① Damage airway epithelial cells and ciliary movement, reducing airway purification ability;

② Promote the proliferation and hypertrophy of bronchial mucus glands and goblet cells, and increase mucus secretion;

③ Stimulates parasympathetic nerves to cause bronchial smooth muscle contraction and increase airway resistance;

④ Increase the production of oxygen free radicals, induce neutrophils to release proteases, destroy pulmonary elastic fibers, and induce the formation of emphysema;

①Cilia: adhesion, lodging, shedding

②Mucosal epithelium: degeneration, necrosis, and shedding

① Squamous metaplasia (ciliated columnar epithelium to squamous epithelium)

② Increased goblet cells (secreting a large amount of mucus, coughing and sputum)

①PaO2 ≤55 mmHg or SaO2 ≤88%, with or without hypercapnia

②PaO2 55-60 mmHg or SaO2 <89%, and edema or polycythemia caused by pulmonary hypertension, heart failure

① Episodic: When encountering predisposing factors, it becomes episodic and worsens;

② Rhythmicity: often attacks or worsens at night and early in the morning;

③Seasonality: often occurs or worsens in autumn and winter;

④Reversibility: Symptoms can usually be relieved and there can be an obvious remission period;

① Recurrent wheezing, shortness of breath, chest tightness or cough often have triggers;

② During the attack, the wheeze is scattered or diffuse, mainly in the expiratory phase, and the expiratory phase is prolonged;

③Symptoms are relieved or relieved after treatment;

①Positive bronchial provocation test;

②Positive bronchodilation test;

③The average daily PEF diurnal variation rate is >10% or the PEF weekly variation rate is >20%;

Epinephrine is used for bronchial asthma, not for cardiac asthma;

Morphine (three depressants and one depressant - sedative, antitussive, antiasthmatic, and respiratory depressant) is used for cardiac asthma, but not for bronchial asthma;

Use theophylline for acute asthma of unknown cause;

Ketotifen - restores receptor downregulation; formoterol - does not produce receptor downregulation; glucocorticoids - upregulates receptors and increases their affinity;

Level 1 No use or low dose use

Level 2 Low-dose ICS or leukotriene receptor antagonist single agent

Level 3 Low-dose ICS LABA or low-dose ICS leukotriene receptor antagonist

Level 4: Medium to high dose ICS LABA or high dose ICS leukotriene receptor antagonist

Level 5 (medium and high dose ICS LABA or high dose ICS leukotriene receptor antagonist) oral glucocorticoids

Lobar (alveolar) pneumonia: causes alveolar inflammation and spreads to other alveoli through the inter-alveolar pores (Cohn's pores), usually without involving the bronchi. X-ray images show consolidation shadows in pulmonary lobes or lung segments;

Lobular (bronchial) pneumonia: causes inflammation of the bronchioles, terminal bronchioles, and alveoli. X-ray images show irregular patchy shadows distributed along the lung texture without signs of consolidation;

Interstitial pneumonia: Involves the bronchial wall and peribronchial tissue. X-ray images show irregular shadows in the lower part of one or both lungs;

Community-acquired pneumonia (CAP): air inhalation, bloodstream dissemination, adjacent site infection, aspiration of colonized bacteria in the upper respiratory tract; mainly G-cocci, with pneumococci accounting for 40-50%; ❤ (Streptococcus pneumoniae - the most common, Mycoplasma, Chlamydia, Haemophilus influenzae - the most common gram-negative bacilli, respiratory viruses, etc.)

Hospital-acquired pneumonia (HAP): aspiration of gastrointestinal colonization bacteria/aspiration of gastroesophageal reflux material (common), inhalation through artificial airway; mainly G-bacilli, increased MDR❤ (MRSA, Pseudomonas aeruginosa bacteria, Acinetobacter baumannii)

Streptococcus pneumoniae (SP): Gram-positive cocci, a normal flora that resides in the oral cavity or nasopharynx. It does not produce toxins, cause tissue necrosis or form cavities. Its pathogenicity is due to the invasive effect of the capsule of high molecular polysaccharides on tissues (many types, prone to mutation, prone to drug resistance, sensitive to bile salts, positive bile bacteriolysis test)

Routine blood test: white blood cell count increased, neutrophils were more than 80%, and nuclei shifted to the left;

Sputum smear: G ( ), encapsulated diplococci or streptococci;

Chest X-ray (preferred): The lung segments or lobes show large inflammatory infiltration shadows or consolidation shadows;

CT: Air bronchus sign can be seen in consolidation;

1. Penicillin G is preferred; enzyme-resistant → semi-synthetic penicillin;

2. For penicillin allergy or penicillin-resistant Streptococcus pneumoniae pneumonia, third-generation cephalosporins and fluoroquinolones (floxacin) should be used

3. For those with multidrug-resistant strains (MDR), vancomycin, teicoplanin, and linezolid can be used

4. Supportive treatment and symptomatic treatment of complications.

1. The pathogenic substances of Staphylococcus aureus are mainly toxins and enzymes, such as hemolytic toxins, leukocidins, enterotoxins, etc., which have the effects of hemolysis, necrosis, killing leukocytes and vasospasm;

2. The pathogenicity of Staphylococcus aureus can be measured by plasma coagulase. Those who are positive (such as Staphylococcus aureus) are highly pathogenic;

Note: Staphylococcus infection accounts for 11% to 25% of hospital-acquired pneumonia.

