Therpay Exam QA Flashcards
- Methodology of diagnosis: the methodology of preliminary diagnosis, the methodology of
differential diagnosis, the principles of clinical diagnosis.
- Methodology of Diagnosis:
- The process of identifying a disease or condition from its signs and symptoms.
- Preliminary Diagnosis:
- The initial assessment of a patient’s condition.
- Based on presenting symptoms, patient history, and basic examinations.
- Helps to build a provisional diagnosis to guide further investigation.
- Differential Diagnosis:
- A systematic method used to identify a disease that is causing the patient’s symptoms.
- Considers all possible conditions that might produce the patient’s symptoms.
- Involves comparing and contrasting the likelihood of various diseases.
- Tests and procedures may be used to exclude certain diagnoses.
- Principles of Clinical Diagnosis:
- Integration of patient history, examination findings, and diagnostic test results.
- Utilizing medical knowledge, clinical experience, and understanding of epidemiology.
- Making use of reasoning, pattern recognition, and clinical decision-making skills.
- Continual assessment and refinement of diagnosis as new information becomes available.
Each step in this methodology is critical to identifying the correct diagnosis and prescribing the most effective course of treatment
- Pneumonia. Social significance. Etiology and pathogenesis. Classification.
- Social Significance:
- Pneumonia is one of the leading causes of morbidity and mortality worldwide, especially in children under five years of age and in the elderly.
- It has a substantial impact on public health systems, contributing to high hospitalization rates and substantial healthcare costs.
- In developing countries, the burden of pneumonia is exacerbated by factors like poor access to healthcare, malnutrition, and crowded living conditions.
- Etiology:
- Pneumonia can be caused by a variety of pathogens including bacteria, viruses, fungi, and parasites. The most common causative agent in adults is Streptococcus pneumoniae.
- Viral pneumonia can be caused by influenza, respiratory syncytial virus (RSV), and COVID-19, among others.
- Environmental and lifestyle factors such as smoking, air pollution, and compromised immunity also contribute to the risk of developing pneumonia.
- Pathogenesis:
- The pathogenesis of pneumonia involves the invasion of the lung parenchyma by infectious agents, followed by the host’s immune response to these pathogens.
- This leads to inflammation and consolidation in the lung tissue, impairing gas exchange and resulting in the typical symptoms of pneumonia such as cough, fever, and difficulty breathing.
- Severity can vary from mild to life-threatening, depending on the pathogen, the individual’s immune response, and other coexisting conditions.
- Classification:
- Pneumonia can be classified based on different criteria such as the setting of acquisition (community-acquired pneumonia CAP and hospital-acquired pneumonia HAP), the pathogen involved, and the area of lung affected.
1- Community-acquired pneumonia (CAP) is acquired outside of hospital settings and is the most common form of pneumonia.
2- Hospital-acquired pneumonia (HAP), including ventilator-associated pneumonia (VAP), occurs in hospital settings and often involves more resistant bacteria.
3- Aspiration pneumonia results from the inhalation of foreign matter into the lungs.
4- Based on the causative agent, pneumonia can also be classified as bacterial, viral, fungal, or parasitic.
- Pneumonia can be classified based on different criteria such as the setting of acquisition (community-acquired pneumonia CAP and hospital-acquired pneumonia HAP), the pathogen involved, and the area of lung affected.
- Clinic and diagnosis of pneumonias. General signs of pneumonias.
—Clinical Features and Diagnosis of Pneumonias:
1. Symptoms:
- Cough: Can be productive (yielding phlegm) or non-productive (dry).
- Fever: Often accompanied by chills and sweating.
- Dyspnea: Difficulty breathing or shortness of breath.
- Pleuritic Chest Pain: Pain in the chest that may worsen with breathing or coughing.
- General Malaise: Feeling of overall weakness and discomfort.
- Headaches.
- Myalgia: Muscle pain.
- Confusion: Especially in the elderly, can indicate more severe illness.
2. Signs (Clinical Observations):
- Tachypnea: Increased rate of respiration.
- Crackles or Rales: Abnormal lung sounds heard with a stethoscope.
- Tachycardia: Elevated heart rate.
- Cyanosis: A bluish discoloration of the skin, indicating inadequate oxygenation.
- Hypotension: Can indicate severe infection or sepsis.
- Consolidation: Dullness on percussion and enhanced breath sounds over affected areas, indicating fluid in the alveoli.\
——-DIAGNOSIS :
1. Clinical Assessment
2. Chest Radiography
3. Blood Tests:
- Routine tests such as Complete Blood Count (CBC) may show elevated white blood cell count indicating infection.
- Inflammatory markers such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) can be elevated.
- Blood cultures may identify the causative organism, especially in cases of bacteremia.
