1
Q
What are chronic obstructive pulmonary disease?
A
Disorders associated with airflow obstruction
2
Q
Do patients with airflow obstruction have more of a problem with expiration or inspiration?
A
Expiration
3
Q
What is maximal expiratory flow rate is influenced by?
A
- Dimensions of airways
- Lung elastic
4
Q
What is emphysema?
A
- Abnormal permanent enlargement of the airspaces distal to the terminal bronchiole accompanied by destruction of their walls without obvious fibrosis
- Enlargement of airspaces leads to overinflation of the lungs
5
Q
What emphysema strongly linked to?
A
- Cigarette smoking or
- Genetic disorder - alpha 1 anti-trypsin deficiency
6
Q
What maintains alveolar wall integrity under normal conditions?
A
A balance between proteases (tissue-destroying enzymes) and anti-proteases (protective enzymes).
7
Q
What happens to the protease–anti-protease balance in emphysema?
A
It becomes imbalanced — excess protease activity leads to alveolar wall destruction.
8
Q
How does smoking contribute to emphysema?
A
Smoking attracts neutrophils to alveoli, which release elastase and oxidants.
9
Q
What is the effect of neutrophil elastase in the lungs?
A
It digests elastin fibers in alveolar walls, causing loss of elasticity and air trapping.
10
Q
How do oxidants and free radicals worsen emphysema?
A
They inhibit α1-antitrypsin (an anti-protease), leading to unchecked tissue destruction.
11
Q
Centriacinar emphysema
A
- Dilatation of the respiratory
bronchioles - Alveolar ducts not affected
- Predominantly occurs in smokers
12
Q
Panacinar emphysema
A
- Mainly dilatation of alveolar ducts and terminal alveoli
- Respiratory bronchiole dilation
occurs in later stages - Predominantly found in patients with genetic deficiency of alpha-1 anti-trypsin
13
Q
When do clinical features of emphysema occur?
A
Until 30% of pulmonary tissue is damaged
14
Q
What are the clinical features of emphysema?
A
- Shortness of breath
- Cough and wheezing
- Prolonged expiration
15
Q
What tools are used to diagnose emphysema?
A
- Spirometry is the primary
diagnostic tool - Chest X-ray and CT
16
Q
What is chronic bronchitis?
A
Inflammation of bronchial airways
17
Q
Chronic bronchitis is defined clinically as presentation of:
A
- a chronic cough (at least 3 months in 2 consecutive years)
- excessive sputum production
18
Q
Simple chronic bronchitis
A
Patients have a productive cough, but no physiologic
evidence of airway obstruction
19
Q
Chronic asthmatic bronchitis
A
Individuals demonstrate hyper-reactive airways, with
intermittent bronchospasm and wheezing
20
Q
Obstructive chronic bronchitis
A
- Chronic airflow obstruction, usually with evidence of
associated emphysema - Particularly in heavy smokers
21
Q
What are the causes of chronic bronchitis?
A
- Chronic irritation bu inhaled substances (cigarette smoking)
- Infections
22
Q
How does cigarette smoking contribute to bronchitis?
A
- Damages epithelium by interfering with cilary action of epithelial cells
23
Q
What changes occur in the airway in chronic bronchitis?
A
- Increased thickness of mucosal layer
- Increased number of mucous secreting goblet cells
- Hypertrophy of sub-mucosal glands
- Narrowed airways
24
Q
Is there respiratory impairment early in chronic bronchitis?
A
No — early stages show no functional impairment.
25
What is the first noticeable symptom as chronic bronchitis progresses?
Shortness of breath on exertion.
26
What COPD-related changes develop over time?
Hypercapnia (↑CO₂), hypoxaemia (↓O₂), and mild cyanosis — “Blue Bloaters.”
27
What cardiac complication can long-standing chronic bronchitis cause?
Cor pulmonale — right ventricular hypertrophy and heart failure due to pulmonary hypertension.
