MindMap Gallery Internal Medicine
Internal medicine is a clinical medical discipline that focuses on the diagnosis and treatment of diseases in various internal systems of the human body. Including respiratory, circulatory, urinary, digestive system, etc.
Edited at 2024-03-11 11:13:16This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
Internal Medicine
respiratory system
Chronic bronchitis, COPD
chronic bronchitis
Clinical manifestations: cough Coughing up sputum: white mucus or serous foamy sputum wheezing or shortness of breath
Laboratory tests: 1. X-ray: Patients with repeated attacks show thickened, disordered, reticular or striped, and speckled lung markings. 2. Respiratory function test 3. Blood test: The total number of white blood cells or neutrophils increases during bacterial infection. 4. Sputum examination: pathogenic bacteria can be cultured
COPD
Pathogenesis: 1. Inflammatory mechanism-activation and aggregation of neutrophils 2. Protease-antiprotease imbalance mechanism 3. Oxidative stress mechanism
Pathology: excessive lung expansion and loss of elasticity. The appearance is pale or gray, with multiple bullae of different sizes visible on the surface. Microscopic examination revealed thinning of the alveolar walls, enlargement, rupture, or bullae formation of the alveolar cavities, reduced blood pressure supply, and destruction of the elastic fiber network.
Pathophysiology: Persistent airflow limitation leading to pulmonary ventilatory dysfunction
clinical manifestations
Symptoms: 1. Chronic cough 2. Sputum: white mucus or serous foamy sputum, occasionally with blood. 3. Shortness of breath or difficulty breathing (the hallmark symptom of COPD) 4. Others: weight loss, loss of appetite
Signs: 1. Inspection: The anteroposterior diameter of the thorax increases, the intercostal space widens - barrel chest 2. Palpation: Bilateral tremor weakened 3. Percussion: The lungs are too voiceless and the heart dullness is narrowed. 4. Auscultation: The breath sounds in both lungs are weakened, the respiratory period is prolonged, and the heart sounds are distant. Some patients can hear crackles or rales.
laboratory tests
1. Pulmonary function monitoring: after inhaling bronchodilators, FEV1/FVC <70%, total lung capacity, functional residual capacity, and residual capacity increase, and vital capacity decreases 2. X-ray: thickened and disordered lung texture 3. CT: COPD small airway lesions can be seen 4. Blood gas analysis: hypoxemia, hypercapnia, acid-base balance disorder, respiratory failure 5. Others: When combined with bacterial infection, peripheral blood leukocytes increase and the nucleus shifts to the left.
Diagnosis and complications
Lung function is persistently limited, and FEV1/FVC <70% after inhalation of bronchodilators is the limit for determining the presence of persistent airflow limitation.
Complications: chronic respiratory failure, spontaneous pneumothorax, chronic cor pulmonale
treat
Stable period treatment: ① Education and management (quit smoking) ② Bronchodilators: β2 adrenergic receptor agonists (albuterol, salmeterol), anticholinergics, theophylline drugs ③Glucocorticoids ④ Expectorants ⑤Other drugs ⑥Long-term home oxygen therapy ⑦Rehabilitation treatment
Treatment for acute exacerbation: ① Bronchodilators; ② Low-flow oxygen; ③ Antibiotics; ④ Glucocorticoids; ⑤ Mechanical ventilation
Bronchial Asthma
Definition: A heterogeneous disease characterized by chronic airway inflammation and airway hyperresponsiveness
Etiology and pathogenesis
Causes: ①Heredity; ②Environmental (allergenic factors (dust mites, pollen, food, drugs)) non-allergenic factors (air pollution, smoking, etc.)
Pathogenesis ① airway inflammation (mainly neutrophil infiltration), ② airway hyperresponsiveness, ③ neural regulation mechanism
clinical manifestations
Symptoms: Paroxysmal expiratory dyspnea with wheezing, which may be accompanied by shortness of breath, chest tightness or cough. Symptoms may occur within minutes, last for hours or even days, and may resolve with antiasthmatic medication or on their own. Onset or worsening at night and early morning
Signs: Extensive wheezing sounds can be heard in both lungs, and expiratory sounds are prolonged. During a severe asthma attack, the wheezing sound weakens or even disappears completely - Silent Lung
laboratory tests
Sputum eosinophil count: increased eosinophil count in sputum Pulmonary function test: ① Ventilation function test shows obstructive ventilatory dysfunction during an asthma attack, forced vital capacity is normal or decreased, FEV1, FEV1/FVC%, and maximum expiratory flow decreases ②Bronchoprovocation test-used to measure airway responsiveness ③ Bronchodilation test-measures reversible changes in the airway. Repeat the lung function test 20 minutes after inhaling the bronchodilator. If FEV1 increases by >12% compared with before taking the drug, and its absolute value increases by ≥200ml, it is positive. ④Measurement of peak respiratory flow rate and its variation rate Chest X-ray/CT: X-ray transparency of both lungs increases, indicating hyperventilation; CT: bronchial wall thickening, mucus obstruction Specific allergen detection: increased allergen-specific IgE in peripheral blood Arterial blood gas analysis: severe hypoxia may cause ischemia, and hyperventilation will cause PaCO2 to decrease and pH to increase, manifesting as respiratory alkalosis.
Diagnostic criteria
1. Diagnostic criteria Typical clinical signs and symptoms of asthma Objective examination of variable airflow limitation ① positive bronchodilation test; ② positive bronchial provocation test; ③ average daily PEF diurnal variation rate > 10% or PEF weekly variation rate > 20%
2. Asthma staging and control level grading 1. Acute attack period: ① Mild: Shortness of breath when walking or going upstairs, anxiety may occur, a slight increase in respiratory rate, and scattered wheezing. ② Moderate: You feel short of breath after doing a little activity, the respiratory rate increases, there may be three concave signs, you can hear loud and diffuse wheezing, the heart rate increases, and you may have an abnormal pulse. ③Severe: Shortness of breath at rest, orthopnea, respiratory rate >30 times/min, often three concave signs, loud and diffuse wheezing, increased heart rate >120 beats/min, abnormal pulse ④ Critical illness: The patient is unable to speak, is drowsy or confused, has contradictory movements of the chest and abdomen, wheeze is weakened or even disappears, severe hypoxemia and capnosis, and reduced pH 2. Chronic duration 3. Clinical remission period
Differential diagnosis
1. Dyspnea caused by left heart failure: sudden shortness of breath, orthopnea, coughing up pink foam, and widespread rales and wheezes. Adrenaline or morphine is contraindicated. 2. Chronic obstructive pulmonary disease 3. Upper airway obstruction 4. Allergic bronchopulmonary aspergillosis
treat
Drug treatment: ① Relief drugs: short-acting β2 receptor agonists, short-acting inhaled anticholinergic drugs, short-acting theophylline, systemic glucocorticoids ② Controlled drugs: inhaled glucocorticoids, leukotriene modulators; long-acting β2 receptor agonists, sustained-release theophylline, sodium cromoglycate, anti-IgE antibodies, anti-IL-5 drugs Treatment of acute attack: ① Mild: SABA inhaled through MDI ② Moderate: Inhalation of SABA ③Severe to critical: continuous atomized inhalation of SABA combined with atomized inhalation of short-acting anticholinergics, hormone suspensions and intravenous theophylline drugs, etc. Chronic duration treatment: Periodically make rapid adjustments based on long-term treatment grading to maintain the patient's level of control. Immunotherapy
bronchiectasis
Etiology and pathogenesis: congenital and secondary Causes: infection (Pseudomonas aeruginosa), immune deficiency or abnormality, congenital genetic disease
Pathology and pathophysiology
Destruction and inflammatory changes in the wall of segmental or subsegmental bronchus: ① columnar shape, ② cystic dilation, ③ irregular dilation
clinical manifestations
Symptoms: Persistent or recurring cough, phlegm, and thick phlegm. Sputum is mucinous, mucopurulent or purulent and can be yellow-green in color Stratification of sputum (4 layers): upper layer of foam, middle layer of turbid mucus, lower layer of purulent components, and the lowest layer of necrotic tissue Major bleeding is often caused by erosion of small arteries or destruction of proliferated blood vessels. Some patients have hemoptysis as the only symptom - dry bronchiectasis
Physical signs: Dry and wet rales can be heard
laboratory tests
chest High-resolution chest CT: dilated bronchi show "double-track sign" or "string of beads" changes Blood routine fiberoptic bronchoscopy
Differential diagnosis: chronic bronchitis, lung abscess, tuberculosis, congenital pulmonary cyst, diffuse panbronchiolitis, bronchial carcinoma
Treatment: ①Treat basic diseases ②Infection control: antibiotics (second- and third-generation cephalosporins, ampicillin) ③Improve airflow limitation: monitor patient’s lung function ④ Clear airway secretions ⑤Immune modulators ⑥Surgical treatment: For those whose bronchiectasis is localized and still recurs after adequate medical treatment, surgical removal of the diseased tissue may be considered.
pulmonary infectious diseases
Pneumonia Overview
Definition: Refers to inflammation of the terminal airways, alveoli, and alveolar interstitium, which can be caused by pathogenic microorganisms, physical and chemical factors, immune damage, allergies, and drugs.
Causes: 1. Community-acquired pneumonia: ① air inhalation; ② hematogenous spread; ③ spread adjacent to the infected site; ④ aspiration of colonizing bacteria in the upper respiratory tract 2. Hospital-acquired pneumonia: Aspiration of colonized bacteria in the gastrointestinal tract or inhalation of pathogenic bacteria in the environment through artificial ventilation ducts
Classification
Anatomical classification: Lobar pneumonia, lobular pneumonia, interstitial pneumonia
Cause classification: bacterial pneumonia, pneumonia caused by atypical pathogens, viral pneumonia, fungal pneumonia, pneumonia caused by other pathogens
Category of disease environment: community-acquired pneumonia, nosocomial pneumonia
Clinical manifestations: Cough and sputum, or aggravation of original respiratory symptoms, purulent sputum or bloody sputum, with or without chest pain Signs: dullness to percussion, increased voice tremor, bronchial breath sounds
Diagnosis: 1. Confirm the diagnosis of pneumonia 2. Assess the severity 3. Determine the pathogen
bacterial pneumonia
Streptococcus pneumoniae pneumonia
Cause and pathogenesis: Streptococcus pneumoniae
Pathology: congestive phase, red hepatoid degeneration phase, gray hepatoid degeneration phase, dissipation phase
Clinical manifestations:
Symptoms: Before the onset, there are often cold, rain, fatigue, sudden onset, high fever, chills, muscle aches all over the body, body temperature rising to 39-40°C within a few hours, little phlegm, which may be bloody or rust-colored.
