Respiratory

Question 1

Classification of Pneumonia

Answer 1

• Aetiology: viral, bacteria, fungal
• Community vs hospital
• Typical vs atypical

Question 2

Stages of Lobar Pneumonia

Answer 2

1. Congestion: oedema in alveoli
2. Red hepatisation: RBCs in alveolar space (leaky septa), neutrophils, capillaries congested
3. Grey hepatisation: Neutrophils, macrophages and fibrin
4. Resolution

Question 3

Outcomes of lobar pneumonia

Answer 3

• resolution
• abscess formation
• empyema

Question 4

Bronchopneumonia

Answer 4

• patchy distribution
• infection starts in bronchioles or bronchi and can spread
• usually hospital acquired
• immunosupression

Question 5

TB

Answer 5

• SE asia and africa
• Bacterial infection
• M tuberculosis
• Chronic inflam
• Can be infected with bacteria but not have the disease

Question 6

Factors predicting TB outcome

Answer 6

• No of organisms ingested and virulence of organisms
• Immune resp: malnutrition, old, co-morbidities e.g. HIV
• Administration of appropriate antibiotics

Question 7

Granuloma

Answer 7

1. central core of caseous necrosis
2. activated macrophages
3. giant cells
4. lymphocytes
5. fibroblasts

Question 8

Primary TB - Ghon complex

Answer 8

1. ghon focus: granulomas +

2. lymph node involvement

Question 9

Primary TB - development

Answer 9

1. exposure to M. tuberculosis: inhalation
2. alveolar macrophage endocytosis
3. t lymphocyte hypersensitivity
4. cell mediated immune response
5. granuloma formation
6. healed or latent lesion

Question 10

Progressive primary TB

Answer 10

• 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

Question 11

Secondary TB

Answer 11

• 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

Question 12

TB Bronchopneumonia

Answer 12

Infected lymph node erodes into bronchus

- Numerous confluent caseating granulomatous lesions

Question 13

COPD

Answer 13

• Regular obstruction of airflow in the pulmonary airways

- Progressive and accompanied by inflammation

Question 14

Risk factors for COPD

Answer 14

• Smoking
• Hereditary deficiency of alpha-1 antitrypsin
• Asthma

Question 15

Symptoms

Answer 15

• Decreased FEV1 due to:
• Increased resistance = narrowed airways (chronic bronchitis)
• Decreased outflow pressure = loss of elastic recoil (emphysema)

Question 16

COPD Pathogenesis

Answer 16

1. inflam and fibrosis of bronchial wall
2. hypertrophy of submucosal glands
3. hypersecretion of mucus
4. loss of elastic lung fibres
5. loss of alveoli

Question 17

COPD treatment

Answer 17

• stop smoking
• O2 therapy
• bronchodilators (B2 adrenergic agonists)

Question 18

Chronic bronchitis

Answer 18

• 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

Question 19

Emphysema

Answer 19

• abnormal permanent enlargement of the airspaces
• destruction of alveolar wall
• increased airspaces
• > hyperventilation of lungs
• > increased total lung capacity
• > ventilation is impaired

Question 20

Emphysema: Pathogenesis

Answer 20

• 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

Question 21

Emphysema: clincal feature

Answer 21

• 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

Question 22

Chronic bronchitis: pathogenesis

Answer 22

• 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

Question 23

CB: clinical features

Answer 23

• persistant cough
• dyspnea of exertion
• cyanosis
• cor pulmonale
• ‘blue bloaters’ = cyanosis and oedema

Question 24

Small cell carcinoma

Answer 24

• only in smokers

- highly malignant

Question 25

squamous cell carcinoma

Answer 25

- keratin pearls | - slower growing

Question 26

Adenocarcinoma

Answer 26

- lots of disorganised glands | - women and nonsmokers

Question 27

large cell carcinoma

Answer 27

- highly anaplastic (very poorly differentiated) | - poor prognosis