Respiratory Pathology

Mind Map by , created almost 6 years ago

Doctorate Pathology (Systems Pathology) Mind Map on Respiratory Pathology, created by melian.yates on 11/20/2013.

Created by melian.yates almost 6 years ago
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Respiratory Pathology
1 Routes of Invasion
1.1 1) Aerogenous
1.1.1 Trachea: High speed Bronchi/bronchioles: Slower speed => Aerogenous particles settle (Cranioventral areas)
1.1.2 Cranial & Medial lobes
1.2 2) Haemotogenous
1.2.1 Random scattering of multifocal lesions Ex. Metastases
1.3 3) Transcoelomic
1.3.1 Ex. Traumatic Reticulitis (Entry through Diaphragm)
2 Nasal Cavity
2.1 Normal flora:
2.1.1 Variable (Gram +ve) Prevent adherence by pathogenic (often Gram -ve bacteria)
2.2 Circulatory Problems
2.2.1 Epistaxis
2.2.2 Ex. Equine Ethmoid Haematoma Chronic nasal bleeding Old horses Pedunculated mass in ethmoidal region Expansive, but non-neoplastic Progressive Ethmoid Haematoma (PEH) Gets bigger over time
2.3 Rhinitis
2.3.1 Infectious (Upper Resp. tract infections) Viruses Bacteria Fungi Ex. Aspergillus fumigatus Chronic necrotizing inflammation => destruction of turbinates & septum Cryptococcus neoformans Nasal cavity often affected Sneezing, nasal discharge, nasal swelling (Granulomatous rhinitis) +/- Skin, ocular & CNS lesions Has a thick, non-staining mucoid capsule Ex. Atrophic rhinitis Strangles (Streptococcus equi) Lymphadentitis, Pharyngitis, Rhinitis, Metastatic abcesses, Guttural pouch empyema, Purpura haemorrhagica Ex. Feline viral rhinotracheitis, Canine distemper, Infectious Bovine Rhinotracheitis, Equine Rhinovirus
2.3.2 Allergens
2.3.3 Toxins
2.3.4 Trauma/foreign bodies
2.3.5 Classification Serous Catharral Mucopurulent Purulent Fibrinous Ulcerative + Fibrinonecrotic => Full thickness of epithelium exposed Fibrin deposits Overproduction of Mucous (Goblet cells) + Neutrophil Infiltration => Snotty nose Overproduction of mucous by Goblet cells Overproduction of Serous fluid (by Serous cells)
2.3.6 Chronic Rhinitis Consequence of Acute Rhinitis failing to resolve Chronic purulent rhinitis Nasal Polyps
2.3.7 Allergic Rhinitis Hypersensitivity to inhaled allergens Nasal epithelium damaged by cytokines Succeptible to 2ndary bacterial infections Eosinophils often the dominant infiltrating leukocyte
2.4 Pseudostratified columnar epithelium
2.5 Sinusitis
2.5.1 Common sequel to Rhinitis
2.5.2 Close proximity of sinuses to nasal cavity (Blockage of sinus drainage)
2.5.3 Purulent inflammation of the sinuses -> Chronic (poor drainage)
2.5.4 Dental or peridontal disease (maxillary sinus) Penetration of infections from dehorning wounds & fractures of the facial bones (Frontal sinus)
2.6 Neoplasia (Nasal Cavity & Sinuses)
2.6.1 Generally rare (more common in Dogs)
2.6.2 Can arise from any of the tissues in the region Adenoma/carcinoma (Glands/epthelium) Sarcoma (Cartilage, bone, connective tissue)
2.6.3 Most are malignant & are usually 2ndarily infected
2.6.4 Ex. Endemic ethmoid tumors (Ruminants): Retroviral origin - Carcinomas
3 Conducting Airways
3.1 Larynx & Trachea
3.1.1 Airflow obstruction
3.1.2 Aspiration pneumonia
3.1.3 Necrotic Laryngitis Ex. Calves: Fusobacterium necrophorum Friable appearance Cranial /Ventral lung lobes Massive inflammatory rxn (rupture onto surface)
3.1.4 Laryngeal Chondritis Texels & Southdowns (Other breeds) Rams > Ewes Chronic suppuration w/in the arytenoid cartilages of the larynx resulting in swelling & occlusion of the lumen (of larynx)
3.1.5 Filaroides Osleri Parasite (Canine) Nodules around tracheal bifurcation Foreign body nodular rxn develops around dead parasites