Signs: Acute facial appearance, flushed cheeks; flaring nose, burning and dry skin, herpes simplex at the corners of the mouth and around the nose. Increased tactile fremitus and audible bronchial breath sounds
laboratory tests
Elevated white blood cell count The lung texture is thickened, and the affected lung lobes and lung segments are slightly blurred.
treat
Antimicrobial treatment: penicillin Supportive therapy: bed rest, adequate protein, calories and vitamin supplements Management of complications
Staphylococcal pneumonia
Pathogen: Staphylococcus aureus
Symptoms: Sudden onset, high fever, chills, chest pain, purulent sputum, Signs: moist rales scattered in both lungs
Other laboratory signs: increased leukocytes in peripheral blood and increased proportion of neutrophils Chest X-ray shows segmental or lobar consolidation, early stage cavities, and lobular infiltration with single or multiple fluid cysts.
Treatment: Use sensitive antibiotics
Pulmonary infections caused by other pathogens
Mycoplasma pneumonia
Etiology and pathogenesis: Streptococcus pneumoniae
Clinical manifestations: fatigue, headache, sore throat; muscle aches, cough, paroxysmal dry cough, severe at night, and thick phlegm may also be produced
Laboratory tests: The total number of white blood cells is normal or slightly increased, and about 2/3 of the patients have positive agglutination tests.
Treatment: Macrocyclic ester antibiotics are preferred (erythromycin, azithromycin)
chlamydial pneumonia
Etiology and pathogenesis: Chlamydia pneumoniae
Clinical manifestations: Insidious onset, mild symptoms, accompanied by fever, chills, myalgia, dry cough, non-pleuritic chest pain, and headache
Diagnosis: tuberculosis respiratory symptoms and systemic symptoms, X-ray examination, etiology and serology tests
Treatment: Macrocyclic ester antibiotics are the first choice
viral pneumonia
Causes: Common influenza viruses A and B, adenovirus, and parainfluenza virus
Clinical manifestations: acute onset, fever, headache, body aches, and fatigue
Laboratory tests: white blood cell count is normal, slightly high, or low Chest X-ray shows increased lung markings, ground-glass shadows, small patchy infiltrates or extensive infiltrates
Treatment: mainly symptomatic treatment, oxygen therapy when necessary
lung abscess
Etiology and pathogenesis
Inhalation lung abscess: The pathogen inhales pathogenic bacteria (Streptococcus pneumoniae, Staphylococcus aureus) through the mouth and nasopharynx.
secondary lung abscess
Hematogenous lung abscess: due to skin trauma infection, furuncle, otitis media or osteomyelitis
Clinical manifestations: Symptoms: fever, night sweats; fatigue, anorexia, coughing up sputum, mucus sputum, and the sputum may have a rancid smell. Signs: Large lesions, a large amount of inflammation around the abscess, dull or solid sounds upon percussion; decreased breath sounds on auscultation, and sometimes crackles can be heard.
laboratory tests
Biochemical examination: leukocytosis, neutrophils above 90%, nuclear shift to the left, and often toxic particles
Microbiological examination: sputum culture
Imaging examination: X-ray: large, dense and fuzzy inflammatory infiltration shadows with unclear edges; CT mostly shows a round-like thick-walled abscess cavity, and there may be a fluid level in the abscess cavity.
fiberoptic bronchoscopy
Differential diagnosis: bacterial pneumonia; cavitary tuberculosis, bronchial carcinoma, secondary infection of bullae or cysts,
Treatment: 1. Antibiotic treatment: penicillin, beta-lactamase-resistant penicillin or cephalosporin, vancomycin 2. Drainage of pus: Those with thick phlegm that is difficult to drain can use expectorants or atomized inhalation of normal saline. 3. Indications ① The duration of lung abscess is more than three months, and the abscess cavity does not shrink after medical treatment, or the abscess cavity is too large to be easily closed; ② Severe cough of blood that is ineffective or life-threatening after medical treatment; ③ accompanied by bronchopleural fistula or Patients with empyema who have poor efficacy through aspiration, drainage and irrigation; ④ Bronchial obstruction restricts airway drainage
tuberculosis
Pathogen: Mycobacterium tuberculosis
pathology
Basic pathological changes: inflammatory exudation, hyperplasia and caseous necrosis; the pathological process is characterized by destruction and repair often occurring simultaneously.
Outcome of pathological changes: absorption and healing are very slow, often worsening and spreading
clinical manifestations
Symptoms: Respiratory system: cough, sputum production, dry cough or a small amount of mucus sputum Systemic symptoms: long-term afternoon low-grade fever, fatigue, fatigue, night sweats, loss of appetite and weight loss
Signs: When exudative lesions are large in scope or caseous necrosis occurs, there may be signs of pulmonary consolidation: increased tactile fremitus, percussion dullness, auscultation, bronchial breath sounds, and fine crackles.
Diagnosis: ① Medical history and symptoms and signs; ② Imaging diagnosis (chest X-ray is the preferred method for diagnosis) ③ Sputum culture test for Mycobacterium tuberculosis; ④ Fiberoptic bronchoscopy; ⑤ Tuberculin test; ⑥γ-interferon release test
Differential diagnosis: pneumonia, chronic obstructive pulmonary disease, bronchiectasis, lung cancer, lung abscess, mediastinal and hilar disease, other diseases
treat
Principles: early stage, regularity, whole process, appropriate amount, combination
Drugs: isoniazid, rifampicin, pyrazinamide, ethambutol, streptomycin ① Intensive period: isoniazid, rifampicin, pyrazinamide, ethambutol ②Consolidation period: isoniazid, rifampicin
lung cancer
Cause and pathogenesis
Risk factors: smoking, occupational carcinogens, air pollution, ionizing radiation, diet and physical activity, heredity and genetic changes
Classification
According to anatomical location: central lung cancer, peripheral lung cancer According to histopathology: non-small cell lung cancer (squamous cell carcinoma, adenocarcinoma, large cell carcinoma), small cell lung cancer
clinical manifestations
Symptoms and signs caused by the primary tumor: cough, expectoration or blood, shortness of breath or wheezing, chest pain, fever, weight loss
Symptoms and signs caused by local extension of tumor: chest pain, hoarseness, dysphagia, pleural effusion, pericardial effusion, superior vena cava obstruction syndrome, Horner syndrome
Symptoms and signs caused by distant metastasis of tumors: Central nervous system metastasis (headache, nausea, vomiting) Bone metastasis (local pain and tenderness, pathological fracture) Abdominal metastasis (loss of appetite, liver area pain or abdominal pain, jaundice, hepatomegaly) Lymph node metastasis
Imaging and other tests
Chest X-ray: Central lung cancer: The tumor grows in the main bronchus, lobe or segmental branch, "inverted S-shaped image" Peripheral lung cancer: Occurs in the subsegmental bronchi, with lobular shape, umbilical recess sign, fine spicules, Chest computed tomography scan: Magnetic resonance imaging radionuclide scintigraphy
Tests to obtain pathological diagnosis: sputum exfoliated cytology, pleural effusion cytology, respiratory endoscopy, needle aspiration biopsy, open lung biopsy
Tumor marker examination
Differential diagnosis: tuberculosis, pneumonia, lung abscess, tuberculous pleurisy, pulmonary cryptococcosis
Treatment: ① Surgical treatment (the best treatment for early-stage lung cancer): NSCLC, SCLC ②Drug treatment (chemotherapy and targeted therapy) ③Radiotherapy ④Interventional treatment ⑤TCM treatment
pulmonary heart disease
Causes: Bronchopulmonary disease, thoracic dyskinesia, pulmonary vascular disease, others
Pathogenesis and pathophysiological changes
Formation of hepatic arterial hypertension: pulmonary vasoconstriction (hypoxia, hypercapnia, respiratory acidosis), long-term recurrent COPD and peribronchial inflammation, thrombosis, pulmonary vascular remodeling, increased blood viscosity, blood volume increase
Heart disease, heart failure, and damage to other important organs
clinical manifestations
Lung and heart function compensation period
Symptoms: Cough and phlegm, shortness of breath, palpitations after activity, difficulty breathing, fatigue and decreased work endurance
Signs: There may be varying degrees of cyanosis, dry or moist rales, P2>A2, systolic murmur in the tricuspid valve area or increased cardiac pulsation under the xiphoid process.
Decompensation period of lung and heart function
Symptoms: dyspnea worsens, especially at night, often headaches, insomnia, loss of appetite, daytime drowsiness, even apathy, delirium, shortness of breath, palpitations, lack of appetite, nausea
Signs: Obvious cyanosis, bulbar conjunctival congestion, edema, jugular venous distension, rapid heart rate, arrhythmia, subxiphoid and systolic murmur
Auxiliary inspection
X-ray: signs of pulmonary hypertension
ECG: average frontal axis ≥ +90º; V1R/S ≥ 1; severe clockwise rotation; aVR R/S or R/Q ≥ 1; pulmonary P wave
Echocardiogram, blood gas analysis, blood tests
treat
Pulmonary and heart function compensation period: take comprehensive treatment measures to delay the progression of underlying bronchial and pulmonary diseases
Decompensation period of pulmonary and heart function: control infection, control respiratory failure, control heart failure (diuretics, inotropes, vasodilators), prevent complications
pleural disease
pleural effusion
circulation mechanism
The formation of pleural effusion is related to the absorption of pleural blood supply and lymphatic drainage.
