MindMap Gallery respiratory diseases
Pathology summarizes and organizes knowledge points to help learners understand and remember. Straight to the point, it can be used as study notes and review materials to help you systematically review and consolidate the knowledge you have learned. The knowledge points are systematic and comprehensive. I hope it will be helpful to everyone! Suitable for exam review.
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This is a mind map about a commercial solution for task speech recognition. The main content includes: text file content format:, providing text files according to the same file name as the voice file.
respiratory diseases
Respiratory tract anatomy (understand)
upper respiratory tract
Warm and moist air
Secrete mucus and serous fluid to attach larger dust and expel it
lower respiratory tract
Conducting part
composition
Bronchial tubes (with cartilage)
small bronchi
Bronchioles
terminal bronchioles
epithelium
Pseudostratified or single-layer ciliated columnar epithelium
Cilia, wall goblet cells, mucus glands = mucus-ciliary drainage system
Less than 2μm enters the alveoli and is phagocytosed by macrophages
terminal bronchioles
Features
single layer ciliated columnar epithelium
No goblet cells
No glands and cartilage
Lobules of the lungs (lobular pneumonia)
3-5 terminal bronchioles and their branching alveoli
Between adjacent pulmonary lobules: interlobular veins, lymphatic vessels and fibrous tissue
Pulmonary acini
Level 1 respiratory bronchioles within pulmonary lobules Distal lung tissue
Alveoli
Type 1 epithelium (95%)
Cells are flat and broad with basement membrane
Type 1 epithelium, capillary endothelium, basement membrane = air-blood barrier
Type 2 epithelium (5%)
Cubic type, embedded between type 1 epithelium
Secrete surfactants to reduce surface tension
Interalveolar pores (Cohn's pores)
On the alveolar walls, connecting adjacent alveoli
pneumonia
Bacterial pneumonia (parenchymal) (both lower lungs)
Lobar pneumonia
Overview
Cause
Streptococcus pneumoniae infection
involve
All large lobes of lung
People prone to hair loss
young adults
Features
opportunistic disease
No transparent film appears
Nature of the lesion
Fibrinitis in the alveolar space
Predisposed areas
Lower lobes of both lungs
Pathological changes
Course of disease (every 2 days)
congestive edema stage
in general
The diseased lung lobes are swollen and dark red
under the mirror
Diffuse capillary congestion of alveolar septa
A large amount of serous exudate in the alveolar cavity, mixed with a small amount of blood cells
Red hepatoid degeneration
in general
The diseased lung lobes are swollen and dark red
The texture becomes firm, the cut surface is gray-red, and the shape resembles liver.
under the mirror
The alveoli are filled with a large amount of fiber and red blood cells, and a small amount of inflammatory cells
Cellulose can pass through the interalveolar pores
clinical manifestations
Coughing rust-colored sputum (macrophages phagocytose and digest red blood cells and disintegrate hemosiderin)
Impaired pulmonary ventilation, cyanosis and hypoxia (when the lesions are extensive)
Fibrinous pleurisy, chest pain (when pleura is involved)
gray hepatoid stage
in general
The lungs are enlarged, but not congested (red to gray), and are as solid as liver
under the mirror
Increased fibrin and neutrophils in the alveoli, and disappearance of red blood cells
The phenomenon of cellulose passing through the interalveolar pores is more common
clinical manifestations
Coughing up mucus and thick phlegm
Hypoxia improved
Dissolution and dissipation period
under the mirror
Neutrophils undergo necrosis, release hydrolytic enzymes, and dissolve cellulose
Insufficient dissolution
Lung flesh changes
Complications (rare)
Flesh changes in the lungs (organizing pneumonia)
Brown flesh-like appearance
Too few neutrophils in the alveoli (insufficient number)
Cellulose cannot be dissolved and becomes organic
Pleural hypertrophy and adhesions
Intrapleural fiber is not completely absorbed
Lung abscess and empyema
Highly virulent pathogenic bacteria or low resistance
Sepsis and Sepsis
Severe infection that invades the bloodstream
septic shock
severe cases
Lobular pneumonia (bronchopneumonia)
Overview
Cause
Suppurative bacterial infection
Nature of the lesion
Purulent inflammation centered on bronchioles
Mainly neutrophil exudation
People prone to hair loss
The old, the weak, the sick and the disabled
belong
aspiration pneumonia
Predisposed areas
Lower lobes of both lungs
Pathological changes
naked eye
Grayish-yellow, solid lesions distributed on the surface of both lungs
The lesion is within 1cm in diameter, and the diseased bronchioles can be seen in the center
In severe cases, the lesions merge into sheets or even involve the entire large lobes (confluent lobular pneumonia)
under the mirror
Early days
Congestion and edema of diseased bronchiolar mucosa
No changes in surrounding lung tissue
progress
Neutrophils, red blood cells, and exfoliated alveolar epithelial cells (hyaline membrane) appear in the diseased bronchioles and surrounding alveoli.