28
What cellular change can occur in the airway epithelium?
Atypical metaplasia, which can progress to squamous cell carcinoma.
29
What commonly causes death in chronic bronchitis?
Acute bacterial infections leading to severe respiratory failure.
30
Chronic Bronchitis vs Pure Emphysema
Chronic Bronchitis ("Blue Bloater") – Caused by long-term airway irritation from smoking or pollutants leading to inflammation and mucus overproduction. Patients often appear overweight, cyanotic, and may develop hypoxaemia, hypercapnia, and cor pulmonale. They commonly suffer from frequent productive coughs and recurrent infections.
Pure Emphysema ("Pink Puffer") – Caused by alveolar wall destruction due to an imbalance between proteases and anti-proteases (often from smoking). This leads to loss of elasticity, air trapping, and barrel chest. Patients are typically thin, non-cyanotic, with dyspnoea and pursed-lip breathing. Oxygen and CO₂ levels are often near normal until late stages.
31
Blue Bloaters vs Pink Puffers
32
What is the general management of CODP?
Pharmacological:
- Bronchodilators
- Corticosteroids
Life-style modifications:
- SMoking cessation
- Avoid environmental and occupational irritants
- Stay hydrated
33
What is asthma?
Reversible airway obstruction, bronchial hyperreactivity and increased mucus production
34
What are the predisposing factors of asthma?
* Hypersensitivity of airways associated with inflammation
* Genetic predisposition to type I hypersensitivity (atopy)
* Bronchial hyperresponsiveness
35
What are contributing factors of asthma?
* Air Pollution
* Diet
* Respiratory Infections
* Cigarette smoke
* Drugs
* Cold air
* Allergens
* Stress
36
What is the pathophysiology of asthma?
* Bronchoconstriction is triggered by stimuli that would have little or no effect on individuals with normal airways
* Often, no allergic trigger can be identified
* Rarely, a state of unremitting attacks (status asthmaticus)
may prove fatal
37
What are the patterns of inflammation of asthma?
Varied but:
- Eosinophilis
- Neutrophilis
- Mixed inflammatory
- Pauci-granulocytic
38
What are the features of the airway in asthma?
* Variable, reversible airways obstructions
* Bronchial smooth muscle constriction
* Vasodilation and oedema
* Excessive thick mucus production
* Inflammation
* Fibrosis
39
Which mediators play a major role in asthma pathophysiology?
Leukotrienes (C4, D4, E4) and Acetylcholine (ACh).
40
What is the role of Leukotrienes C4, D4, and E4 in asthma?
They are key in Type I hypersensitivity and cause powerful bronchospasm and vasoconstriction (C4 & D4 most potent).
41
How does Acetylcholine contribute to asthma?
Released from intrapulmonary nerves, acts on M3 receptors in airway smooth muscle → bronchoconstriction.
42
What is the role of Histamine in asthma?
It’s a potent airway constrictor, but blocking it provides little clinical benefit.
43
How does Prostaglandin D2 affect the airways?
Causes bronchoconstriction and vasodilation.
44
What does Platelet Activating Factor (PAF) do in asthma?
Stimulates histamine and serotonin release, worsening inflammation and constriction.
45
What is the most common type of asthma?
Atopic (Allergic) Asthma — accounts for about 80% of cases and usually begins in childhood.
46
What type of hypersensitivity reaction is atopic asthma?
Type I hypersensitivity (IgE-mediated) reaction.
47
What is commonly seen in the family history of atopic asthma patients?
Atopic diseases such as allergic rhinitis, eczema, and hives.
48
What triggers atopic asthma?
Environmental allergens — dust, animal dander, pollens, and certain foods.
49
How is atopic asthma diagnosed?
Skin prick test (immediate wheal-and-flare reaction) or RAST test for allergen-specific IgE.
50
Does non-atopic asthma usually have a family history of allergies?