Intracapillary fluid hydrostatic pressure parietal pleura -30cmHg, visceral pleura -24cmHg Colloidal osmotic pressure in parietal and visceral layers -34cmHg Intrathoracic pressure--5cmHg Intrathoracic colloid osmotic pressure-5cmHg
Etiology and pathogenesis
Increased hydrostatic pressure within pleural capillaries increased pleural permeability Decreased colloid osmotic pressure in pleural capillaries Parietal pleural lymphatic drainage disorder damage Iatrogenic
clinical manifestations
Symptoms: It is not obvious when the amount of effusion is less than 0.3~0.5L. When there is a large amount of effusion, palpitations and dyspnea are obvious, often accompanied by chest pain or cough.
Signs: There are no obvious signs in a small amount of effusion, or pleural friction may be palpable and pleural friction sounds may be heard; in moderate to large amounts of effusion, the affected side's chest will be full, tactile fremitus will be weakened, local percussion dullness, and breath sounds will decrease or disappear.
Laboratory tests and other tests
Diagnostic thoracentesis and pleural effusion examination: appearance and odor, cells, pH and glucose, pathogens, proteins, lipids, enzymes X-ray and radionuclide examination: a small amount of pleural effusion, the costophrenic angle becomes blunt; when a large amount of effusion occurs, the chest on the affected side is dense, and the trachea and mediastinum are pushed to the healthy side. Ultrasonography Pleural needle biopsy Thoracoscopic or thoracotomy biopsy Bronchoscopy
treat
Tuberculous pleurisy: ① General treatment ② Fluid extraction treatment ③ Anti-tuberculosis treatment ④ Glucocorticoids
pneumothorax
Causes and pathogenesis: ① A breach occurs between the alveoli and the thoracic cavity, ② Chest trauma creates communication with the thoracic cavity, ③ There are gas-producing microorganisms in the thoracic cavity
Clinical types: closed pneumothorax, communicating pneumothorax, tension pneumothorax
clinical manifestations
Symptoms: Before the onset of the disease, patients have triggers such as holding heavy objects, holding back their breath, and strenuous physical activity. Most of them have a sudden onset, sudden chest pain, acupuncture-like or knife-like pain on one side; the duration is short, followed by chest tightness and dyspnea.
Signs: In a small amount of pneumothorax, the signs are not obvious. In a large amount of pneumothorax, the trachea is displaced to the unaffected side, the chest on the affected side is bulged, respiratory movement and tactile vibrato are weakened, and there is a voiceless or tympanic sound upon percussion.
Film degree exam
chest Chest CT: Very low-density gas shadow appears in the chest, accompanied by varying degrees of lung atrophy. Pneumothorax volume assessment
Differential diagnosis: asthma and chronic obstructive pulmonary disease, acute myocardial infarction, pulmonary thromboembolism, bullae
Treatment: Purpose - to promote recruitment of the affected lung, eliminate the cause and reduce recurrence ① Conservative treatment: suitable for stable small-volume pneumothorax; ② Exhaust method (thoracic puncture, closed chest drainage) ③ Chemical pleurodesis ④ Endobronchial occlusion ⑤ Surgical treatment ⑥ Complications and their treatment
Respiratory failure and respiratory failure support technology
Cause
Airway obstructive disease, lung tissue disease, pulmonary vascular disease, heart disease, thoracic and pleural disease, neuromuscular disease
Classification
Type I respiratory failure: PaO2 <60mmHg, PaCO2 reduced or normal
Type II respiratory failure: PaO2<60mmHg, accompanied by PaCO2>50mmHg
Pathogenesis and pathophysiology
The mechanisms of hypoxemia and hypercapnia: pulmonary hypoventilation, diffusion disorder, ventilation/blood flow imbalance, increased intrapulmonary anatomical shunting of intrapulmonary anatomy, and increased oxygen consumption.
Effects of hypoxemia and hypercapnia on the body: effects on the central nervous system, effects on the nervous system, effects on the respiratory system, effects on renal function, digestive system,
acute respiratory failure
Causes: Respiratory system diseases, acute pulmonary edema caused by various causes, pulmonary vascular diseases
clinical manifestations
Difficulty breathing Cyanosis Psychological and neurological symptoms: confusion, mania, coma, convulsions Circulatory system manifestations: Most patients have tachycardia, which in severe cases can lead to myocardial damage, peripheral circulatory failure, decreased blood pressure, and arrhythmias. Digestive and urinary system manifestations: elevated alanine aminotransferase and plasma urea nitrogen may occur in some cases
treat
Keep airway open Oxygen therapy: Oxygen concentration - try to reduce the oxygen concentration as much as possible while ensuring that PaO2 quickly increases to 60mmHg or the pulse volume and blood oxygen saturation reaches more than 90% Oxygen device (nasal cannula or nasal prongs, mask, nasal main flow oxygen therapy) Positive pressure mechanical ventilation and extracorporeal model oxygenation Cause treatment general supportive care
chronic respiratory failure
Cause: Mostly caused by bronchial-pulmonary diseases
clinical manifestations
Dyspnea and: labored breathing accompanied by prolonged expiration, which may develop into shallow and rapid breathing in severe cases
Nervous symptoms: As PaCO2 increases, it may first be excited and then suppressed. Exciting symptoms include insomnia, irritability, agitation, insomnia at night and sleepiness during the day. Do not use sedatives or hypnotics at this time.
Circulatory system manifestations: peripheral surface vein filling, skin congestion, warmth and sweating, elevated blood pressure, and increased cardiac output.
treat
Oxygen therapy positive pressure mechanical ventilation Anti-infective respiratory stimulants Correct acid-base balance imbalance
circulatory system
heart failure
Summary
type
Left heart failure, right heart failure and total heart failure acute and chronic heart failure Heart failure with reduced ejection fraction, heart failure with preserved ejection fraction
Cause
Basic cause: myocardial damage (myocardial infarction, chronic myocardial ischemia, inflammation and immune myocardial damage; myocardial damage caused by endocrine and metabolic diseases) Overload of the heart (hypertension, aortic stenosis, heart valve insufficiency insufficient ventricular preload Causes: infection, arrhythmia, increased blood volume, excessive physical exertion or emotional agitation; improper treatment
Pathophysiology
Frank-Starling mechanism Neurohumoral mechanisms (increased sympathetic nerve excitability, RAAS activation, changes in other humoral factors ventricular remodeling
chronic heart failure
Cause: coronary heart disease, hypertension
clinical manifestations
Left heart failure: Symptoms: ① Different degrees of dyspnea (exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, acute pulmonary edema) ② Cough, sputum, and hemoptysis; ③ Fatigue, tiredness, decreased exercise tolerance, Dizziness, palpitation and other organs; ④ Symptoms of oliguria and renal damage Signs: moist rales in the lungs, cardiomegaly, and relative mitral regurgitation
Right heart failure: Symptoms: ① Gastrointestinal symptoms: abdominal distension, lack of appetite, nausea and vomiting; ② exertional dyspnea Signs: ① Edema; ② Jugular venous signs (enhanced, filling, and distended jugular vein pulses); ③ Hepatomegaly; ④ Cardiac signs: significant enlargement of the right ventricle.
Heart failure grade
Level I: Patients with heart disease have no restrictions on their daily activities and general activities do not cause fatigue; they have heart failure symptoms such as dyspnea. Level II: Patients with heart disease have mild limitations in physical activity, no conscious symptoms at rest, and symptoms of heart failure may occur during normal activities. Level III: Patients with heart disease whose physical activities are significantly limited and lower than usual activities will cause symptoms of heart failure. Level IV: Heart disease patients cannot engage in any physical activity and have symptoms of heart failure even at rest, which worsen after activity.
Auxiliary inspection
Laboratory tests: natriuretic peptide, troponin, routine examination electrocardiogram Echocardiography, X-ray examination, cardiac magnetic resonance, coronary angiography, cardio-pulmonary exercise test
Differential diagnosis
Bronchial asthma, pericardial effusion, constrictive pericarditis, cirrhosis, abdominal effusion with lower extremity edema
treat
General treatment: lifestyle management, rest and activity, treatment of cause
Drug therapy: diuretics (loop diuretics, thiazide diuretics, potassium-sparing diuretics) RAAS inhibitors (ACEI, ARB, ARNI, aldosterone receptor antagonists, renin inhibitors); β-receptor antagonists, positive Sexual inotropic drugs (digital drugs, phosphodiesterase inhibitors)
acute heart failure
type
Acute left heart failure: Myocardial contractility is significantly reduced, cardiac load is aggravated, resulting in a sudden drop in cardiac output, a sudden increase in pulmonary circulation pressure, and an increase in peripheral circulation resistance. Acute right heart failure: a sharp decrease in right ventricular myocardial contractility or a sudden increase in right ventricular preload, and a sharp decrease in right ventricular blood output
clinical manifestations
Sudden severe dyspnea, forced sitting, ashen complexion, cyanosis, profuse sweating, irritability, frequent coughing, and coughing up pink frothy sputum Main manifestations of cardiogenic shock: persistent hypotension, systolic blood pressure falling to 90mmHg for more than 30 minutes, accompanied by tissue hypoperfusion, clammy skin, paleness, and cyanosis
treat
General treatment: ① Position: semi-recumbent or upright sitting position, legs drooping ②Oxygen inhalation: high-flow nasal cannula oxygen supply ③Preparation for treatment, intravenous channel opening, indwelling urinary catheter, ECG monitoring, and transcutaneous blood oxygen saturation monitoring
Drug treatment: ① Morphine; ② Rapid diuresis; ③ Aminophylline; ④ Digitalis drugs
vasoactive drugs
Vasodilators: sodium nitroprusside, nitrates, alpha receptor antagonists Positive inotropes: β-receptor stimulants, phosphodiesterase inhibitors; levosimendan Vasoconstrictors: norepinephrine, epinephrine
Mechanically assisted circulatory support device
Mechanical Ventilation continuous renal replacement therapy Mechanically assisted circulatory support device
Arrhythmia
sinus arrhythmia
sinus tachycardia
Adult sinus rhythm has a frequency of more than 100 beats/minute
Treatment: Treatment of the cause and removal of predisposing factors, combined with β-blockers and non-dihydropyridine calcium channel blockers if necessary
sinus bradycardia
Adult sinus rhythm has a frequency of less than 60 beats/minute
Asymptomatic sinus bradycardia does not require treatment; if symptoms of insufficient cardiac output occur, atropine or isoproterenol can be used
sinus arrest
The sinus node cannot generate impulses
Electrocardiogram: No P wave occurs during the interval that is significantly longer than the normal PP interval, or neither P wave nor QRS wave appears. There is no multiple relationship between the long PP interval and the basic sinus PP interval.