4. Microbiological Tests:
- Sputum culture: Sputum sample can be cultured to identify the causative bacteria.
- Throat swabs and nasopharyngeal samples may be taken for viral PCR tests.
5. Urine Antigens: Tests for antigens from specific bacteria like Streptococcus pneumoniae or Legionella pneumophila.
- Differential diagnosis of pneumonias.
- Bronchitis: Both acute and chronic bronchitis can present with cough and production of sputum, similar to pneumonia, but typically lack the systemic symptoms of fever and the chest radiographic findings seen in pneumonia.
- Asthma: Asthma can cause wheezing, shortness of breath, and cough. However, it is characterized by episodic attacks and a history of allergic triggers, distinguishing it from pneumonia.
- Tuberculosis (TB): Pulmonary TB can mimic pneumonia with its presentation of cough, fever, night sweats, and weight loss. Chest X-rays and sputum cultures for Mycobacterium tuberculosis are essential for diagnosis.
- Pulmonary Embolism (PE): PE can present with acute onset shortness of breath, chest pain, and sometimes cough. The presentation can resemble pneumonia, but the diagnosis is confirmed with imaging studies like CT pulmonary angiography.
- Pulmonary Edema: Caused by fluid accumulation in the alveoli, it presents with shortness of breath, crackles on auscultation, and hypoxia. It is distinguished from pneumonia by the clinical context (such as heart failure) and imaging studies.
- COPD Exacerbation: Patients with Chronic Obstructive Pulmonary Disease (COPD) can have exacerbations presenting with increased dyspnea, cough, and sputum production. Distinguishing between a COPD exacerbation and pneumonia can be challenging and often requires a chest X-ray.
- Lung Cancer: Can present with cough, weight loss, and hemoptysis. While these symptoms may overlap with pneumonia, lung cancer might also present with persistent, localized abnormalities on chest imaging, prompting further investigation.
- Viral Respiratory Infections: Influenza or respiratory syncytial virus (RSV), especially in specific seasons, can present similarly to pneumonia with fever, cough, and malaise. Laboratory testing and clinical context help differentiate these conditions.
- Complications of pneumonias. Diagnosis and treatment of infectious toxic shock, nonhaemodynamic (toxic) pulmonary oedema and acute respiratory failure.
–Complications of pneumonia :
1. Pleurisy and Pleural Effusion: Inflammation of the pleura (the membrane surrounding the lungs) can lead to sharp chest pain. Fluid can also accumulate in this space, termed a pleural effusion, which can complicate breathing.
2. Lung Absces
3. Septicemia/Bacteremia: The infection can spread to the bloodstream, leading to a potentially life-threatening condition known as sepsis.
4. Acute Respiratory Distress Syndrome (ARDS)
5. Empyema: The collection of pus in the pleural cavity, which can result from the spread of infection from the lungs.
6. Respiratory Failure: The lungs can become so damaged from the infection or its complications that they can no longer perform their function of gas exchange efficiently.
7. Pericarditis and Myocarditis
——–DIAGNOSIS
–Diagnosis:
- Clinical Assessment: Sudden onset of high fever, rash, hypotension, and multi-organ involvement are key indicators.
- Laboratory Tests: Cultures of blood, urine, cerebrospinal fluid, or any other suspected site of infection can identify the causative bacteria. Tests may also show signs of organ dysfunction (e.g., elevated liver enzymes, high creatinine indicating kidney issues).
- Supportive Laboratory Findings: These may include thrombocytopenia (low platelet count), elevated creatinine, evidence of liver impairment, and high creatine kinase levels, among others.
### Toxic Pulmonary Edema:
Pulmonary edema caused by exposure to toxins or as part of an acute allergic reaction needs immediate treatment to reduce lung inflammation and support oxygenation.
Treatment might include:
- Diuretics (like Furosemide): Helps reduce fluid in the lungs.
- Oxygen Therapy: To ensure adequate oxygen levels in the blood.
- Corticosteroids (such as Methylprednisolone): To reduce inflammation in the lungs caused by allergic reactions or toxins.
- Mechanical Ventilation: In severe cases, to support breathing and manage oxygen and carbon dioxide levels in the blood.
Identifying and removing the source of the toxic exposure is crucial, along with supportive care.
### Acute Respiratory Failure:
This condition requires immediate medical attention to support the lungs and ensure the body gets the oxygen it needs.
- Etiological diagnosis of pneumonias:
1) according to the place of origin of the disease;
2)according to clinical and radiological data;
3) according to laboratory tests.