No — family history is less common and skin tests are negative.
51
What are common triggers of non-atopic asthma?
Viral respiratory infections (e.g. rhinovirus, parainfluenza) and air pollutants (sulfur dioxide, ozone, nitrogen dioxide).
52
What do atopic and non-atopic asthma share in common?
Similar inflammatory mediators (humoral and cellular) causing airway obstruction.
53
What causes occupational asthma?
Repeated exposure to workplace substances that trigger bronchoconstriction or hypersensitivity reactions.
54
How much exposure is needed to trigger occupational asthma?
Only minute quantities after repeated exposure.
55
What are common occupational asthma triggers?
Fumes (epoxy resins, plastics), gases (toluene), and dusts (wood, cotton, platinum).
56
How does the mechanism of occupational asthma vary?
Depends on the substance — can involve immune hypersensitivity or direct release of bronchoconstrictors.
57
Which drugs can provoke asthma?
Aspirin, codeine, and morphine.
58
How does aspirin induce asthma?
By inhibiting arachidonate metabolism (COX pathway) while leaving the lipoxygenase route active, increasing leukotriene production → bronchoconstriction.
59
What other symptom often accompanies aspirin-induced asthma?
Skin rash (urticaria).
60
How do codeine and morphine trigger asthma?
They stimulate mast cells, leading to histamine release and bronchoconstriction
61
What are the signs of asthma?
- Frequent episodes of breathlessness, chest tightness, wheezing or coughing
- Worse at night or morning
62
How is asthma diagnoses?
- CLinical features
- Objective measures in lung functions (spirometry)
63
What is the pharmacological intervention?
- Bronchodilators (prevent or reverse the bronchoconstriction)
- Anti-inflammatory drugs
64
What are non-immune defence response of respiratory system?
- Nasal clearance, sneezing or blowing
- Cough reflex
65
What is immune response of the respiratory system?
- Phagocytosis
- IgA
- Serum IgG, IgM
- T cells
66
What does upper respiratory tract infection include?
- Nose
- Sinuses
- Pharynx
- Larynx
- Large airways
67
What does URTI usua;;y involve?
- Direct invasion of upper airway mucosa
- Acquired by inhalation of infected droplets
68
What are the risk factors for a URTI?
- Close contact with children
- Medical disorder
- Smoking
- Immunocompromised
- Anatomical anomalies
69
What causes URTI?
Variety of viruses and bacteria
- Most common Rhinovirus
- FLu
- Adenovirus
- Enterovirus
- Covid
70
What is Rhinovirus?
Most common causes of the common cold
- Acute, self limited, limited to the mucosal membranes of URT
71
What are the signs and symptoms of rhinovirus?
* Cough
* Sore throat
* Runny nose
* Nasal congestion
* Headache
* Low-grade fever
* Facial pressure
* Sneezing
* Malaise/Fatigue
* Myalgias/muscle pain
72
How to diagnose viruses?
* Viral culture
* Antigen detection
* PCR (Polymerase Chain Reaction)
73
Treatment / Management of URTI
- Decongestants and combination antihistamine/decongestant medications
- Vit C
- Early antiviral treatment
- Vaccination
74
How can micro-organism gain access to the lung?
- Aspiration
- Inhalation
- Blood spread
75
What is pneumonia?
Inflammation of the terminal airways of lung resulting in altered gas exchange
76
What are the classifications of pneumoniae?
- Based on area of lung affected
- Duration/Onset
- Causative agent
- Clinically
77
Community-acquired pneumonia
* Streptococcus pneumoniae
* Mycoplasma pneumoniae
* Haemophilus influenzae
* Chlamydia pneumoniae
* Influenza and other viruses
78
Hospital-acquired pneumonia
* Staphylococcus aureus
* Pseudomonas aeruginosa
* Klebsiella pneumoniae
* Legionella spp
* E. Coli
79
What are the clinical manifestations of pneumonia?
