PATHOLOGY OF THE RESPIRATORY
SYSTEM, PART II
ASTHMA BRONCHIALE
Episodes of paroxysmal dyspnoe
Expiratory dyspnoe with bronchospasm, oedema of brochial walls and mucus hypersecretion)
Histamin, brydykinin, leukotrien, PAF,
1) Astma extrinsic (1 type hypersensitivity - dust, pollen, mites, Aspergillus
2) A. intrinsic (hypereactivity – cold, exertion, stress, aspirin)
Status asthmaticus (hypoxia, hypercapnia)
Microscopically : occlusion of brochi and bronchioles + excess of mucus (Curschmanns´ spirals), eosinophils, Charcot-Leyden crystals, basement membrane thickenig, oedema, chronic infiltrate (CD4+ lymphocytes, macrophages, mast cells) hypertrophy of mucous gland, goblet cells, and smooth muscle
2
3
CONGENITAL ABNORMALITIES
Agenezis or hypoplasia of the lungs: may affect one lobe or the whole lung (Down sy, diafragmantic herniation, oligohydramnion, deformitie of the thorax)
Others
Congenital adenomatous malformation,
Congenital lobar emphysema (vessel pressure, abnormities of cartilage (thread of spontaneous pneumothorax)
Congenital bronchogenic cysts, cystic malformation
Intralobular and extrapulmonal lobar sequstration (lung lobes or segments supplied by an abnormal systemic artery, often without connection with respiratory pathways – reccurent infections)
RESPIRATORY MEMBRANE
PNEUMOCONIOSES, OCCUPATIONAL LUNG
DISEASES
Disseases caused by
inhalation of dust
(particles less than 2-3 mm)
Dust: mostly inorganic
Reactions: fibrous (massive
fibrosis), neoplastic
transformation
PNEUMOCONIOSES, OCCUPATIONAL LUNG
DISEASES
Silicosis Silica crystals (stone, sand – potters,
miners, glass cutters)
Stages: 1)reticular fibrosis
2) silicotic nodules
3) diffuse interstitial
fibrosis
PNEUMOCONIOSES, OCCUPATIONAL LUNG
DISEASES
Asbestosis Asbestos = inconsumable
Asbestos bodies
5-100 mm X 0,25-0,5 mm
Diffuse fibrosis
Malignant mesothelioma
Lung carcinoma
PNEUMOCONIOSES, OCCUPATIONAL LUNG
DISEASES
Coal miner’s lung
Anthraco-silicosis
Immune complex mediated
fibrosis
Often superinfection by TBC
and atypical mycobakterias
INFLAMMATION OF THE LUNGS
A) Non-specific
Superficial bronchopneumonia
lobar pneumonia
Interstitial 1) Infective
a) normal immunity
Viruses (influenza, RSV, adenoviruses) and mycoplasma
Legionnaires’ disease
b) immunosuppression
Pneumocystis jiroveci (yeast like fungi)
Fungi (Candida, Aspergillus)
Viruses (cytomegalovirus)
HIV lung disease
2) Non- infective (UIP, NSIP, DIP, LIP, eosinophilic pneumonia, hypersensitive pneumonia, BOOP – resulting in lung fibrosis of various intensity)
3) Disintegration (pulmonary abscessus, gangrene)
B) Specific (granulomatous) Tuberculosis
Mykobacterioses (MAI complex) – mostly in immunocompromised patients
Sarcoidosis
INFLAMMATION OF THE LUNGS
SUPERFICIAL PNEUMONIAS
Lobar pneumonia
Large areas = lobar pleumonia
90% Streptococcus pneumonie
Klebsiella (diabetes, alcohol)
Fibrinous – suppurative
inflammation
Young to middle aged adults
Often follows viral infection
Stages 1) congestion
2 red hepatization
3) grey hepatization
4) resolution
Complications: pleuritis+empyema,
carnification, endokarditis,
metastatic suppuration)
Bronchopneumonia
Patchy consolidation of lungs
Centralised on bronchioles
with furhther spread to alveoli
Mostly kids and elderly
Often pre-existing diseases
(terminally ill patients – tumots,
cardiac or renal failure, old man’s
friend that spared prolonged suffering
– terminal events)
Often bilateral and basal localization
BRONCHOPNEUMONIA
LOBAR PNEUMONIA
PNEUMOCYSTIC PNEUMONIA
PULMONARY TUBERCULOSIS
The commonest form of TBC
Risk f: alcohol abuse, diabetes, HIV, old age
Clin. symptoms: variable – depending on the extend of diseases: weight loss, night sweats, cough, dyspnoe
Forms: 1) Primary (initial contact, Ghon complex (granuloma about 10mm + regional lymph ), mostly healed but bacterias survive!!!