- According to the Place of Origin of the Disease:
- Community-Acquired Pneumonia (CAP): This type of pneumonia is acquired outside of hospital or healthcare settings. Common etiological agents include Streptococcus pneumoniae, Haemophilus influenzae, and for certain age groups or situations, Mycoplasma pneumoniae and viral pathogens like influenza.
- Hospital-Acquired Pneumonia (HAP) and Ventilator-Associated Pneumonia (VAP): These pneumonias are acquired in the hospital setting, typically 48 hours or more after admission or within 48 hours of intubation, respectively. They often involve bacteria that are more resistant to antibiotics, such as Pseudomonas aeruginosa, Acinetobacter spp., and MRSA (methicillin-resistant Staphylococcus aureus).
- ## Aspiration Pneumonia: Results from the inhalation of foreign materials into the lungs, often occurring in individuals with impaired gag reflexes or swallowing difficulties. The etiology can include anaerobic bacteria from the oral cavity or stomach.
- According to Clinical and Radiological Data:
- The clinical presentation and radiological findings can offer clues to the causative agent. For example:
- Lobar pneumonia, often seen with Streptococcus pneumoniae,
- Atypical pneumonia, associated with Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella spp.,
- ## Viral pneumonia
- The clinical presentation and radiological findings can offer clues to the causative agent. For example:
- According to Laboratory Tests:
- Microbiological Cultures: Identifying the pathogen from sputum, blood, or pleural fluid cultures is the gold standard for etiological diagnosis, though some pathogens are difficult to culture.
- PCR (Polymerase Chain Reaction)
- Serology
- Antigen Detection
- Urine Antigen Tests
- Treatment of pneumonias. Antimicrobial therapy. Principles of antibiotic selection.
Principles of Antibiotic Selection:
1. Empirical Treatment: Initial treatment is often empirical, meaning it’s based on the most likely pathogens causing pneumonia in the community or hospital setting.
2. Guideline-Conformity: Following established guidelines from organizations like the American Thoracic Society or the Infectious Diseases Society of America, which provide detailed recommendations for different types of pneumonia.
3. Risk Factors Consideration: Taking into account individual patient risk factors for multi-drug resistant pathogens, recent antibiotic use, comorbidities, and hospitalization history.
4. Local Resistance Patterns: Tailoring antibiotic choice to the local antimicrobial susceptibility patterns.
5. De-escalation Strategy: Start with broad-spectrum antibiotics and then narrow based on culture and sensitivity results to minimize the development of resistance.
6. Safety and Tolerability: Considering patient’s allergies, medication interactions, and potential side effects.
### Common Antimicrobial Therapies for CAP:
- Community-Acquired Pneumonia (Outpatient):
- Macrolides (Azithromycin or Clarithromycin) or
- Doxycycline,
For healthy adults with no recent antibiotic use.
- Community-Acquired Pneumonia (Inpatient):
- Beta-lactam (Ceftriaxone, Cefotaxime, or Amoxicillin) plus a Macrolide, or
- Respiratory fluoroquinolone (Levofloxacin or Moxifloxacin),
For those with comorbidities or previous antibiotic use.
### Common Antimicrobial Therapies for HAP/VAP:
- Hospital-Acquired and Ventilator-Associated Pneumonia:
- Antipseudomonal beta-lactam (Piperacillin-tazobactam, Cefepime, Meropenem, or Imipenem) plus
- Antipseudomonal coverage (such as Ciprofloxacin or Levofloxacin) or an aminoglycoside (Amikacin or Gentamicin), and
- Vancomycin or Linezolid for MRSA coverage if risk factors are present
¬¬–The duration of therapy typically ranges from 5 to 7 days for CAP, but it can be longer, especially for more severe infections or if complications arise. For HAP and VAP, the treatment duration might be 7-15 days or more depending on the patient’s response to therapy.
- Pathogenetic and symptomatic methods of pneumonia treatment.
Pathogenetic Treatment:
The cornerstone of pathogenetic treatment in pneumonia is antimicrobial therapy, aimed at eradicating the infectious cause of pneumonia.
1. Antibiotics: The choice of antibiotics depends on whether the pneumonia is community-acquired (CAP), hospital-acquired (HAP), or ventilator-associated (VAP), as well as the patient’s health status, the presence of comorbid conditions, and the local patterns of antibiotic resistance.
- Bacterial Pneumonia: Empirical antibiotic therapy is initiated based on the presumed pathogen and adjusted based on the culture and sensitivity results.
- Viral Pneumonia: Treatment may involve antiviral medications, such as oseltamivir for influenza. For certain viral infections like COVID-19, treatment protocols may include antiviral drugs, corticosteroids, and supportive care.
- Fungal Pneumonia: Antifungal agents are used for fungal pneumonia, selected based on the specific type of fungus identified.