When sinus arrest lasts for too long (>3s) and no escape beat occurs, the patient may experience amaurosis, temporary disturbance of consciousness, or dizziness.
sinoatrial block
A delay or block in the conduction of impulses from the sinoatrial node to the atria
Types
one time Second degree type I: The PP interval progressively shortens until a long PP interval occurs, which is shorter than twice the basic PP interval. Second degree type II: long PP interval is an integral multiple of the basic PP interval Three degrees:
sick sinus syndrome
The sinoatrial node causes conduction dysfunction and produces a variety of comprehensive manifestations of arrhythmias.
Causes: annulus fibrosus and infiltration, sclerosis and degeneration, amyloidosis, hypothyroidism, infection
Clinical manifestations: episodic dizziness, amaurosis, palpitations, fatigue, decreased exercise tolerance, and in severe cases, angina pectoris, heart failure, and temporary disturbance of consciousness.
treat
If the patient has no symptoms related to bradycardia, no treatment is required Symptomatic patients with sick sinus syndrome should receive pacemaker therapy
atrial arrhythmias
premature atrial contractions
Atrial activation originating in any part of the atrium other than the sinoatrial node
Clinical manifestations: palpitations, some patients have symptoms of chest tightness, fatigue, and a conscious feeling of stopping.
ECG characteristics
① The P wave occurs prematurely and is different from the sinus P wave in shape; ② The PR interval is >120 ms; ③ The QRS wave skirt is supraventricular, and some may have intraventricular differential conduction; ④ Mostly incomplete compensatory intervals
Treatment: Usually no treatment is required; treatment should be given when there are obvious symptoms or supraventricular tachycardia due to premature atrial contractions
atrial tachycardia
Tachycardia that originates in the atria and does not require maintenance by the atrioventricular node
Causes: coronary heart disease, digitalis poisoning, chronic lung disease
Clinical manifestations: palpitations, dizziness, chest tightness, breathlessness, fatigue and other symptoms
ECG characteristics
① The atrial rate is usually 150~200 beats/min; ② The shape of the P wave is different from the sinus P wave; ③ Second degree type I or type II atrioventricular block may occur when the atrial rate accelerates; ④ The isoelectric lines between the P waves are still exists; ⑤ Stimulating the vagus nerve cannot terminate tachycardia; ⑥ The heart rate gradually accelerates at the onset of the attack
treat
If the ventricular rate is not too fast and there is no serious hemodynamic disorder, emergency treatment is not necessary. If the heart rate is greater than 140 beats/minute, emergency treatment is required
atrial flutter
Cause: Commonly seen in organic heart disease such as rheumatic heart disease, coronary heart disease, and hypertension
Clinical manifestations: angina and congestive heart failure
ECG characteristics
①The sinus P wave disappears and is replaced by regular sawtooth-like fluttering waves with the same amplitude and spacing, called F waves, with a frequency of 250 to 350 beats/min; ②The ventricular rate is regular or irregular; ③The QRS wave shape is normal
treat
Drug therapy (beta blockers, calcium channel blockers, digitalis preparations) Nonpharmacological treatment: direct current cardioversion
atrial fibrillation
Cause: Often occurs in patients with organic heart disease
Clinical manifestations: angina pectoris, atrial fibrillation complicated by thrombosis
ECG characteristics
① The P wave disappears and is replaced by small and irregular baseline fluctuations, with variable shape and amplitude, called F wave, with a frequency of 350 to 600 beats/min; ② The ventricular rate is extremely irregular; ③ The shape of the QRS wave is usually normal, and when the ventricular rate Too fast, differential indoor conduction occurs, and the QRS wave becomes widened and deformed.
treat
Anticoagulation therapy, conversion and maintenance of sinus rhythm, control of ventricular rate,
atrioventricular junctional arrhythmias
atrioventricular junctional premature contractions
Retrograde P waves are produced, and the QRS wave shape is normal.
Atrioventricular junctional escape beat and heart rate
A rhythm formed by the continuous occurrence of escape beats in the atrioventricular junction zone
Electrocardiogram: Normal QRS wave skirt, frequency 40~60 beats/min, retrograde P wave may be present
nonparoxysmal atrioventricular junctional tachycardia
Related to increased tissue autonomy or triggering activities in the atrioventricular junction zone
Heart rate 70~150 beats/min, heart rhythm is usually normal, QRS wave is normal
Treatment: Treatment of the cause
Atrioventricular junction-related reentrant tachycardia
clinical manifestations
Sudden stop, varying duration, palpitations, chest tightness, anxiety, dizziness
ECG characteristics
① The heart rate is 150 to 250 beats/min, and the rhythm is regular; ② The QRS waveform and duration are normal; ③ The P wave is retrograde and often buried within the QRS wave; ④ The onset is sudden, usually triggered by a premature atrial contraction, which is transmitted downstream The PR interval is significantly prolonged
treat
Acute attack: methods to stimulate the vagus nerve, carotid sinus massage medical treatement
ventricular arrhythmias
premature ventricular contractions
A premature heartbeat that occurs below the bifurcation of the bundle of His and depolarizes the myocardium prematurely.
clinical manifestations
No specific symptoms, palpitations, heartbeat or stopping sensation, accompanied by dizziness, fatigue, and chest tightness
ECG characteristics
① The QRS complex that occurs prematurely often lasts longer than 0.12 seconds and is wide and deformed; ② The direction of the ST segment and T wave is opposite to the direction of the main QRS wave; ③ The period between premature ventricular contraction and the sinus wave in front of it is constant
ventricular tachycardia
Three or more consecutive ectopic heartbeats originating from the special conduction system below the branches of the His bundle or the ventricular myocardium
clinical manifestations
Usually asymptomatic, hypotension, oliguria, shortness of breath; angina, syncope
ECG characteristics
① 3 or more premature ventricular contractions occur continuously; ② The ventricular rate is usually 100 to 250 beats/min; ③ The rhythm is regular or slightly irregular; ④ The independent atrial activity has no fixed relationship with the QRS wave, forming a separate pattern; ⑤ Occasionally It can be seen that ventricular activation reversely captures the atria
Treatment: beta-blockers, amiodarone
Atherosclerosis and coronary atherosclerotic heart disease
atherosclerosis
Causes: age, gender, dyslipidemia, hypertension, smoking, diabetes and glucose intolerance, obesity, family history
Pathogenesis: lipid infiltration theory, endothelial injury-response theory, platelet aggregation and thrombosis hypothesis, smooth muscle cell cloning theory
clinical manifestations
Coronary atherosclerosis, cranial atherosclerosis, renal atherosclerosis, mesenteric atherosclerosis, extremity atherosclerosis
treat
General preventive measures: actively control some risk factors related to the disease, have a reasonable diet, appropriate physical labor and sports activities (reasonable arrangements for work and life, promote smoking cessation and limit alcohol Drug therapy: Adjustment of blood lipid drugs, antiplatelet drugs, thrombolytic drugs and anticoagulant drugs, and corresponding treatment of ischemic symptoms Interventional and surgical treatments
Overview of coronary heart disease
Refers to heart disease caused by atherosclerosis of coronary arteries causing lumen stenosis or occlusion, resulting in myocardial ischemia, hypoxia, or necrosis.
Types
① Occult or asymptomatic coronary heart disease; ② Angina pectoris; ③ Ischemic heart disease; ④ Myocardial infarction; ⑤ Sudden death
Mechanism: There is a conflict between the blood supply of the coronary arteries and the blood demand of the myocardium, and the coronary blood flow cannot meet the metabolic needs of the myocardium, which can cause myocardial ischemia and hypoxia.
chronic myocardial ischemia syndrome
stable angina
Pathogenesis: When coronary arteries are stenotic or partially occluded, their blood flow is reduced and the blood supply to the myocardium is relatively fixed.
clinical manifestations
Symptoms: Triggers: Attacks are often triggered by physical exertion or emotional excitement Location: Mainly behind the sternum, can involve the precordial area and the size of the palm of your hand Nature: Chest pain is often compressive, stuffy or tight, and may also have a burning sensation. The duration generally lasts from a few minutes to more than ten minutes, and generally does not exceed half an hour. Relief method: Generally, relief can be achieved after stopping the activity that originally caused the symptoms. It can also be relieved by taking nitroglycerin and other drugs under the tongue.
Signs: increased heart rate, elevated blood pressure, anxious expression, cold skin or sweating, and sometimes the fourth or third heart sound galloping.