- Chills, shortness of breath, tachypnoea, cough, tachycardia
- Increased sputum, fever, chest pain
- Fatigue anorexia, headache, agitation
80
Lobar Pneumonia
Consolidation of a large portion of a lobe or of an entire lobe
81
Bronchopneumonia
Patchy consolidation
82
Interstitial (atypical) pneumonia
Diffuse infection/inflammation of alveolar walls and interstitial connective tissue
83
Miliary pneumonia (uncommon)
Numerous, small diffuse lesions (millet seeds!) throughout both lungs.
84
What are the causes of lobar pneumonia?
* Streptococcus pneumoniae
* Haemophilus influenza
* Staphylococcus aureus
85
What is congestion in lobar pneomonia result in?
* Vascular engorgement, intra alveolar fluid with few neutrophils, and often the presence of numerous bacteria.
* The lung is heavy, boggy, and red
86
Red hepatization of lobar pneumonia
* Massive confluent exudation, as neutrophils, red cells, and fibrin fill the alveolar spaces
* the lobe is red, firm, and airless, with a liver-like consistency, hence the term hepatization.
87
Grey hepatization of obar pneumonia
* Disintegration of red cells and the persistence of a fibrinosuppurative exudate
* Resulting in colour change to grayishbrown
88
What is the resolution of lobar pneumonia?
Exudates within the alveoli are being enzymatically digested, resorbed, ingested by macrophages or coughed up
89
What are the causes of bronchopneumonia?
* Staph. aureus
* Strep. pyogenes
* Strep. pneumoniae
* Klebsiella
* Haemophilus influenzae
90
What are the predisposing factors of bronchopneumonia?
* Immunosuppression e.g. infancy, old age, general debility, drug induced
* Underlying lung disease eg chronic bronchitis
91
What is the distribution of bronchopneumonia?
Patchy distribution, infection starts in bronchioles or bronchi and spreads to alveoli (opposite of Lobar)
92
What is the diagnosis of pneumonia?
* Phys. Exam
* O2 saturation
* Chest X-ray
* Microbiological assessment: culture etc
93
What is the treatment of pneumonia?
- Empirical antibiotic therapy
- Later tailored to specific causative organism
94
What causes tuberculosis?
Mycobacterium tuberculosis
95
How does tuberculosis transmit?
TB droplets
96
Where tuberculosis more severe?
- Poor natural immunity
- Immunosuppressed bu AIDS of organ transplant
97
What is primary tuberculosis?
TB in previously unexposed person
98
What is secondary tuberculosis?
Reactivation or re-infection of primary TB
99
What are the symproms of secondary tuberculosis?
- Flu-like symptoms
- Increased purulent sputum
- Coughing blood
- Destruction of lung tissue
100
What are the outcomes of secondary TB?
- Untreated can be fatal
- Treated can be cured
101
What is the treatment of secondary tuberculosis?
- Prolonged course of combination of antibiotics
102
What is MDR TB?
Multi Drug Resistant-TB
* is a strain of TB that cannot be treated with the two most powerful first-line treatment antiTB drugs
103
What is XDR TB?
Extensively Drug Resistant TB
* is resistant to both first- and second-line drugs
104
What are the other organs impacted by TB?
* Lymph nodes
* Kidney
* Adrenal gland
* Bones (10%)
* Meninges
* Intestines
* Fallopian tube (salpingitis TB)
* Pleura
105
What are the investigations for TB?
- Chest x-ray
- Sputum smear = acid fast stain
- PCR
106
What is the prevention of tuberculosis?
- Vaccination
- Avoid contact with patient with active disease
107
What is the treatment for TB??
* Directly Observed Therapy (DOT) with
* Anti TB medications:
First-line anti TB
* Isoniazid, rifampin, Pyrazinamide +/– ethambutol
Second-line anti TB:
levofloxacin, moxifloxacin
Systemic Pathology
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