1. Staphylococcal pneumonia caused by respiratory inhalation often presents with lobar distribution or extensive, confluent bronchopneumonia. Air cysts form and rupture, leading to pneumothorax or pyopneumothorax and bronchopleural fistulas. Can be complicated by purulent pericarditis and meningitis;

2. Staphylococci spread from menstrual blood to the lungs, causing multiple lung consolidations, suppuration and tissue destruction, forming multiple or multiple lung abscesses;

1. The onset of this disease is often sudden, with high fever, chills, and chest pain;

2. The sputum is purulent and pus-like (blood in the sputum);

3. Symptoms of toxemia are obvious, and severe cases may suffer early peripheral circulatory failure;

4. There may be no physical signs in the early stage, but later on, there may be signs of moist rales in the lungs, signs of lung consolidation, and corresponding signs of pneumothorax and pyopneumothorax;

Blood routine: peripheral blood white blood cell count increased significantly, the proportion of neutrophils increased, and the nucleus shifted to the left;

X-ray examination: Consolidation of lung segments or lobes, which may lead to early formation of cavities or lobular infiltration with single or multiple fluid-air cysts;

The variability of X-ray is manifested by the disappearance of inflammatory infiltrates in one place and the appearance of new lesions in another place. Or a small single lesion develops into a large shadow. The lesions are absorbed in 2-4 weeks.

1. It is emphasized that the primary lesions of drainage should be removed early and sensitive antibiotics should be used;

2. The resistance rate of Staphylococcus aureus to penicillin G is over 90%;

3. For methicillin-sensitive staphylococci, choose enzyme-resistant semi-synthetic penicillins (oxacillin, cloxacillin) or cephalosporins, combined with aminoglycosides (gentamicin, streptomycin, amikacin);

4. Use amoxicillin/ampicillin enzyme inhibitors for enzyme-producing Staphylococcus aureus;

5. For methicillin-resistant Staphylococcus aureus (MRSA), choose vancomycin, teicoplanin, or linezolid;

[General case description] Children and adolescents with a history of travel, slow onset and self-limiting (can be cured without treatment); sore throat/headache/myalgia/pharyngitis/myringitis (extrapulmonary manifestations are more common), 38° low fever, no infection Toxic shock, persistent paroxysmal severe irritating dry cough, a small amount of mucopurulent sputum (interstitial pneumonia); X-ray patchy infiltrative shadow (flake-like shadow), tympanic membrane congestion, cervical lymph node enlargement; the first choice is within the large ring Esters-erythromycin;

(1) Features:

(2) Clinical manifestations

(3) Laboratory and other inspections

(4) Diagnosis

(5) Treatment

[General case description] The onset of illness was acute, and X-ray showed diffuse ground-glass opacity in both lungs.

(1) Definition: The virus invades the respiratory epithelium and alveolar epithelial cells, causing lung interstitial and parenchymal inflammation.

(2) Causes and pathogenesis

(3) Pathology

(4) Clinical manifestations

(5) Auxiliary inspection

(6) Diagnosis

(7) Treatment

[General case description] Elderly people with chills, high fever, brick-red jelly sputum (yellow-green when blood vessels are not broken); pulmonary lobular consolidation, honeycomb-shaped lung abscess, falling interlobe space (inflammatory exudate in the lesion is thick and heavy); first choice Aminoglycosides (gentamicin, streptomycin, amikacin) third-generation cephalosporins;

[General case description] Middle-aged and elderly; myalgia/headache, chills and high fever, a small amount of mucopurulent sputum, chills and high fever, digestive tract symptoms, low sodium, diarrhea; patchy shadows but no cavities; macrolides are preferred;

[General case description] Inhalation is the most common, the elderly are bedridden, drunk, and comatose; anaerobic bacteria are common; acute high fever and large amounts of purulent sputum (smelly-anaerobic bacteria); large X-ray areas with dense and fuzzy inflammatory shadows and abscess cavities ( Round translucent area) Cavity with air-liquid level; most anaerobic bacteria are effective to penicillin, and the inflammation disappears in 6 to 8 weeks or on X-rays

The more common ones are T wave inversion of V 1 to V 4 and ST segment abnormalities;

S IQ II IT III sign may occur in some cases (i.e. deepening of S wave in lead I, Qq wave and T wave inversion in lead III);

Complete right bundle branch block; pulmonary P wave; right axis deviation;

Signs of pulmonary artery obstruction can be seen: regional lung markings become thinner, sparse or disappear, and lung field translucency increases;

Pulmonary hypertension and right heart enlargement: right lower pulmonary trunk widening or truncation sign, pulmonary artery segment distension and right ventricular enlargement, but these are non-specific;