Auxiliary inspection
Laboratory tests: blood glucose, blood lipids, cardiac troponin, creatine kinase isoenzyme
Electrocardiogram examination: resting electrocardiogram, electrocardiogram during angina pectoris attack, electrocardiogram stress test, continuous dynamic monitoring of electrocardiogram, echocardiogram
treat
Treat during an attack
① Rest; ② Drug treatment (nitrate preparations)
remission treatment
① Lifestyle adjustment; ② Drug treatment: drugs to improve ischemia and relieve symptoms (β-receptor antagonists, nitrate preparations)
Unstable angina and non-ST-segment elevation myocardial infarction
Etiology and pathogenesis: platelet aggregation based on rupture or erosion of unstable atherosclerotic plaques, concurrent thrombosis, spasmodic constriction of coronary arteries, and microvascular embolism
clinical manifestations
Symptoms: Similar to stable angina, usually more severe and longer lasting
Signs: Transient third heart sound or fourth heart sound may be found
treat
Treatment principle: immediate relief of ischemia and prevention of serious adverse consequences
General treatment: bed rest, eliminating tension and worries, keeping the environment quiet
Drug therapy: anti-myocardial ischemia drugs, nitrate preparations, β-receptor antagonists), antiplatelet drugs, anticoagulation therapy, lipid-lowering therapy, ACEI or ARB, coronary revascularization
hypertension
High blood pressure classification and definition
Etiology and pathogenesis
Factors related to the onset of hypertension: genetic factors, environmental factors (diet, mental stimulation, smoking), other factors
Pathogenesis: ①psychological mechanism; ②renal mechanism; ③hormonal mechanism; ④vascular mechanism; ⑤insulin resistance;
Clinical symptoms
Symptoms: often onset slowly, common symptoms include dizziness, headache, neck stiffness, fatigue, and heart palpitations
Signs: peripheral vascular pulsation, vascular murmur, heart murmur
complication
Cerebrovascular disease, heart failure and coronary heart disease, chronic renal failure, aortic dissection
Laboratory tests:
Basic items: blood chemistry, complete blood count, hemoglobin and hematocrit Recommended items: 24-hour ambulatory blood pressure monitoring, echocardiography, carotid artery ultrasound, and 2-hour postprandial blood glucose Selected items: Plasma renin activity, blood and urinary aldosterone
treat
Purpose and Principles: Therapeutic lifestyle intervention, Antihypertensive drug treatment targets: ① Patients with high blood pressure level 2 or above; ② Patients with high blood pressure combined with diabetes, or patients with heart, brain, and kidney target organ damage or complications; ③ Anyone whose blood pressure continues to rise and has not yet achieved improvement in lifestyle Effective control Antihypertensive drugs; diuretics, beta receptor antagonists, calcium channel blockers, ACEI
cardiomyopathy
dilated cardiomyopathy
Etiology and pathogenesis: infection, inflammation, poisoning, endocrine and metabolic abnormalities, genetics
Pathological anatomy and pathophysiology: mainly cardiac chamber enlargement, ventricular dilation visible to the naked eye, multiple thinning of ventricular walls, and fibrous scar formation; often accompanied by mural thrombus
Clinical symptoms
Symptoms: The onset is insidious and may be asymptomatic in the early stage. The main symptoms are dyspnea during activity and decreased activity tolerance.
Signs: enlargement of the heart, weakened heart sounds on auscultation, audible third or fourth heart sounds, a galloping rhythm when the heart rate accelerates, and sometimes a systolic murmur can be heard at the apex of the heart.
Auxiliary inspection
Chest X-ray: enlarged heart shadow, cardiothoracic ratio >50% Electrocardiogram: poor R wave progression, intraventricular block, and left bundle branch block Echocardiogram: Mild enlargement of the left ventricle; later, all cardiac chambers were enlarged cardiac magnetic resonance Coronary angiography and cardiac catheterization Blood and serology tests endocardial biopsy
treat
Treatment of causes and aggravating factors: control the infection, strictly limit or quit drinking, and actively search for the cause of the disease Drug treatment for heart failure: ACEI or ARB drugs, beta-blockers, mineralocorticoid receptor antagonists, diuretics, digitalis
hypertrophic cardiomyopathy
Cause: often autosomal dominant inheritance
Pathophysiology: forward movement of the anterior leaflet of the mitral valve, aggravating obstruction
Pathological changes: mainly ventricular hypertrophy, especially ventricular hypertrophy
clinical manifestations
Symptoms: The most common ones are exertional dyspnea and fatigue, and 1/3 of patients may have exertional chest pain.
Signs: Mild enlargement of the heart, audible fourth heart sound
Auxiliary inspection
Chest X-ray: The heart shadow can be normal in size or the left ventricle can be enlarged Electrocardiogram: The main manifestations are QRS complex left ventricular high voltage, inverted T wave and abnormal q wave. Echocardiography: asymmetric ventricular hypertrophy without ventricular cavity enlargement Cardiac MRI, cardiac catheterization and coronary angiography, endomyocardial biopsy
treat
Drug therapy: ① Reduce left ventricular outflow tract obstruction ② Treat heart failure ③ Treat atrial fibrillation
Non-drug treatment: ① surgical treatment ② alcohol septal ablation ③ pacing treatment
restrictive cardiomyopathy
Pathological changes and pathophysiology Myocardial fibrosis, inflammatory cell infiltration and endocardial scarring
Clinical manifestations: Main manifestations include decreased activity tolerance, fatigue, dyspnea, and severe right heart failure. Jugular venous distension, galloping rhythm can be heard on heart auscultation, hepatomegaly, positive moving dullness, and pitting edema in the lower limbs.
Auxiliary inspection
Laboratory tests: BNP is significantly elevated in patients with restrictive cardiomyopathy Electrocardiogram: Abnormal QRS complex and ST-T changes Echocardiogram: biatrial enlargement and ventricular hypertrophy X-ray, CTA, CMR cardiac catheterization Endocardial biopsy
treat
There is no specific treatment, mainly to avoid fatigue, respiratory infection and other factors that aggravate heart failure.
valvular heart disease
Common causes: inflammation, myxoid degeneration, congenital malformations, avascular necrosis, trauma
mitral stenosis
Cause: Mainly rheumatic fever
Pathology: fibrosis and contracture of valve leaflets and chordae tendineae, mutual adhesion of valve leaflet interfaces
Pathophysiology: left ventricular filling is obstructed and pressure difference persists throughout ventricular diastole
clinical manifestations
Symptoms: dyspnea, cough, hemoptysis, thromboembolism, hoarseness, difficulty swallowing, loss of appetite, bloating, nausea
Signs: Mitral valve appearance-bizygomatic cyanosis; Heart sounds: An elevated first heart sound can be heard at the apex of the heart, which is like a beating. Open valve sounds, P2 hyperactivity and splitting can also be heard. Heart murmur: a low-key, rumble-like murmur in mid-to-late diastole in the apical region, with an increasing pattern
Laboratory and other tests
X-ray examination: enlarged hilus, blurred edges, thickened lung texture, and enlarged left atrium Electrocardiogram: mitral P wave, QRS complex showing right axis deviation and right ventricular hypertrophy. Echocardiography: The anterior leaflet of the mitral valve shows "city wall-like" changes
Complications: atrial fibrillation, acute pulmonary edema, thromboembolism, right heart failure, infective endocarditis, pulmonary infection
treat
General treatment: prophylactic antirheumatic fever treatment, long-term or even lifelong use of benzathine penicillin Treatment of complications: sitting position, diuretics to reduce pulmonary artery pressure, ventricular rate control, embolism prevention Surgical treatment: percutaneous mitral valvuloplasty, mitral valve separation, artificial valve replacement
Mitral valve insufficiency
Pathophysiology: The blood flow ejected by the left ventricle with each stroke and part of the reflux, such as the left atrium, reduce the forward blood flow and increase the left atrial load and left ventricular diastolic load.
clinical manifestations
Symptoms: acute - only mild exertional dyspnea, severe left heart failure, acute pulmonary edema Chronic - fatigue, reduced activity tolerance, exertional dyspnea, orthopnea
Signs: The apical beat is hyperdynamic, lifting-like beat, P2 hyperactivity, and the fourth heart sound may appear in the apical area. Holosystolic blowing murmur in the apical region ≥ grade 3/6
Laboratory and other tests
X-ray examination: left atrium and left ventricle were significantly enlarged, Electrocardiogram: In mild cases, the electrocardiogram is normal, but in severe cases, left ventricular hypertrophy and strain may be present. Echocardiogram:
treat
Medical treatment: reduce reflux volume, lower pulmonary veins, increase cardiac output Surgical treatment:
aortic stenosis
Causes: congenital lesions, degenerative lesions, inflammatory lesions
Pathophysiology: There is an obvious systolic pressure gradient between the left ventricle and the aorta, concentric hypertrophy of the left ventricular wall, increased thickness of the left ventricular free wall and interventricular septum, and decreased compliance.
clinical manifestations
Symptoms: dyspnea, angina, syncope
Signs: The heart boundary is normal or slightly enlarged to the left, and a lifting-like pulse can be palpated in the apex area. First heart sound normal Rough and loud jet murmur in the 1st to 2nd intercostal space on the right edge of the sternum, grade 3/6 or above
Laboratory and other tests
X-ray examination: The heart shadow is generally not large, and its shape may change slightly. Electrocardiogram: increased QRS complex voltage with mild ST-T changes Echocardiogram: Aortic valve leaflets thickened and echo enhanced
Complications: arrhythmia, sudden cardiac death, congestive heart failure, infective endocarditis, systemic embolism, gastrointestinal bleeding
treat
Medical Treatment: Prevention of Endocardial Infection Surgical treatment: ① artificial valve replacement ② aortic valve shunt under direct vision ③ percutaneous aortic valve balloon formation ④ percutaneous aortic valve replacement
aortic valve insufficiency
Causes: infective endocarditis, aortic dissection hematoma, rheumatic heart disease, congenital malformations, aortic root dilation
clinical manifestations
Symptoms: Paroxysmal dyspnea and orthopnea at night, inability to lie down, sweating all over the body, frequent coughing, irritability, and confusion
Signs: The heart boundary expands to the lower left The first heart sound is weakened and the second heart sound in the aortic area is weakened or disappeared. The diastolic murmur in the aortic area is a high-pitched descending sigh-like murmur. Peripheral vascular signs: increased systolic arterial blood pressure, decreased diastolic blood pressure, and widened pulse pressure
Laboratory and other tests
X-ray examination: left ventricle is significantly enlarged, heart and waist are deepened, and "boot-shaped heart" Electrocardiogram: left ventricular hypertrophy and strain with left axis deviation Echocardiography: rapid high-frequency vibration of the anterior mitral valve leaflet during diastole
treat
Medical treatment Surgical treatment
pericardial disease
acute pericarditis
Cause: Most common viral infection
clinical manifestations
Symptoms: pain behind the sternum and precordium, which can radiate to the neck; pain in the left shoulder and left arm that is sharp in nature and related to respiratory movements, and can be aggravated by coughing and deep breathing
Signs: pericardial rub, rough high-frequency sound like scratching
Auxiliary inspection
Serological examination: elevated white blood cell count, elevated C-reactive protein, and accelerated erythrocyte sedimentation rate Electrocardiogram: ST segment is arched and elevated downward. Chest X-ray: enlarged heart shadow echocardiogram cardiac magnetic resonance imaging pericardiocentesis
treat
Treatment of the cause, relief of cardiac tamponade and symptomatic supportive treatment
Pericardial effusion and cardiac tamponade
Cause: The common cause is tumors
clinical manifestations Beck's triad: hypotension, muffled heart sounds, jugular venous distention
Symptoms: dyspnea, orthopnea, shallow breathing, pale complexion, cyanosis
Signs: apical pulse weakened, heart percussion dullness expanded to both sides
Cardiac tamponade: sinus tachycardia, decreased blood pressure, decreased pulse pressure, and significantly increased venous pressure
Auxiliary inspection
X-ray examination: The heart shadow increases to both sides and looks like a flask. Electrocardiogram: P wave can be seen with low QRS voltage and large amounts of fluid exudation. Echocardiogram: Fluid between the visceral and parietal pericardium is visible throughout the cardiac cycle.
