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