Direct signs: semilunar or annular filling defect of pulmonary vessels, complete obstruction, orbit sign;

Indirect signs: lung blossoms, strip-shaped high-density areas, atelectasis;

Oral warfarin should be taken for at least 3 months; for first-time cases of unknown source of emboli, anticoagulation should be given for at least 6 months; for those with concurrent pulmonary heart disease or long-term risk factors, the anticoagulant treatment should be extended to Anticoagulation for 12 months or more, or even lifelong - warfarin bleeding can be antagonized with vitamin K;

Since warfarin takes several days to exert its full effect, it needs to be overlapped with heparin drugs for at least 5 days. When the international normalized ratio (INR) reaches 2.5 (2.0-3.0) and lasts for at least 24 hours, heparin can be stopped. For anticoagulant therapy with warfarin alone, adjust its dose according to the INR, and maintain the target INR value at generally 2.0 to 3.0;

① Mainly suitable for cases of large-scale pulmonary thromboembolism (obvious dyspnea, chest pain, hypoxemia, etc.);

②For sub-large areas, thrombolysis can be considered if there are no contraindications, but there is controversy;

③For cases with normal blood pressure and right ventricular motor function, thrombolysis → anticoagulation is not suitable;

① Long-term recurrent COPD and peribronchial inflammation can involve adjacent pulmonary arterioles, causing vasculitis, wall thickening, lumen stenosis or fibrosis, or even complete occlusion, increasing pulmonary vascular resistance and producing pulmonary hypertension;

② Emphysema causes the intra-alveolar pressure to increase, compressing the alveolar capillaries, causing capillary lumen stenosis or occlusion. Alveolar wall rupture causes damage to the capillary network, and pulmonary circulation resistance increases when the alveolar capillary bed loss exceeds 70%;

③ Pulmonary vascular remodeling: Chronic hypoxia causes pulmonary vasoconstriction and increases tube wall tension. At the same time, a variety of growth factors (such as polypeptide growth factors) are produced in the lungs during hypoxia, which can directly stimulate tube wall smooth muscle cells, intimal elastic fibers and collagen fiber proliferation;

④ Thrombosis: Autopsy found that some patients with acute exacerbation of chronic pulmonary heart disease had multiple in situ thrombosis of pulmonary microarteries, which caused increased pulmonary vascular resistance and aggravated pulmonary hypertension;

idiopathic pulmonary hypertension

Chronic obstructive pulmonary disease (COPD)

(1) Actively control infection; (very important)

(2) Unblock the respiratory tract and improve respiratory function;

(3) Correct hypoxia and carbon dioxide retention in pigs;

(4) Control breathing and heart failure;

(5) Actively deal with complications;

(1) Diuretics

(2) Positive inotropic drugs

(3) Vasodilator drugs

(4) Control of arrhythmia: Generally, arrhythmia can disappear on its own after treatment of infection and hypoxia in chronic pulmonary heart disease. If it persists, drugs can be selected according to the type of arrhythmia.

(5) Anticoagulation treatment;

(6) Strengthen care: turn over and pat the back;

The main mechanism of hypoxemia in COPD-decreased alveolar ventilation

The main mechanism of hypoxemia in interstitial diseases-diffusion dysfunction

The main mechanism of hypoxemia in pulmonary thromboembolism - imbalance of ventilation/blood flow ratio

The main mechanism of hypoxemia in ARDS - intrapulmonary shunt

hypoxia

CO2 retention

Manifestation: Psychoneurological symptoms

A certain degree of decrease in PaO2 and increase in PaCO2 → a reflex increase in heart rate, increase in myocardial contractility, and increase in cardiac output;

Hypoxia, CO2 retention → sympathetic nerve excitement → vasoconstriction of skin and abdominal organs, coronary vasodilation, and increased blood flow;

Severe hypoxia and CO2 retention → Directly inhibit the cardiovascular center → Inhibit cardiac activity and vasodilation, drop in blood pressure, and arrhythmia;

Manifestations: cardiovascular dysfunction—palpitations in severe cases, conjunctival congestion and edema (a manifestation of CO2 retention), arrhythmia, and cardiac arrest;

hypoxia

CO2 retention (respiratory center stimulant)

Manifestation: Respiratory dysfunction

Manifestation: Cyanosis

Manifestations: Digestive and urinary system-ulcer disease symptoms; upper gastrointestinal bleeding; abnormal liver function, renal insufficiency;

Acute respiratory dysfunction → respiratory acidosis combined with metabolic acidosis, intracellular acidosis, hyperkalemia (energy deficiency, sodium pump dysfunction);

Chronic respiratory failure→compensated respiratory acidosis (hypercapnia) combined with metabolic alkalosis (CO2 increases for a long time, HCO3- remains at a high level, and renal HCO3- excretion decreases), hypochloremia (only a small amount of HCO3- in the blood) Anions HCO3- and Cl The sum of - is relatively constant, and when HCO3- continues to increase, blood Cl- decreases accordingly);