treat
pericardiocentesis drainage
constrictive pericarditis
Cause: Tuberculosis is the most common in my country
Pathophysiology: pericardial constriction limits ventricular diastolic expansion, reduces filling, and decreases stroke volume.
clinical manifestations
Symptoms: Mainly related to decreased cardiac output and systemic circulation congestion, myocardium, exertional dyspnea, decreased activity tolerance, and fatigue
Signs: increased jugular venous pressure, often smaller pulse pressure, weakened or absent apical pulse
Auxiliary inspection
Check with X first: the heart shadow is slightly enlarged and appears triangular or spherical, and there may be pericardial calcification. Electrocardiogram: tachycardia, low QRS voltage, flat or inverted T wave Echocardiogram, cardiac CT, MRI
treat
pericardiectomy
urinary system
primary glomerular disease
Overview
Classification
Clinical classification: ① Acute glomerulonephritis ② Rapidly progressive glomerulonephritis ③ Chronic glomerulonephritis ④ Asymptomatic hematuria or proteinuria ⑤ Nephrotic syndrome
Pathological classification: ① Mild glomerular lesions ② Focal segmental glomerular lesions ③ Diffuse glomerulonephritis
Pathogenesis
Immune response: humoral immunity, (circulating immune complex deposition, in situ immune complex formation, autoantibodies) cellular immunity Inflammatory response: inflammatory cells, inflammatory mediators, non-immune factors
Clinical manifestations: protein, hematuria, edema, hypertension, abnormal renal function
acute glomerulonephritis
Etiology and pathogenesis
Mainly beta-hemolytic streptococci infection
Pathology: Diffuse glomerular capillary endothelial cells and mesangial cell proliferation are seen under light microscopy, which may be accompanied by neutrophil and monocyte infiltration in the acute phase.
Clinical manifestations: acute onset, typical manifestations of acute nephritic syndrome, clinical glomerulogenic hematuria, and may be accompanied by mild or moderate proteinuria.
Laboratory tests: Serum C3 and total complement decreased, gradually returning to normal within 8 weeks, and serum anti-streptococcin "O" titer increased.
Treatment: Mainly supportive and symptomatic treatment
Rapidly progressive glomerulonephritis
Cause and pathogenesis
Type I (anti-glomerular basement membrane type) Type II (immune complex type) Type III (low immune deposition type)
Pathology: Under light microscopy, most glomeruli are formed with large crescents. In the early stage of the disease, they are cellular crescents and in the later stages, they are fibrous crescents.
Clinical manifestations: The onset is sudden, the condition can progress rapidly, oliguria or anuria appears in the early stage, and the patient is accompanied by varying degrees of anemia.
treat
Intensive therapy ① Plasma exchange ② Methylprednisolone shock
Support symptomatic treatment
nephrotic syndrome
Causes: Primary (① smile lesion nephropathy ② mesangial proliferative glomerulonephritis ③ focal segmental glomerulosclerosis ④ mesangial nephropathy ⑤ mesangial capillary glomerulonephritis Secondary
Pathophysiology
massive proteinuria hypoalbuminemia Edema Hyperlipidemia
Pathological types and clinical features
Minimal change nephropathy: No obvious glomerular changes under light microscopy, fatty degeneration can be seen in the proximal tubular epithelial cells
Mesangial proliferative glomerulonephritis: Diffuse proliferation of glomerular mesangial cells and mesangial matrix can be seen under light microscopy
Focal segmental glomerulosclerosis: The lesions are focal and segmentally distributed under light microscopy, showing sclerosis of the affected segments, corresponding to tubular atrophy and interstitial fibrosis.
Membranous nephropathy: Diffuse glomerular nephrosis can be seen under light microscopy. In the early stage, only a small number of scattered Ferythrophilic granules are seen on the epithelial side of the glomerular basement membrane.
Mesangial capillary glomerulonephritis: The pathological changes under light microscopy are diffuse and severe proliferation of mesangial cells and mesangial matrix.
complication
Infection, thrombosis and embolism, acute kidney injury, protein and fat metabolism disorders
Differential diagnosis
Hepatitis B virus-related nephritis, lupus nephritis, Henoch-Schonlein purpura nephritis, diabetic nephropathy, renal amyloidosis
treat
General treatment: proper rest, avoidance of public places and infection prevention
Symptomatic treatment: diuresis and swelling (thiazide diuretics, loop diuretics, osmotic diuretics), reducing proteinuria
Immunosuppressive treatment: glucocorticoids (prednisone), cytotoxics (cyclophosphamide, chlorambucil), calcineurin inhibitors, mycophenolate mofetil
urinary tract infection
Etiology and pathogenesis
Pathogenic microorganisms (Gram-negative bacilli)
Pathogenesis: route of infection (ascending infection, blood infection, direct infection, lymphatic infection)
clinical manifestations
Cystitis: Frequent urination, urgent urination, dysuria, pain or tenderness above the pubic bone, and some patients have difficulty urinating.
Pyelonephritis
Acute pyelonephritis: systemic symptoms: fever, chills, headache, body aches, nausea and vomiting, body temperature usually above 38°C Urinary system symptoms: frequent urination, urgency, painful urination, difficulty urinating Low back pain: Low back pain varies in degree, mostly dull pain or soreness Chronic pyelonephritis: clinical manifestations are complex, with atypical systemic and urinary system local manifestations
Asymptomatic bacteriuria, complicated urinary tract infection
Laboratory and other tests
Urine test: urine shows leukocyturia, hematuria, and proteinuria; White blood cell excretion rate, bacteriological examination: smear bacterial examination, bacterial culture, nitrate reduction test Blood tests: increased white blood cell count, increased neutrophils, left nuclear shift, decreased glomerular filtration rate, and increased serum creatinine Imaging examination: B-ultrasound, plain abdominal X-ray,
treat
General treatment: rest, drink plenty of water, and urinate frequently Anti-infective treatment: Choose antibiotics that are sensitive to pathogenic bacteria, choose antibiotics with less nephrotoxicity and fewer side effects
acute kidney injury
Pathogenesis and pathophysiology
Prerenal AKI - caused by insufficient renal blood perfusion
① Insufficient effective blood volume ② Decreased cardiac output ③ Dilation of systemic blood vessels ④ Constriction of renal arteries ⑤ Impaired renal blood flow autonomic regulation response
Renal AKI-renal ischemia and nephrotoxic substances cause renal tubular epithelial cell damage
Postrenal AKI-bilateral urinary tract obstruction or unilateral urinary tract obstruction in patients with solitary kidney
Pathology: The kidneys are enlarged, soft, the medulla is dark red in cross-section, the cortex is swollen, and the kidneys are pale due to ischemia.
clinical manifestations
Initiation phase: hypotension, ischemia, sepsis and nephrotoxins
Progression phase and maintenance phase: generally last 7 to 14 days, with loss of appetite, nausea and vomiting, diarrhea and abdominal distension, gastrointestinal bleeding, acute pulmonary edema, infection, hypertension, heart failure, water and sodium retention, electrolyte imbalance, anemia, acidosis, Disorder of consciousness, restlessness, delirium
Recovery period: GFR gradually increases and returns to normal or close to normal levels
Laboratory and other tests
Blood tests: anemia, increased serum potassium concentration, decreased serum calcium, increased serum phosphorus, pH and decreased bicarbonate ion concentration
Urine examination: In prerenal AKI, there is no proteinuria and hematuria, and a small amount of transparent casts can be seen.
Film degree exam:
kidney biopsy
treat
Early cause intervention and treatment nutritional support treatment Treatment of complications renal replacement therapy
chronic renal failure
Definition and staging
Chronic kidney disease: Abnormal kidney structure or function caused by various reasons for ≥ 3 months
Chronic renal failure: a syndrome composed of decreased GRF caused by chronic kidney disease and related metabolic disorders and clinical symptoms
clinical manifestations
Water and electrolyte metabolism disorders
metabolic acidosis Water and sodium metabolism disorders Potassium metabolism disorders Calcium and phosphorus metabolism disorders Magnesium metabolism disorders
Protein, carbohydrate, lipid and vitamin metabolism disorders
Cardiovascular system manifestations
Hypertension and left ventricular hypertrophy heart failure uremic myocarditis pericardial lesions Vascular calcification and atherosclerosis
Respiratory symptoms: Shortness of breath, shortness of breath, and severe acidosis may occur when there is excess body fluid or acidosis.
Gastrointestinal symptoms: lack of appetite, nausea and vomiting; smell of urine in mouth
Hematologic manifestations: renal anemia, bleeding tendencies, and thrombosis
Neuromuscular symptoms: fatigue, insomnia, and difficulty concentrating in the early stage; personality changes, depression, and memory loss may occur later.
endocrine dysfunction
Bone changes: high-conversion bone disease, low-conversion bone disease, mixed bone disease
treat
Early prevention and treatment strategies and measures: ① Timely and effective control of hypertension ② Application of ACEI and ARB ③ Strict control of blood sugar ④ Control of proteinuria
Nutritional therapy: protein-restricted diet
Drug treatment of chronic renal failure and its complications: ① Correction of acidosis and water and electrolyte disorders ② Treatment of hypertension ③ Treatment of anemia ④ Prevention of infection ⑤ Treatment of hyperlipidemia ⑥ Oral adsorption therapy and cathartic therapy
renal replacement therapy
digestive system
Summary
Digestive physiology and biochemical functions related to common diseases
Physiological esophageal reflux defense mechanism: ① esophageal-gastric anti-reflux barrier, ② esophageal clearance, ③ esophageal mucosal barrier
Gastric mucosal barrier: Pyloric glands are located in the gastric antrum and pylorus and are the main glands that secrete mucus and gastrin Fundic glands are distributed in the fundus and body of the stomach. They are composed of chief cells, cell walls, cervical mucus cells and endocrine cells. They are the main glands that secrete gastric acid, pepsin and intrinsic factor. The cardia gland is located near the cardiac cardia of the stomach. It is a single gland duct and mainly secretes mucus. The pH of gastric juice is about 0.9~1.5, and the secretion volume of normal people is 1.5~2.5L/d. Pepsinogen is activated in an acidic environment.