3.1.6 Tracheitis Thickening, hyperplasia of lamina propria 2ndary bacterial infections Clumps of necrotizing debris Runny nose, runny eyes High morbidity, low mortality Ex. Infectious Bovine Rhinotracheitis
3.1.7 Non-inflammatory Tracheal Diseases Tracheal Collapse Dorsoventral tracheal flattening Tracheal ligament has become stretched Older, small breed dogs Tracheal Neoplasia (Uncommon)
3.2 Bronchi
3.2.1 Bronchitis Acute Chronic Goblet cell hyperplasia & hypersecretion Squamous metaplasia Bronchiectasis Permanent dilation of bronchi (as a result of accumulation of purulent exudate in the lumen) Partial rupture of bronchial walls (irreversible) Usually 2ndary to chronic bronchitis Grape bunch appearance Dogs: Chronic cough Excess airway exudate Thickened mucosa Chronic inflammation => Stimulation of muscular hypertrophy in walls of small arteries Pulmonary hypertension => Cor pulmonale (RT heart failure)
3.2.2 Infectious tracheobronchitis (Kennel Cough) Common Persistent tracheobronchial inflammation If severe => Rhinitis or Bronchopneumonia Bordetella bronchiseptica PI2 CAV2
3.2.3 Bronchioles Epithelium highly susceptible to injury: Presence of Clara cells (contain oxidases that can locally generate metabolites that are toxic) Vulnerability to free radical damage Bronchiolitis Bronchiolar Obstruction Bronchioles much more prone to obstruct when inflamed than Bronchi Not much cartilage (rigid structure) -> Fills w/ inflammatory cells Where collateral ventilation is poor (Ruminants) obstructed bronchiole -> Atelectasis Extension of or concurrently w/ Bronchitis & Pneumonia Certain viral infections (pulmonary toxicity) When exudate cannot be cleared -> infiltration by fibroblasts -> development of organized polyp-like masses w/in the bronchiolar lumen => Bronchiolitis Obliterans
4 Alveoli
4.1 Structure
4.1.1 Simple squamous epithelium Type 1 Pneumocytes: Flattened, fried egg, cover 97% of septal surface Type 2 Pneumocytes: Cuboidal, cover approx. 3% of septal surface Produce Surfactant Progenitor of Type I & Type II Pneumocytes Repair surface of lungs (Damage)
4.2 Response to Injury
4.2.1 Aveolar Epithelialisation Marked lung damage (Type II Pneumocytes predominate)
4.2.2 Hyaline Membrane Formation Severe & Acute lung disease Stain pink
4.3 Pneumonia
4.3.1 Consolidation = altered texture of lung (firmer) due to accumulation of exudates (fluid & cellular infiltrate)
4.3.2 Inflammation that takes places in the alveoli & their walls
4.3.3 Classification via: Nature of inflammatory process Aetiological agent Pattern
4.3.4 Bronchopneumonia From terminal bronchioles Aerogenous portal of entry => Cranioventral Common (Bacterial, Mycoplasmal) Neutrophils & cell debris => Sequella: Resolution (mucociliary escalator, resolves 3 -4 weeks) Progression => Chronic Suppurative Bronopneumonia Consequences: Bronchiectasis Pulmonary abcessation Pleuritis & adhesions Atelectasis or overinflation BALT hyperplasia Fibrinous Bronchopneumonia Acute (tends to be more severe than suppurative) => Sudden death (possible) - toxaemia (Pasteurella) => Fibrosis & adhesions (b/w visceral & parietal pleura) Bronchointerstitial Pneumonia Hybrid of Bronchopneumonia & Interstitial Pneumonia Caused by viruses damaging both airway & alveolar epithelial cells (Ex. RSV)