2) Secondary (reactivation of primary complex or superinfection), cavities in upper lobes – open TBC
3) Miliary
primary and secondary TBC, inadequate immune response- dissemination – lungs, meninges, kidneys, bones, liver, peritoneum, often fatal
PULMONARY TUBERCULOSIS
Accumulation of fluid in alveoli
Exsudate (s.w over 1020 kg/m3) x Transudate
Interstitial X alveolar
Increased capillary permeability and increased intraluminal pressure
Increased hydrostatic pressure
Damage of alveolar or capillary walls (iritant gases, toxemia, embolism)
Decreased oncotic pressure
Blockade of lymph drainage
Symptoms: Dyspnoe, cough, foamy Respiratory failure, hypoxia!!
PULMONARY OEDEMA
EDÉM PLIC
Trombembolism
Fat embolism (12-24h, DAD, petechiae, cerebral symptoms – confusion, coma
Bone marrow embolism (after cardiac resucitation)
Air embolism (trauma, criminal abortions, Keson disease, more than 100 cc of air)
Amniotic fluid embolism
Tumour embolism
PULMONARY EMBOLISM
80% from deep veins of LE
60-80% emboli are silent
(manifested only when succesive
– p. hypertension)
PE with infarction - when
bronchial artery insufficiency =
left ventricle failre, mitral stenosis,
reduction of pulmonary circulation
Suden death
Symptoms: dyspnoe, tachykardia,
pleural or chest pain – may mimic
cardiac infarction, hemoptysis,
sudden death)
TROMBEMBOLISM
EMBOLUS
Types
primary pulmonary hypertension – with unknown etiology (young females), occlusion of small arterioles due tu endothelial damage.
Bad prognosis (withun 3 yrs cardiac failure)
Symtoms: dyspnoe, cyanosis, chest pain, malaise
secondary pulmonary hypertension
1) pre- capillary (COPD, fibroses, pneumokonioses)
2) post -capillary ( LV failure)
3) hyperkinetic (cardiac shunts, increased minute volume – hyperthyroidism)
COR PULMONALE
Middle pressure (mm
Hg)
Systolic pressure (mm Hg)
normal < 25 < 35
mild 26–35 36–45
moderate 36–45 46–60
severe > 45 > 60
PULMONARY HYPERTENSION
Rapidly progressive respiratory failure with hypoxemia
Causes:
1)trauma, shock, fat embolism
2) infections – bacterial (sepsis)+ viral (SARS)
3) aspiration
4) drugs, intoxications (heroin, oxygen, radiation, cytotoxic agents)
Phases: Exudative (pneumocytes necroses+ hyaline membrane)
Proliferative
Fate: Acute respiratory failure - fatal
Recovery with normal function
Honeycomb lung
DIFFUSE ALVEOLAR DAMAGE, DAD
Benign:
Adenoma, papilloma, leiomyoma, fibroma, chondrohamartoma, papillární pneumocytoma (sklerosin hemangioma), solitary fibrous tumor
Malignant:
Carcinoma – M:F=2:1, over 55 yrs (smoking, radiation, fibrosis, arsenic, mutation of p16, K- ras, TP53, pRB)
Small cell carcinoma (30%): often paraneoplastic sy
Non- small cell carcinomas: adenocarcinoma (10%)
squamous cell carcinoma (50%) large cell carcinoma (10%)
Neuroendocrine
Carcinoid
Atypical carcinoid
Mezenchymal Angiosarcom,a synovial sarcoma, lymphoma
PULMONARY TUMORS
Macroscopic forms - Central
- Lobar
- Peribronchial
- Lymfagitic
- Pulmomediastinal
- Pleuropulmonal
- Pancoast tumor (apical - compressison of cervical sympathetic plexus –
Horner´s trias= ptosis, miosis, enopthalmos)
- Carcinoma in scar (TBC, pneumokonises)
- Multinodular
PULMONARY CARCINOMAS
Cought
Hemoptysis
Reccurent pneumonias
Bronchiectasis
Paraneoplastic syndromas
Pleural effusions
Cachexia
Metastases
CARCINOMA – SYMPTOMS
Peribronchial type
PLEURAL PATHOLOGY
pleuritis serous: frequent, good prognosis
pleuritis fibrinous: complicated by adhesions
pleuritis hemorrhagic: TBC, haemorrrhagic diatesis, tumour
pleuritis purulent: empyema
Inflammation
Usually associted with pneumonia, abscessus, gangrene, septic infarction,
or from chest wall and mediastinum inflammation, less frequently
hematogenic spread
Primary
mesothelioma: malignant, epitheloid, sarcomatoid, biphasic
synovial sarcoma
epitheloid hemangioendotelioma
adenomatoid tumor: benign
solitary fibrous tumor: benign
Secondary = metastases (more frequent)
PLEURAL TUMORS