Secretion and regulation of gastric acid: The information sensed by the gastric antrum from food prompts the G cells of the pyloric gland to secrete gastrin
Intestinal mucosal barrier: mechanical barrier, chemical barrier, immune barrier, biological barrier, intestinal motility
Intestinal microecology
Composed of bacteria, fungi, viruses, etc.
Function: ① Metabolic function (can secrete complex proteases, has redox effect, can promote the decomposition of components in food, and decompose, metabolize and transform endogenous and exogenous other substances ②Nutrition function: Synthesize a variety of vitamins, amino acids, peptides, exercise fatty acids, and microbial metabolites to promote the absorption of minerals and nutrients. ③Host immune function: regulates the development and maturation of host immune organs ④Intestinal defense function: It is an important part of the intestinal mucosal barrier
gastrointestinal peptides
Cholecystokinin, somatostatin, intestinal vasoactive peptide, substance P
It plays an important and complex regulatory role in the secretion, motility, material transport, immunity and intestinal epithelial cell repair of the gastrointestinal tract.
Digestion, absorption of major nutrients and metabolism of the liver
Sugar: hydrolyzed by pancreatic amylase into disaccharides, part of which supplies energy to the body; part of which is stored in the form of glycogen in the liver and muscles. Fat: After emulsification by bile salts in the small intestine, it is digested by pancreatic lipase into monoglycerides, fatty acids and cholesterol, and then absorbed into the portal vein in the upper intestine. protein
Metabolism and detoxification functions of the liver
Oxidation, reduction, hydrolysis, combination
Coordinated movement of the biliary tract
Liver cells produce bile, and secretion begins in the bile canaliculi; the general gallbladder can hold 20~50ml of bile
Pancreatic enzyme synthesis and activation and the physiological mechanism of fat glands preventing self-digestion
Important Diagnostic and Treatment Techniques for the Digestive System
Endoscopic diagnosis: gastroscopy, enteroscopy, capsule endoscopy, enteroscopy, endoscopic retrograde cholangiopancreatography, endoscopic ultrasound
Laboratory testing: diagnosis of B viral infection, Helicobacter pylori detection (non-invasive method, invasive method), liver function assessment
Diagnostic imaging: ultrasound, computed tomography, magnetic resonance imaging
gastroesophageal reflux
Etiology and pathogenesis
①Abnormal structure and function of the anti-reflux barrier, ②Reduced esophageal clearance, ③Reduced esophageal mucosal barrier function
pathology
Reflux esophagitis (RE): esophageal mucosal epithelial necrosis, inflammatory cell infiltration, mucosal erosion and ulcer formation
Non-erosive reflux disease (NERD): ① basal cell proliferation ② elongation of papillae of lamina propria and proliferation of blood vessels ③ infiltration of inflammatory cells ④ enlargement of squamous epithelial cell gaps
clinical manifestations
Esophageal symptoms
Typical symptoms: Reflux and heartburn.
Atypical symptoms: chest pain, which can radiate to the precordium, back, neck, shoulders, and behind the ears, difficulty swallowing, and foreign body sensation behind the sternum.
Extraesophageal symptoms: pharyngitis, chronic cough, asthma and dental erosion. Some patients report pharyngeal discomfort, foreign body sensation or blockage sensation.
Complications: upper gastrointestinal bleeding, esophageal stricture, Barrett's esophagus
Auxiliary inspection
Gastroscopy (the most accurate method to diagnose RE), 24-hour esophageal pH monitoring (to determine whether there is excessive acid and alkali reflux in the esophagus), esophageal barium angiography, and esophageal manometry
treat
Drug therapy: acid-suppressing drugs (PPI, histamine H2 receptor antagonists), gastrointestinal motility drugs (domperidone, mosapride), antacids, maintenance treatment patient education Antireflux surgical treatment Treatment of complications
Esophageal cancer
Cause
Nitrosamines and mycotoxins Chronic physical and chemical irritation and inflammation nutritional factors genetic factors
pathology
The lesions of esophageal cancer are mostly in the middle section, followed by the lower section, and least in the upper section. Gross pathology: early esophageal cancer: the lesions are limited to the mucosa and superficial submucosal layers, without lymph node metastasis Intermediate and advanced esophageal cancer; cancer tissue gradually affects the entire circumference of the esophagus, protrudes into the cavity, or penetrates the wall to invade adjacent organs. Spread and metastasis modes of esophageal cancer: direct spread, lymphatic metastasis, hematogenous metastasis
clinical manifestations
Early symptoms: The main symptoms are retrosternal discomfort, burning sensation, and pinprick or pulling-like pain. There may be slow passage of the esophagus, retention, or mild choking sensation. Symptoms in the middle and late stages: progressive dysphagia, food regurgitation, and pain when swallowing Signs: wasting, anemia, malnutrition, dehydration, or cachexia
Auxiliary inspection
Gastroscopy, barium esophagography, CT, EUS
Differential diagnosis
Achalasia, gastroesophageal reflux disease, benign esophageal stricture, globus hysteria
treat
Endoscopic treatment, surgery, radiotherapy, chemotherapy
gastritis
acute gastritis
Common causes and pathophysiological mechanisms
Stress, drugs, alcohol, trauma and physical factors
Clinical manifestations: upper abdominal pain, fullness; nausea and vomiting, loss of appetite
Diagnosis: based on clinical symptoms and incentives; confirmed diagnosis relies on gastroscopy
Treatment: Remove the cause and aggressively treat underlying disease and trauma
chronic gastritis
Etiology and pathogenesis: Hp infection, duodenal-gastric reflux, drugs and poisons, autoimmunity, age factors and others
Gastroscopy and histopathology: The mucosa of chronic non-atrophic gastritis may be congested and edematous or the mucosal folds may be swollen and thickened; the mucosa of atrophic gastritis may become lighter in color, the folds may become thinner and flatter, the mucus may be reduced, and sometimes mucosal vascular striae may be visible.
The main histological changes in chronic gastritis are: inflammation, atrophy, metaplasia, and dysplasia
clinical manifestations
Discomfort, fullness, dull pain, burning pain in the middle and upper abdomen, and may also present with lack of appetite, belching, pantothenic acid, and nausea
Diagnosis: gastroscopy + histological examination
treat
Treatment for the cause: Hp-related gastritis (antibiotics, PPI, bismuth) Symptomatic treatment
Special types of gastritis or stomach problems
corrosive gastritis
Caused by swallowing strong acid, strong alkali, arsenic, phosphorus, mercury chloride
For corrosive gastritis, temporary fasting, parenteral nutrition, and close monitoring should be
peptic ulcer
Definition: Refers to inflammatory defects in the gastrointestinal mucosa, usually related to gastric acid and digestion of gastric juice. The lesions penetrate the muscularis mucosa or reach deeper layers.
Etiology and pathogenesis
Gastric acid and pepsin: Pepsinogen is easily activated when the pH is 2~3, and when the pH is >4, pepsin is inactivated.
Helicobacter pylori, drugs, mucosal defense barrier, genetic susceptibility, heavy drinking, long-term smoking
pathology
Gastric ulcers are more common in the corners of the stomach and the lesser curvature of the gastric antrum, while duodenal ulcers are more common in the bulb.
clinical manifestations
Symptoms: Upper abdominal pain (dull pain (burning, distending, severe pain)). Characteristics ① chronic process, ② recurring or periodic attacks, ③ some patients have rhythmic epigastric pain related to meals, ④ abdominal pain can be treated with acid suppressants or antacid relief
Signs: There may be localized tenderness under the xiphoid process, upper abdomen or right upper abdomen
special ulcer
Compound ulcer: refers to gastric and duodenal ulcers, more common in men
Pyloric ulcer: pain occurs soon after meals, and complications such as pyloric obstruction, bleeding and perforation are prone to occur
Retrobulbar ulcer: an ulcer that occurs in the descending and horizontal segments of the duodenum. The ulcers are mostly on the posteromedial wall. The pain can radiate to the right upper quadrant and back.
