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Respiratory Disease Flashcards

1
Q

Asthma

A

heterogeneous, chronic inflammatory disorder of the airways characterised by

variable and recurring symptoms- cough
airflow obstruction
bronchial hyperresponsiveness
underlying airway inflammation

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2
Q

risk factors of asthma

A

environment- allergies/ viral infection
occupation- with chemical and dust
poor housing
pollution

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3
Q

clinical signs

A

symptoms- cough, wheezing, dyspnoea, chest tightness

episodic symptoms

polyphonic expiratory wheezing, prolonged expiration, accessory muscle use in serve attack

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4
Q

Development of asthma

A

complex immunologic, strucutral and neural mechanisim that culminate in episodic symmptoms and progressive airway dysfucntion

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5
Q

Airway Inflammation asthma

A

Mast cells, Eosinophils and T cells infiltrate bronchial mucosa

leads to oedema, increase mucus production, desquamtion of epithelial cells, increase vascular permability

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6
Q

Bronchial hyperresponsiveness asthma

A

exaggerated bronchial restrictors

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7
Q

Bronchoconstriction asthma

A

triggered by
direct exsposure to allergens
exercise
narrowing of airways

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8
Q

muscus hypersecretion asthma

A

goblet cells hyperplasia leads to excess mucus production

mucus forms obstruction

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9
Q

airflow obstruction in asthma from

A

bronchospasm
mucosal oedema
mucus plug

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10
Q

contributing systemic factors to asthma

A

atopy- invloves hightened IgE antibodies due to allergies

obesity- inflammation

enevironmental pollutans

smoking and infection

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11
Q

immune sensitisation

A

inhaled allergens dendritic cells present antigen to T helper which goes to a TH2 cell

TH2 cells then promote IgE antibody production which will prime cells for future allergen exsposure

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12
Q

Allergen response in asthma
Early phase: bronchoconstriction and mast cell activation

A

Re-exsposed to allergen- cross link form between IgE antibodies triggering Mast cell degeranulation

leads to rapid release of histamine

cause smooth muscle to contract, increased vascular permability, mucus hypersecretion, and airway narrows

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13
Q

late phase: inflammatory cell recruitment

A

recruitment of eosinophils, basophils, neutrophils to the airways

cytokines- goblet cell metaplasia and overporduction

inflammation of epithelial cell damage= mucus plug

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14
Q

airway hyperresponsiveness asthma

A

airways overreact to the trigger

enhanced smooth muscle cell contractibility, increased vagal tone, great sensitivity to stimuli

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15
Q

airway remodel asthma

A

hypertrophy and hyperplasia of smooth muscel

thickened membrane

goblet cell hyperplasia

loss of epithelial integrity

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16
Q

Chronic obstructive pulmonary disorder COPD

A

PERSISTANT AIRWFLOW LIITATION
PROGRESSIVE AND NOT FULLY REVERSIBLE AIRFLOW OBSTRUCTION
CHRONIC INFLAMMATORY RESPONSE TO NOXIOUS PARTICLES OR GASES

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17
Q

RISK FACTORS AND CASUES OF COPD

A

smoking
air pollution
occupation with fumes and dust
genetics

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18
Q

subtype of COPD
Chronic bronchitis

A

progressive cough
prominant mucus production/ air way narrow
ABG- acidosis

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19
Q

subtype of COPD emphysema

A

destruction of alveolar walls- decreased surface area for gas exchange

hyperinflation and air trap
ABG- hypoxaemia- acidosis

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20
Q

features of COPD

A

-airways= increase goblet cells, mucus gland hyperplasia/ fibrosis nd narrowing

emphysema- airway collapse
chronic bronchitis

-lung parenchyma
emphysema affects alveolar ducts, sacs, alveoli = permenant dilation or destruction

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21
Q

types of emphysema

A

proximal acinus
panacinar emphysema
distal acinar emphysema

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22
Q

Proximal acinar emphysema:

A

abnormal dilation or destruction of respiratory bronchiole, the central portion of the acinus

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23
Q

Panacinar emphysema:

A

enlargement or destruction of all parts of the acinus

24
Q

Ddistal acinar emphysema:

A

alveolar ducts predominantly affected

25
chronic bronchitis
bronchi and bronchioles mucus hypersecretion Goblet cell metaplasia mild hypoxaemia ABG- chronic compensated respiratory acidosis image- increased markings and cardiomegly
26
emphysema
alveoli and distal airspaces alveolar wall destroyed decrease elastic recoil macrophages hypoxaemia with hyperinflation decrease PaCO2 flat diaphragm on images
27
chronic suppurative lung disease
clinical syndrome in children/adolescents or adults that involves irreversible dilatation of the bronchi due to structural airway injury. It is diagnosed based on clinical symptoms (chronic productive cough, recurrent infections) and confirmed by high-resolution chest CT revealing bronchial dilatation.
28
CAUSES AND RISK FACTORS OF CSLD
Post-infectious (e.g., pneumonia, tuberculosis, pertussis) Cystic fibrosis (CF) or CFTR-related disorders Primary ciliary dyskinesia (PCD) Allergic bronchopulmonary aspergillosis (ABPA) Autoimmune and systemic diseases (e.g., rheumatoid arthritis, Sjögren’s syndrome) Immunodeficiencies (e.g., CVID, IgG subclass deficiencies) Foreign body aspiration or airway obstruction (e.g., tumors, broncholiths) Alpha-1 antitrypsin deficiency Nontuberculous mycobacterial (NTM) infections Recurrent aspiration or reflux Tracheobronchomalacia and congenital syndromes
29
INITIAL AIRWAY INSULT CSLD
serve lower repsiratory infection airway obstruction impaired host defence mechansims Epithelium injury Compromises epithelial integrity Triggers an aberrant immune response Disrupts mucociliary clearance
30
impaired mucociliary clearence CSLD
Ciliary damage or dysfunction impairs mucus transport (as in primary ciliary dyskinesia) Goblet Cell Hyperplasia: resulting in excessive mucus production CFTR dysfunction (seen in cystic fibrosis and CFTR-related disorders) dehydrates the airway surface liquid, increasing mucus viscosity​
31
chronic infection CSLD
Pseudomonas aeruginosa (notorious for biofilm formation, virulence factors like pyocyanin) Haemophilus influenzae Staphylococcus aureus NTM (e.g., Mycobacterium avium complex) Fungal elements (e.g., Aspergillus in ABPA)
32
key features of chronic infection CSLD
Biofilms → resist immune clearance and antibiotics Disruption of epithelial repair Promotion of chronic neutrophilic inflammation
33
neutrophil inflammation CSLD
neutrophil elastase- degrades extracellular matrix oxidative stress/ epithelial damage myeloperoxdiase- enhances oxidative killing but kills host tissue pregnancy zone protein traps pathogens but damages airway in process Promote mucosal ulceration, oedema and angiogenesis Correlate with disease severity, sputum purulence and exacerbation risk
34
structural lung damage In CSLD
transmural inflammation Ulceration, capillary leakage, neovascularisation Loss of structural proteins Elastin and cartilage degradation → weakened airway walls Bronchial dilation and wall thickening Irreversible distortion seen on HRCT (in bronchiectasis) Goblet cell hyperplasia and smooth muscle hypertrophy Contributes to airflow obstruction and mucus hypersecretion Epithelial-mesenchymal transition Leads to fibrosis and remodeling
35
factors that amplify CSLD
vitamin D insurficent impaired neutrophil function atopy
36
what are the stages of CSLD
infection inflammation structural damage impaired mucocillary clearence
37
clinical symptoms of CSLD
chronic wet cough dyspnoea on exertion wheeze chest tightness crackles in breathing
38
cystic fibrosis
autosomal recessive caused by mutation in CFTR gene defective chloride and bicarbonate transport resulting in dehydrated and thick secretions in lungs
39
cystic fibrosis risk factors
genetic- mutation in CFTR gene inheritance pattern autosomal recessive
40
pathogenesis Cystic fibrosis CFTR dysfunction
it codes of a protien which losses its function decreased chloride and bicarbonate secretion leads to dehydrated lung surface Mucus stasis ciliary dysfunction airway obstruction
41
pathogenesis of cystic fibrosis airway inflammation and infection
neutrophilic inflammation form biofilm increase oxidative stress release protease
42
pathogenesis of cystic fibrosis tissue destruction and bronchiectasis
inflammation cause bronchial wall thickens irreversible airway dilation loss of elastin and airway remodel
43
pathogenesis of cystic fibrosis extrapulmonary effects
pancreatic insurficent male infertility intestinal obstruction
44
cystic fibrosis respiratory symptoms
chronic cough wheezing dyspnoea hypoxia
45
cystic fibrosis gastrointestinal function
failure to thrive fatty stools malnutrition lack of vitamin
46
other sysmptoms of cystic fibrosis
male infertility salt loss osteopenia osteoporsis chronic sinus disease
47
pneumonia
infection of alveolar spaces
48
typical pneumonia
Streptococcus pneumoniae, Haemophilus influenzae
49
atypical pneumonia
Mycoplasma pneumoniae, Legionella, Chlamydophila pneumoniae
50
tuberculosis
Airborne transmission from an infectious person - Latent or active reactivation - Increased risk in immunocompromised (e.g. HIV) or undernourished individuals
51
covid 19
Transmission via respiratory droplets, aerosols, and fomites - Viral variants (e.g. Delta, Omicron) influence severity and transmission
52
pneumonia pathogenesis
inhaled pathogen aspiration heamotgenous spread failure of hot defences inflammatory response= inate immune activation- local tissue injury alveolar damage and consolidation typical- lobar consolidation atypical- patchy interstital infiltrates
53
TB Pathogenesis
airborne droplet inhaled MTB INHIBTS PAHGOSOME AND LYSOSME FUSION this allows it to survie in macrophage adapative immunity means it is then criculated latent- controlled infection reactivation- breakdown and MTB spreads to lungs
54
covid pathogenesis
spike protein binds to receptor evasion and viral replication in host cell release of proinflammatory cytokines microvascular thombosis and capilary leak diffuse alveolar damage thombosis
55
pneumonia symptoms
Transmission via respiratory droplets, aerosols, and fomites - Viral variants (e.g. Delta, Omicron) influence severity and transmission
56
TB symptoms
Chronic productive cough (often with haemoptysis) - Weight loss, anorexia - Night sweats - Low-grade fever - Fatigue
57
COVID 19 Symptoms
Fever, fatigue, dry cough - Loss of smell/taste (anosmia) - Sore throat, headache, myalgias - GI symptoms (diarrhoea, nausea)

Pathophysiology (18 decks)

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