4.3.5 Interstitial Pneumonia Inflammation primarily in alveolar walls Haematogenous spread (Most cases) Diffuse damage (May)=> Protein & fluid exudation => Hyaline membrane formation Exudative phase followed by proliferative phase (Type II pneumocytes proliferate to replace damaged Type I cells) Acute May be transient (Ex. viral infections) May be severe & associated with life threatening pulmonary oedema (Ex. Acute Resp. distress syndrome -ARDS) Examples: Fog Fever (Acute Bovine Pulmonary Oedema & Emphysema) Adult beef cattle Autumn (change to lush pasture) Ingestion of Tryptophan (3 methyl indole) in rumen Local generation of Free Radicals => Necrosis of Type I Pneumocytes Hyaline formation => Acute interstitial Pneumonia => Chronic Interstitial Pneumonia Paraquat Poisoning Weed killer (uncommon) Dogs & Cats Acute & Chronic lesions Extrapulmonary lesions Necrosis of adrenal zona glomerulosa Necrosis of Renal tubular epithelium Chronic Dominated by fibrosis of alveolar walls & proliferation of Type II Pneumocytes
4.3.6 Embolic Pneumonia Haematogenous spread Most often Caudal (Can occur anywhere) B/c more lung tissue Oriented around blood vessels (Embolis must come in vascular supply)
4.3.7 Granulomatous Pneumonia Dominated by macrophages, +/- giant cells Varying associated lymphocytes & neutrophils Multiple granulomas scattered throughout the lungs
4.3.8 Pulmonary Abscesses 1) Extension from Pneumonia 2) Septic emboli Ex. Suppurative mastitis 3) Aspiration of foreign material 4) Direct penetration Ex. Traumatic reticulocarditis
4.3.9 Enzootic Pneumonia Young animals in close contact (Calves, Lambs & Pigs)
4.3.10 Parasitic Disease Dictyocaulus viviparus Lifecycle Penetration phase In transit Prepatent phase Sequential alveolitis -> bronchiolitis -> bronchitis Patent Phase Parasitic bronchitis & pneumonia Postpatent Phase recovery Acute signs due to: Alveolar epithelialisation Superimposed infection Wedge-shaped lesions Dictyocaulus filaira Dictyocaulus arnfeldi Common (rarely clinical disease) Horses & Donkeys Gross pathology Raised focal over-inflated areas in the caudal lung lobes Histology Central parasites & associated chronic catharral bronchitis Hyperplastic bronchial epithelium & surrounding lymphoid infiltration Metastrongylus (Pigs) Muellerius capillaris Common (rarely clinical sig.) Firm "lead shot" nodules Dorsal regions of caudal lobes Aerostrongylus abstrusus Cat lungworm Firm, yellow nodules in parenchyma Eggs & larvae -> Foreign body type Rxn Chronic coughing & airway Eosinophilia (can resemble asthma) Angiostrongylus vasorum (Heart worm) Pulmonary arteries & RT ventricle Dogs & Foxes Can cause proliferative change in blood vessels => Pneumonia => Pulmonary Oedema & Hypertension Echinococcus granulosus Intermediate stage (Lungs) Little clinical significance Zoonosis & carcass condemnation Hydatid Cyst Hypersensitivity Diseases Type I Hypersensitivity Mast cell mediated (Through Ag- IgE complexes) => Degranulation Constriction of airways Feline Asthma/ Allergic Bronchitis Inhaled Ags Recurrent episodes of bronchoconstriction Inflammation (Eosinophil dominated) +/- Circulating Eosinophilia Pulmonary Infiltration w/ Eosinophilia Dog Predominance of Eosinophils in airways Inhaled Ags Type III Hypersensitivity Ag-Ab Complex mediated Can settle in alveolar blood vessels Extrinsic Allergic Bronchio-alveolitis Repeat inhalation of spores Chronic inflammation Thickening of alveolar septae Housed Dairy Cows (Winter) Diffuse Fibrosing Alveolitis (DFA) COPD - Chronic Obstructive Pulmonary Disease (SPAOPD -Summer pasture associated) Chronic coughing, poor performance Airway inflammation, excess mucus Heaves (Heave line) Gross: Affected lungs unremarkable (except in extreme cases - alveolar emphysema) Histologically: Chronic generalized bronchitis Plugging of airways w/ mucous, inflammatory cells, goblet cell metaplasia & smooth muscle hypertrophy