Compensatory emphysema (overexpansion) of some alveoli
viral pneumonia
lesion site
interstitium
naked eye
Pulmonary congestion and edema (mild)
under the mirror
Pulmonary interstitial congestion and edema, lymphomononuclear infiltration
Alveolar septa widened, internal blood vessels dilated
diagnosis
Viral inclusion bodies (epithelial cells or multinucleated giant cells)
measles virus pneumonia
Easiest to form a transparent film
Mycoplasma pneumonia
Nature of the lesion
interstitial pneumonia
Characteristics of lesions such as viral pneumonia, culture identification
Severe acute respiratory syndrome SARS
Nickname
infectious atypical pneumonia
lung
naked eye
Consolidation of both lungs, dark red surface, hemorrhage and necrosis
under the mirror
diffuse alveolar damage
Extensive transparent membrane formation in the alveolar space
visible inclusion bodies
spleen and lymph nodes
slightly
chronic obstructive pulmonary diseaseCOPD
COPD
Damage to lung parenchyma and small airways (difficulty expiration)
leading to chronic irreversible airway obstruction
chronic bronchitis
Pathological changes
Early days
Impaired respiratory mucus-ciliary drainage system
Squamous metaplasia occurs (most common)
Necrosis and shedding of ciliated columnar epithelium
Increased regenerative epithelial goblet cells
other
Submucosal gland hyperplasia and hypertrophy
serous epithelial mucinous metaplasia
Congestion and edema of the vessel wall, chronic inflammatory cell infiltration
Smooth muscle rupture and atrophy of the tube wall (hypertrophy in patients with wheezing type)
recurring attacks
Increased number of bronchioles involved, causing fibrous thickening of the tube wall
Inflammation spreads to surrounding tissues, forming peribronchiolar inflammation
clinical manifestations
White frothy phlegm
complication
Emphysema and Cor pulmonale
bronchiectasis
Basis of disease
Bronchial wall is damaged
Pathological changes
naked eye
More common in left lower lobe of lung
Cylindrical or cystic dilation of bronchi, honeycombing of lungs (characteristic lesions)
Intraluminal purulent exudation of dilated bronchioles
under the mirror
bronchial wall thickening
Mucosal epithelial hyperplasia with squamous metaplasia
Bronchial structural damage and scar repair
clinical manifestations
Coughing up purulent sputum and coughing up blood (bronchial wall blood vessels are damaged)
Late complications of pulmonary hypertension and pulmonary heart disease
Severe pulmonary dysfunction (shortness of breath, cyanosis, finger clubbing)
bronchial asthma
Basis of disease
Bronchiolar spasm and mucus plug obstruction
Characteristic lesions
Reversible paroxysmal bronchial spasm
Pathological changes
naked eye
Excessive inflation of the lungs
intraluminal mucus plug
under the mirror
Localized shedding of mucosal epithelium
Submucosal edema, mucous gland hyperplasia, increased goblet cells
Hyperplasia and hypertrophy of smooth muscle of tube wall
Infiltration of eosinophils in all layers
Eosinophil disintegration products: Charcot-Leyden crystals
clinical manifestations
expiratory dyspnea
Emphysema
Basis of disease
Chronic obstructive bronchitis and peripheral inflammation
concept
Excess air content in peripheral lung tissues (respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli) accompanied by destruction of alveolar septa
Causes lung tissue elasticity to weaken, volume to expand, and ventilation function to decrease
Pathogenesis
obstructive ventilatory disorder
Decreased levels of alpha1-antitrypsin (chronic inflammation)
Decreased elasticity of respiratory bronchioles and alveolar walls
Classification
Alveolar emphysema (parenchymal)
Centrilobular emphysema (most common)
Bronchioles
Perilobular emphysema
Alveoli
panalveolar emphysema
are expanding
Caused by reduced levels of alpha1-antitrypsin
interstitial emphysema
Strings of small bubbles appear in the alveolar septa
Pathological changes
Decreased pulmonary capillary bed (alveolar expansion compressing the pulmonary interstitium)
causing pulmonary hypertension
Adjacent alveoli fuse to form larger cysts
Soft lungs
clinical manifestations
Expiratory dyspnea (obstructive)
barrel chest
late stage pulmonary heart disease
Chronic cor pulmonale (cor pulmonale)
Cause: COPD (most common)
Chronic bronchitis complicated by obstructive emphysema (most common)
other
Silicosis
pulmonary embolism
key links
pulmonary hypertension
Pathological changes
lung disease
Decreased capillaries (spasm)
Caused by hypoxia
Small blood vessel structural changes
Amuscular arteriole muscularization
Muscular arteriole media hyperplasia
Massive destruction of pulmonary capillary bed
Interfering item: fibrinoid necrosis of medium-sized arteries
Heart disease (mainly right ventricle)
Right ventricular hypertrophy with anterior wall muscle thickness exceeding 5 mm (diagnosis)
Myocyte lysis, fiber atrophy
clinical manifestations
Respiratory insufficiency
Right ventricular insufficiency
Pulmonary encephalopathy (severe)
pneumoconiosis
Pulmonary silicosis (silicosis)
Cause
The smaller the SiO2 particles, the more pathogenic they are (1-2μm)
Pathogenesis
Macrophages are unable to digest SiO2 and autolysis causes lung damage
Pathological changes
Silicon nodules (basic lesions)
Collection of macrophages engulfing silica dust (primary)
Fibroblast proliferation within nodules, nodular fibrosis
Adjacent silicon nodules can fuse, and central ischemia and necrosis can lead to silicosis cavities.
