinusitis.
ciliary mobility
IMMUNODEFICIENCY:
* Persons with humoral immunodeficiency syndromes
– — , — & — (i.e. Hypogammaglobulinaemia)
* Immunodeficiency due to malignancy e.g. — , —
* Immunoglobulin replacement reduces the — of infections and
prevents ongoing airway —
BRONCHIAL OBSTRUCTION:
Obstruction of — bronchi by:
* — / — foreign bodies
* Tumour
* — plugs in asthma
* Compressive —
* Chronic aspiration
IgG IgM IgA
myeloma and lymphoma
frequency
destruction
central
inhaled / aspirated
mucus
compresive lymphodenpathy
“RHEUMATIC” CONDITIONS
* Sjogrens Syndrome
* Systemic — Erythematosus
* Rheumatoid arthritis
* Inflammatory — disease especially —
pathogenesis :
* The induction of bronchiectasis requires two factors:
▪ An — insult
▪ Impaired — airway obstruction
* Involved bronchi are — , inflamed & easily — , resulting in airflow — & impaired — of secretions
lupus
bowel
ulcerative colitis
infectious
drainage
dilated
collapsible
obstruction
clearance
CLINICAL FEATURES OF BRONCHIECTASIS:
Symptoms
* — cough with — sputum
* Sputum may be — , — , — or — or smelly !!
* —-streaked sputum or copious — may result from erosive airway damage due to acute infection
* Dyspnoea & wheezing in 75%
* —- pain in 50%
* Recurrent —
Physical Findings
* — , coarse crepitations & — on auscultation
* Clubbing a common finding in the past, rare now 3%
* Major confounding disease is —
productive
purulent
mucoid , mucopurlent , thick or viscous
blood
haemtpysis
pleuritic
LRTI
crackles
ronchi
copd
COMPLICATIONS OF BRONCHIECTASIS:
* Massive —
* Respiratory failure
* Pneumonia
* —
* – abscess
* —
Pathogens include
— Aureus, — Influenza & Pseudomonas —
haemoptsysis
pleural effusion
brain
amyloidosis
staphylococcus , homophiles m aeruginosa
pleural effusion:
* Accumulation of — in the —
space
* Empyema: accumulation of — in the —
* Normally a small amount of—,
—- fluid is present in the
pleural space to allow— of
the visceral pleural against the
parietal pleura
* Pleural effusions are classified as — or —
* Transudates have — specific
gravity, — protein and — cells
– Causes include heart failure, fluid overload, nephrotic syndrome,
Peritoneal dialysis
* Exudates have — specific
gravity, — protein and — of
cells
– Causes include infection, malignancy,
pulmonary emboli
fluid
pleural space
infected fluid
pleural sace
thin
pale yellow
movement
trasudate or exuate
low , low, few
high , high , lots
pleural effusion:
Pleural fluid accumulates when
the rate of pleural fluid — >
rate of pleural fluid — by —
– A transudative effusion occurs
when alterations & balance in
the — factors that
influence pleural fluid — result in a pleural
effusion e.g.
* — capillary pressure with
heart failure
* ↓—serum oncotic pressure
with — syndrome,
hepatic —
* Pleural fluid accumulates when
the rate of pleural fluid formation >rate of pleural fluid removal by
lymphatics
– An exudative effusion occurs
when the — are altered. Inflammation of the
pleura, leading to increased — in the pleural space is the most common cause of
exudative effusion
diganosis:
* CXR
* +/- CT Thorax
* Blood tests
* Thoracocentesis → Examine — & Request Help from the
Laboratory [Chemical Pathology Cytology etc. ]
formation > removal
systemic factors
movement
high
low
nephrotic syndrome , hepatic cirrhosis
pleural surface
proteins
fluid
vascular lung diseases:
1. Pulmonary —
2. Pulmonary —
3. —
4. —
- Pulmonary embolism
- Pulmonary infarction
- Haemorrhage
- Vasculitis
pulmonary thromboembolism:
* —- followed by — of — to the —- or its branches
– Source: — & — side of heart
▪ >95% arise from — in — of — legs (— or—)
▪ Thromboemboli do not usually arise from — or – leg veins
* 50,000 deaths / year in USA
* True incidence of non-fatal pulmonary emboli is unknown
risk factors:
1- * — & Poor —
– Prolonged bed rest
– Surgery
– Severe trauma
– Congestive Cardiac Failure
– Pregnancy
2-* — states:
– Factor V leiden mutation
– Protein C, Protein S deficiency
– Antithrombin III deficiency
– Lupus anticoagulant
– Homocystynuria
– Oral Contraceptive Agent
– Malignancy
* Connective tissue disease
Deep vein thrombosis
migration
ditched clot
pulmonary artery
venous and right
thrombi
deep veins
lower
popliteal vein or above
superficial or small
immobilisation and poor venous return
hypercoaguable
pulmonary embolus pathophysiology :
* Depends on — of the embolism, which in turn dictates the size of the occluded pulmonary artery
– Increase in —- from blockage of flow & — caused by neurogenic mechanisms & release of mediators
– — of downstream pulmonary parenchyma
* Occlusion of a major vessel causes a sudden ↑ — , ↓ — , acute Cor Pulmonale & possibly sudden death
* Occlusion of a smaller vessel is — catastrophic and may even be
clinically —
size
pulmonary artery pressure
vasospasm
ishcemeia
pulmonary artery pressure
cardiac output
less
silent
