Respiratory Flashcards
1
Q
Classification of Pneumonia
A
- Aetiology: viral, bacteria, fungal
- Community vs hospital
- Typical vs atypical
2
Q
Stages of Lobar Pneumonia
A
- Congestion: oedema in alveoli
- Red hepatisation: RBCs in alveolar space (leaky septa), neutrophils, capillaries congested
- Grey hepatisation: Neutrophils, macrophages and fibrin
- Resolution
3
Q
Outcomes of lobar pneumonia
A
- resolution
- abscess formation
- empyema
4
Q
Bronchopneumonia
A
- patchy distribution
- infection starts in bronchioles or bronchi and can spread
- usually hospital acquired
- immunosupression
5
Q
TB
A
- SE asia and africa
- Bacterial infection
- M tuberculosis
- Chronic inflam
- Can be infected with bacteria but not have the disease
6
Q
Factors predicting TB outcome
A
- No of organisms ingested and virulence of organisms
- Immune resp: malnutrition, old, co-morbidities e.g. HIV
- Administration of appropriate antibiotics
7
Q
Granuloma
A
- central core of caseous necrosis
- activated macrophages
- giant cells
- lymphocytes
- fibroblasts
8
Q
Primary TB - Ghon complex
A
- ghon focus: granulomas +
2. lymph node involvement
9
Q
Primary TB - development
A
- exposure to M. tuberculosis: inhalation
- alveolar macrophage endocytosis
- t lymphocyte hypersensitivity
- cell mediated immune response
- granuloma formation
- healed or latent lesion
10
Q
Progressive primary TB
A
- 10% of patient, infection develops to PPTB
- Life-threatening: caused by high bacterial load and bacterial virulence or immunosupression
- initial lesion enlarges -> producing large necrotic areas with central liquefaction resulting in cavities
- Can spread into: 1. pulm arteries = miliary TB or 2. ersion into bronchi = TB bronchopneumonia
11
Q
Secondary TB
A
- previous exposure
- reactivation
- reinfection
- little lymph node involvement due to pre-existing hypersensitivity and prompt inflam response
- can lead to miliary spread, TB bronchopneumonia or TB empyema
12
Q
TB Bronchopneumonia
A
Infected lymph node erodes into bronchus
- Numerous confluent caseating granulomatous lesions
13
Q
COPD
A
- Regular obstruction of airflow in the pulmonary airways
- Progressive and accompanied by inflammation
14
Q
Risk factors for COPD
A
- Smoking
- Hereditary deficiency of alpha-1 antitrypsin
- Asthma
15
Q
Symptoms
A
- Decreased FEV1 due to:
- Increased resistance = narrowed airways (chronic bronchitis)
- Decreased outflow pressure = loss of elastic recoil (emphysema)
16
Q
COPD Pathogenesis
A
- inflam and fibrosis of bronchial wall
- hypertrophy of submucosal glands
- hypersecretion of mucus
- loss of elastic lung fibres
- loss of alveoli
17
Q
COPD treatment
A
- stop smoking
- O2 therapy
- bronchodilators (B2 adrenergic agonists)
18
Q
Chronic bronchitis
A
- Increased mucus production
- obstruction of small airways
- chronic productive cough
- Diagnosis: persistant cough with sputum production for at least 3 months in at least 2 consecutive years
19
Q
Emphysema
A
- abnormal permanent enlargement of the airspaces
- destruction of alveolar wall
- increased airspaces
- > hyperventilation of lungs
- > increased total lung capacity
- > ventilation is impaired
20
Q
Emphysema: Pathogenesis
A
- Protease/anti-protease imbalance
- inherited deficiency in alpha1-antitrypsinogen (1% of pateints)
- Normally elastin production and destruction is balanced
- Alpha-1 antitryspinogen = protects lungs from protease/elastase activity
- cigarette smoke (and other irritants) increases free radicals -> causes infiltration of neutrophils and activation of alveolar macrophages
1. Neutrophils and macrophages release proteases/elastases -> increased protease/elastase activity
2. Cigarette smoke -> decreased alpha-1 antitrypsin levels - Loss of elastin -> decreased outflow pressure
21
Q
Emphysema: clincal feature
A
- 60yrs and older
- Dyspnea on exertion
- minimal cough
- weight loss
- lungs overinflated (barrel chest)
- ‘pink puffer’: lack of cyanosis, use of accessory muscles and pursed lips
22
Q
Chronic bronchitis: pathogenesis
A
- Hypersecretion of mucus in large airways
- hypertrophy of submucosal glands -> excessive mucus production -> obstruction of airways
- increase in goblet cells of smaller airways
- may also increase SM -> bronchial hyperactivity
23
Q
CB: clinical features
A
- persistant cough
- dyspnea of exertion
- cyanosis
- cor pulmonale
- ‘blue bloaters’ = cyanosis and oedema
24
Q
Small cell carcinoma
A
- only in smokers
- highly malignant
25
Q
squamous cell carcinoma
A
- keratin pearls
- slower growing
26
Q
Adenocarcinoma
A
- lots of disorganised glands
- women and nonsmokers
27
Q
large cell carcinoma
A
- highly anaplastic (very poorly differentiated)
- poor prognosis