intracellular silica nodules
early stage lesions
diffuse fibrosis of lung tissue
advanced disease
Predisposed areas
hilum
complication
tuberculosis
chronic pulmonary heart disease
Lung infections and emphysema
Pulmonary asbestosis (asbestosis)
Cause
Inhalation of asbestos (containing Fe, Mg, Al, etc.)
Pathological changes
Asbestos bodies (diagnostic basis)
diffuse interstitial pulmonary fibrosis
Hypertrophy of the visceral layer of the pleura; formation of pleural plaques in the parietal layer
complication
Pleural mesothelioma
respiratory distress syndrome
Adult respiratory distress syndrome ARDS
Overview
Severe trauma, infection and severe lung disease throughout the body
Characterized by progressive respiratory distress and hypoxemia
acute respiratory failure syndrome
Pathogenesis (respiratory membrane damage)
Pulmonary capillary damage
Intra-alveolar and interstitial edema
Massive exudation of cellulose in the alveoli
Alveolar epithelial damage
After type 2 epithelial injury, active substances are reduced, alveoli collapse, and a transparent membrane forms on the alveolar surface.
Pathological changes
Hyaline membrane: plasma protein, necrotic alveolar epithelium (typical lesion)
Division: Respiratory bronchioles, alveolar ducts, alveoli
interstitial congestion
Alveolar cavity proteinaceous exudate
complication
Diffuse fibrosis of alveoli and lung tissue
It is not caused by cellulose leakage, but by protein deposition in blood cells.
Neonatal respiratory distress syndrome NRDS
Lesion characteristics
A transparent membrane forms in the lungs
Cause
Type 2 alveolar epithelial underdevelopment (premature infants)
Respiratory system tumors
Nasopharyngeal cancer
special causes
Epstein-Barr virus
Predisposed areas
roof of nasopharynx
general shape
Nodular type
squamous cell carcinoma
differentiated squamous cell carcinoma
Nonkeratinizing squamous cell carcinoma (most common)
Keratinizing squamous cell carcinoma (well differentiated squamous cell carcinoma, keratinized beads)
undifferentiated squamous cell carcinoma
alveolar cell carcinoma
Diffusion pathway
Lymphatic metastasis (early stage)
Metastasis to: deep upper cervical lymph nodes
A painless nodule appears on the posterior edge of the sternocleidomastoid muscle on the ipsilateral side
Direct spread (understanding)
Destroys the bones at the base of the skull upward and into the skull, damaging the cranial nerves.
Invades the piriform recess, epiglottis and upper larynx downward
Lateral damage to the Eustachian tube such as the middle ear
forward to the nasal cavity or orbit
Destroys the upper cervical vertebrae and spinal cord backwards
lung cancer
diagnosis
fiber bronchial biopsy
Pathological changes
Adenocarcinoma and squamous cell carcinoma
Squamous cell carcinoma is mostly central lung cancer
Central (hilar) (most common) (squamous cell carcinoma)
In the early stage, the mass compresses the bronchus to the point of stenosis and progresses to surround the bronchus.
Hilar mass and hilar lymph node metastasis, which can be fused
Squamous cell carcinoma (origin: large bronchial mucosal epithelium)
Formation of keratinized beads and intercellular bridges (keratinized type)
No keratinized beads, no intercellular bridges (non-keratinized type)
diffusion
lymphatic tract
Adenocarcinoma is mostly peripheral lung cancer
Adenocarcinoma (origin: small bronchial epithelium)
Most common type of lung cancer in women
Peripheral (adenocarcinoma) (95%)
Originating from lung segments or distal bronchi
Prevalent site: around the lungs near the lung membrane
Diffuse type (well differentiated adenocarcinoma) (5%)
Originates from peripheral lung tissue
Diffuse infiltration and growth, forming miliary-sized nodules
diffusion
blood channel
Other histological types
Small cell carcinoma (oat cell carcinoma)
neuroendocrine cancer
Can be secreted
Lung cancer is the most poorly differentiated (worst prognosis)
Mostly central
adenosquamous carcinoma
Adenocarcinoma combined with squamous cell carcinoma
carcinoid
The least malignant
Neuroendocrine tumors that secrete
Lung cancer without lymph node metastasis
early stage lung cancer
Central type (limited to the lumen)
Peripheral type
Latent lung cancer
Carcinoma in situ or early invasive carcinoma of bronchial mucosa
Imaging recessive, cytology positive