Huge ulcer: an ulcer with a diameter >2cm, the pain can be severe and stubborn
Ulcers in the elderly and childhood ulcers
Refractory ulcers: ulcers that have not healed despite regular anti-ulcer treatment
complication
Bleeding: In mild cases, the symptoms are positive for drinking blood in the stool and black stools, and in severe cases, massive bleeding. Perforation: Sudden severe abdominal pain that persists and becomes severe, with physical signs such as stiffness of the abdominal wall, tenderness, rebound tenderness, and disappearance of liver dullness Pyloric obstruction: clinical symptoms include upper abdominal pain, aggravated after meals, and abdominal pain can be relieved after vomiting cancer
Auxiliary inspection
Gastroscopy and biopsy: Gastroscopy is the preferred method and gold standard for peptic ulcers X-ray barium CT Laboratory tests: HP testing
treat
Treatment goals: remove the cause, control symptoms, promote ulcer healing, prevent recurrence and avoid complications
Intestinal tuberculosis and tuberculous peritonitis
Intestinal tuberculosis
Etiology and pathogenesis: Mainly caused by Mycobacterium hominis
Pathology: Mainly located in the ileocecal region, but may also involve the colorectum
clinical manifestations
Abdominal pain: mostly located in the right lower abdomen or around the umbilicus, with intermittent attacks, aggravation after meals, and often accompanied by borborygmi Changes in bowel habits: The stools are pasty, often without pus and blood, and without tenesmus. Abdominal wall mass: mostly located in the right lower abdomen, in the middle mass, relatively fixed Systemic symptoms and manifestations of extraintestinal tuberculosis
Laboratory tests and other tests
Laboratory tests: The erythrocyte sedimentation rate is significantly accelerated, and a small amount of pus cells and red blood cells are seen in the stool. CT, X-ray barium enema Colonoscopy: mucosal congestion, edema, and ulcer formation in the ileocecal area and other areas
treat Eliminate symptoms, improve general condition, promote lesion healing and prevent complications
Anti-tuberculosis chemical drug treatment Symptomatic treatment Surgical treatment: Indications ① Complete intestinal obstruction or incomplete intestinal obstruction that fails medical treatment ② Acute intestinal perforation, or chronic intestinal perforation fistula that cannot be closed after medical treatment ③ Massive intestinal bleeding that cannot be effectively stopped by active rescue ④ Diagnosis is difficult and requires laparotomy
tuberculous peritonitis
Cause: Mostly secondary to pulmonary tuberculosis or tuberculosis in other parts of the body
pathology
Exudative type: peritoneal bleeding, edema, surface covered with fibrin exudate Proliferative type: A large amount of fibrous tissue proliferation and protein deposition make the peritoneum and mesentery significantly thickened cheese type
clinical manifestations
Systemic symptoms: low-grade fever, night sweats, flaccid fever or residual fever Abdominal pain: located around the umbilicus, lower abdomen or entire abdomen, persistent or paroxysmal dull pain Abdominal palpation: There is often a rubbing sensation Abdominal distention, abdominal effusion: accompanied by abdominal distension Abdominal wall mass: more common in adhesion type or cheese type Diarrhea: usually 3 to 4 times/min, and the stools are mostly paste-like.
Laboratory and other tests
Blood test: Mild to moderate anemia may be present Tuberculin test and gamma-interferon release test Ascites Abdominal imaging tests Laparoscopy
treat
1. Anti-tuberculosis chemical drug treatment 2. If there is a large amount of abdominal effusion, the abdominal effusion can be appropriately drained to relieve symptoms. 3. Surgical treatment 4. Patient education
inflammatory bowel disease
ulcerative colitis
Etiology and pathogenesis
Environmental factors, genetic factors, intestinal microecology, immune imbalance
Pathology: The lesions are mainly limited to the large intestinal mucosa and submucosal base, with a continuous and diffuse distribution.
clinical manifestations
Digestive system: diarrhea, mucus, pus and bloody stools, abdominal pain, bloating, loss of appetite, nausea and vomiting, Mild and moderate patients only have tenderness in the left lower abdomen, while severe patients have obvious tenderness, abdominal muscle tension, tenderness, and rebound tenderness.
Systemic reactions: fever, malnutrition
Extraintestinal manifestations: peripheral arthritis, erythema nodosum, pyoderma gangrenosum, episcleritis
Complications: toxic colitis, cancer
Laboratory and other tests:
Blood: Anemia, increased white blood cell count, accelerated erythrocyte sedimentation rate, and increased C-reactive protein Feces: Mucus, pus and blood are often present to the naked eye. Colonoscope X-ray barium enema
treat
Control inflammatory response: aminosalicylic acid preparations (5-aminosalicylic acid, sulfasalazine) glucocorticoids, immunosuppressants
Symptomatic treatment: timely correction of water and electrolyte imbalances, blood transfusion for severe anemia, supplementation of white list for hypoalbuminemia
Surgical treatment: The indications for emergency surgery are those complicated by massive bleeding, intestinal perforation and toxic megacolon that fail to respond to aggressive medical treatment.
Crohn's disease
pathology
Gross morphological characteristics: ① The lesions are segmental ② The mucosa of the lesions presents longitudinal ulcers and cobblestone-like appearance, which may appear as thrush ulcers in the early stage ③ The lesions involve the entire intestinal wall, with thickening and hardening of the intestinal wall and narrow intestinal lumen
Histological characteristics: ① Non-caseating granuloma, composed of epithelial-like cells and multinucleated giant cells, can occur in all layers of the intestinal wall and local lymph nodes ② Fissure ulcers, slit-shaped, can penetrate deep into the submucosal muscle layer, muscle layer and even Serosal layer ③ Inflammation of all layers of the intestinal wall, accompanied by lymphocyte accumulation at the bottom of the lamina propria and submucosa, and widening of the submucosa
clinical manifestations The onset of symptoms is mostly insidious and slow.
Digestive system manifestations: abdominal pain - mostly located in the right lower quadrant or around the umbilicus, intermittent attacks, diarrhea, abdominal mass, fistula formation, and perianal lesions
Systemic manifestations: fever, malnutrition, weight loss, anemia, hypoalbuminemia
Complications: Intestinal obstruction is the most common
Laboratory and other tests
Endoscopy: Colonoscopy is the test of choice for Crohn’s disease Imaging examination: CT, MRI
treat
Control inflammatory response: aminosalicylic acids, glucocorticoids, immunosuppressants, antibacterial drugs, biological agents, total enteral nutrition
Symptomatic treatment: correct water and electrolyte imbalance, and blood transfusion can be used in patients with anemia
Surgical treatment: mainly for complications
Cirrhosis
Cause
Cholestasis, circulatory disorders, parasitic infections, genetic and metabolic diseases, unknown causes
Pathogenesis: The liver experiences chronic inflammation, fatty degeneration, hepatocyte reduction, diffuse fibrosis, and extrahepatic and extrahepatic vascular proliferation, and gradually develops into cirrhosis.
clinical manifestations
Compensation phase: asymptomatic or mild symptoms, including abdominal discomfort, fatigue, loss of appetite, indigestion and diarrhea
decompensation period
Decreased liver function: maldigestion, malnutrition, jaundice, bleeding and anemia, endocrine disorders, irregular low-grade fever, hypoalbuminemia
Portal hypertension: formation of portal collateral circulation (esophageal and gastric varices, abdominal wall varices, hemorrhoidal varices, retroperitoneal anastomotic varices, splenorenal shunt) hypersplenism and splenomegaly; peritoneal effusion
complication
Gastrointestinal bleeding (esophageal and gastric variceal bleeding, peptic ulcer, portal hypertensive gastroenteropathy) cholelithiasis Infections (spontaneous bacterial peritonitis, biliary tract infections, lung, intestinal and urinary tract infections) Hepatic encephalopathy (ammonia poisoning, pseudoneurotransmitters, tryptophan, manganese ions) Portal vein thrombosis or cavernous degeneration Electrolyte and acid-base balance disorders Hepatorenal syndrome Hepatopulmonary syndrome primary liver cancer
diagnosis
Determine if there are any complications: Finding the cause of cirrhosis Liver function assessment Diagnosis of complications
treat
Protect or improve liver function ① Remove or reduce the cause of the disease ② Use drugs that damage the liver with caution ③ Maintain enteral nutrition ④ Protect the liver
Treatment of symptoms of portal hypertension and its complications: ① Ascites (restriction of sodium and water intake, diuresis; transvenous intrahepatic portacaval shunt) ② Treatment and prevention of EGVB
hepatic encephalopathy
Early identification and removal of triggers of HE attacks, nutritional support and treatment, promotion of ammonia metabolism in the body, regulation of neurotransmitters, and blocking of porto-systemic shunts
Treatment of other complications
Operation
pancreatitis
acute pancreatitis
Cause
Biliary tract disease, alcohol, pancreatic duct obstruction, descending duodenal disease, surgery and trauma, metabolic disorders, drugs, infection and systemic inflammatory response, overeating
Pathogenesis: ① Damage to acinar cells, activation of the hub molecule nuclear factor of inflammatory response and other factors lead to massive inflammatory exudation ② Pancreatic microcirculation disorder causes pancreatic hemorrhage and necrosis
pathology
Pancreatic acute inflammatory disease local complications of pancreas Pathology of multi-organ inflammatory injury caused by acute pancreatitis
clinical manifestations
Acute abdominal pain: often severe, often located in the left upper abdomen or even the entire abdomen, and in some patients the pain radiates to the back
Acute multiple organ dysfunction and failure: abdominal pain persists, abdominal distension gradually worsens, and circulatory, respiratory, intestinal, liver, and renal failure may occur one after another.
local complications of pancreas
Auxiliary inspection
Important serum markers for diagnosing AP: ①Amylase: Serum amylase begins to increase 2 to 12 hours after the onset of illness and begins to decrease at 48 hours ②Lipase: It begins to increase 24 to 72 days after the onset of illness and lasts for 7 to 10 days.
Laboratory test indicators that reflect the pathophysiological changes of AP: white blood cells, C-reactive protein, blood sugar, white blood list, blood calcium, and blood triglycerides
Image changes of pancreas and other organs
Abdominal ultrasound, abdominal CT,
diagnosis
Determine the degree of AP: ① Mild acute pancreatitis ② Moderately severe acute pancreatitis ③ Severe acute pancreatitis ④ Critical acute pancreatitis
treat ① Find and remove the cause ② Control inflammation
guardianship
Organ support: fluid resuscitation, respiratory function, intestinal function maintenance, continuous blood purification,
Decreased pancreatic juice secretion: fasting, somatostatin and its analogs
Control inflammation: fluid resuscitation, somatostatin, early enteral nutrition
analgesia
Emergency endoscopic treatment to remove the cause
Prevent and fight infection
chronic pancreatitis
Etiology and pathogenesis
Various bile and pancreatic diseases, alcohol, group B coxsackievirus, idiopathic pancreatitis, hypercalcemia
clinical manifestations
Symptoms: Abdominal pain: recurrent epigastric pain, intermittent at first, then persistent epigastric pain, aggravated when lying down Manifestations of exocrine pancreatic insufficiency: loss of appetite, weight loss, malnutrition, edema Manifestations of pancreatic endocrine insufficiency
Signs: There may be mild tenderness in the abdomen
Auxiliary inspection
Abdominal plain X-ray, abdominal ultrasound and endoscopic ultrasound, abdominal CT and MRI,
treat Eliminate causes, control symptoms, improve pancreatic function, and treat complications