4.3.11 Aspiration Pneumonia Inhaling foreign particle Severity depends on nature of material (ex. food), bacterial load, & distribution w/in lungs Can develop into Severe Necrotizing pneumonia => Gangrenous pneumonia Abscesses
4.3.12 Gangrenous Pneumonia Tissue becomes necrotic -> invaded by putrefactive saphrophytes (Ex. Clostrdia) Dead tissue undergoes Liquefactive Necrosis Usually Iatrogenic or as a sequel to aspiration pneumonia
4.3.13 Lipid Pneumonia Endogenous Cats > Dogs Subclinical Accumulation of lipids (surfactant) in pulmonary macrophages -> multifocal white nodules Exogenous Associated w/ inhalation of oil, paraffin, etc. Rxn dominated by macrophages which fill the alveoli Interstitial thickening (mononuclear cells & fibrosis) - Inflammation
4.3.14 Uraemic Pneumonia Sever uraemia => increased permeability of the blood -air barrier (May) => Pulmonary Oedema (May) => Degeneration & calcification of smooth muscle & connective tissue
5 Pulmonary Oedema
5.1 Protection Mechanisms
5.1.1 Impermeable epithelium & junctions Interstitial pressure in alveolar septae lower than intraalveolar pressure Efficient lymphatic drainage Pushes fluid out of alveoli
5.2 Excessive fluid in the lung
5.3 Begins as Interstitial Oedema
5.3.1 Expansion of perivascular, peribronchial & peribronchiolar fascia & distension of interstitial lymphatics
5.3.2 Interstitial compartment overwhemled => fluid floods airspces => Alveolar oedema
5.4 Causes
5.4.1 Increased capillary or Type I epithelial permeability Systemic toxins Shock Inhaled caustic gases
5.4.2 Increased capillary hydrostatic pressure (cardiogenic oedema) LT sided or Biventricular Heart failure Increased hydrostatic pressure -> pushes fluid into lungs
5.4.3 Decreased plasma oncotic pressure (Hypoalbuminaemia) Proteins keep fluid in plasma (Decreased proteins -> fluid leaves vascular compartment -> Lungs)
6 Pulmonary Haemorrhage
7 Embolism, Thrombosis & Infarction
7.1 Lung supplied by BOTH Pulmonary & Bronchial Arteries
7.1.1 Infarction doen NOT usually follow embolism or thrombosis, UNLESS pulmonary circulation is already compromised Usually occur w/ emboli/thrombosis during general circulatory collapse or passive congestion of heart failure
8 Pulmonary Hypertension
8.1 Caused by LT -> RT vascular shunts or Increased resistance of the pulmonary vascular system
8.2 Most commonly a sequel of:
8.2.1 Widespread fibrosis in the lung Chronic bronchitis or bronchiolitis (stimulates hypertrophy in the walls of small arteries)
8.3 Severe, Prolonged => Cor Pulmonale
8.3.1 RT-sided Heart failure 2ndary to primary lung disease
9 Neoplasia
9.1 Pulmonary Tumors
9.1.1 Metastatic: Common OPA (Ovine Pulmonary Carcinoma)/ Jaagsiekte Retrovirus induced cancer Intensive management systems - Aerosol transmission 'Wheelbarrow test' Well differentiated carcinoma Can get dry forms of OPA (cells not so active in producing surfactant)
9.1.2 Primary: Relatively Rare Dogs & Cats
9.2 Bronchial papilloma
9.3 Bronchial adenoma/carcinoma
9.3.1 Arising from major airways
9.4 Bronchioloalveolar adenoma/carcinoma
9.4.1 Arising from small airways or alveolar parenchyma (either secretory bronchiolar cells or Type II epithelial cells)
9.4.2 Carcinoid Neuroendocrine cells (Rare in animals)
9.5 Mesothelioma
9.5.1 Most common in Calves (can be congenital)
9.5.2 Often causes Thoracic effusion
9.5.3 Multiple nodular masses on pleural surface & visceral surface
9.5.4 Dx can be difficult due to cytological similarity of reactive & neoplastic mesothelial cells