2. Oxygen Therapy: For patients experiencing hypoxemia, supplemental oxygen is provided to maintain adequate blood oxygen levels.
3. Fluid Management: Careful management of fluids is essential to ensure hydration while avoiding fluid overload, which may worsen pulmonary edema.
4. Corticosteroids: Might be used in specific cases, such as severe viral pneumonia or to reduce inflammation, but their use is based on clinical judgment and current guidelines.
————————-
### Symptomatic Treatment:
Symptomatic treatment is aimed at providing relief from the symptoms of pneumonia and supporting the patient’s general well-being.
1. Fever and Pain Management: Acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs) can be used to reduce fever and alleviate chest pain or discomfort.
2. Cough Management: For a productive cough, expectorants may help loosen and clear secretions. For a dry, irritating cough, antitussives may be used to suppress the cough reflex.
3. Nutritional Support: Adequate nutrition supports immune function and promotes healing. Hydration is particularly important to help loosen lung secretions.
4. Rest: Adequate rest is crucial to support recovery, although patients are also encouraged to engage in limited activity as tolerated to avoid complications associated with prolonged bed rest, such as deep vein thrombosis.
5. Pulmonary Rehabilitation: Techniques such as deep breathing exercises, chest physiotherapy, and incentive spirometry may be recommended to improve lung function and facilitate the clearance of pulmonary secretions.
- Pleurisy. Definition, etiology, pathogenesis, clinic, diagnosis. Treatment of dry and wet pleurisy.
Definition:
Pleurisy, also known as pleuritis, is an inflammation of the pleura, the thin, double-layered membrane surrounding the lungs and lining the rib cage. It can result in sharp chest pain, which is typically aggravated by breathing, coughing, or sneezing.
### Etiology:
The causes of pleurisy can be varied and include:
- Viral Infections: The most common cause.
- Bacterial Infections: Such as pneumonia or tuberculosis.
- Autoimmune Disorders: Like rheumatoid arthritis or lupus.
- Pulmonary Embolism: Blood clots in the lungs.
- Cancer: Particularly lung cancer or pleural mesothelioma.
- Other Causes: Such as chest injury, certain medications, or gastrointestinal disease.
### Pathogenesis:
The pathogenesis of pleurisy follows the inflammation of the pleura, which then leads to friction between the pleural layers.
- Dry Pleurisy (Fibrinous): Characterized by the lack of pleural fluid and the presence of fibrin deposits on the pleura.
- Wet Pleurisy (Effusive): Accompanied by the accumulation of excess fluid, known as a pleural effusion, between the pleural layers.
### Clinic (Clinical Presentation):
- Chest Pain: Sharp and stabbing, worsening with inspiration or coughing.
- Pleural Rub: A scratching sound heard through a stethoscope during breathing.
- Dyspnea: Difficulty breathing or shortness of breath.
- Fever: If an infection is present.
- Cough: Dry or with sputum.
### Diagnosis:
The diagnosis of pleurisy involves:
- Medical History and Physical Examination: Including auscultation for pleural rub.
- Chest X-ray: To look for pleural effusions or underlying lung pathology.
- Ultrasound and CT Scan: For detailed images of the pleura.
- Blood Tests: To check for infection or autoimmune disease.
- Thoracentesis: To sample pleural fluid for analysis.
- Biopsy: In cases where cancer is suspected.
### Treatment:
Treatment of pleurisy is targeted at the underlying cause and relief of symptoms.
#### Dry Pleurisy:
- Anti-inflammatory Medication: Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen can reduce inflammation and pain.
- Pain Management: Acetaminophen can also be used for pain relief. In severe cases, prescription pain relief may be required.
- Treatment of Underlying Cause: If the cause is bacterial, appropriate antibiotics will be used, for tuberculosis, antitubercular therapy is necessary, and for autoimmune conditions, immunosuppressive drugs might be prescribed.
#### Wet Pleurisy:
- Drainage of Excess Fluid: If large, the pleural effusion might need to be drained through thoracentesis or placement of a chest tube.
- Corticosteroids: Might be used to reduce inflammation in cases caused by autoimmune disease.
- Diuretics: In cases where heart failure contributes to fluid accumulation, diuretics such as furosemide can be prescribed.
- Antibiotics or Antifungals: If infection is the suspected cause.
- Antivirals: When a viral infection is identified.
- Chronic obstructive pulmonary disease (COPD). Mechanisms of obstruction. Clinical singes
and diagnostics. + TREATMENT
Chronic Obstructive Pulmonary Disease (COPD) is a long-term, progressive lung disease characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar abnormalities, usually caused by significant exposure to harmful particles or gases.
- Chronic Bronchitis: Characterized by chronic inflammation and thickening of the bronchial tube walls, along with increased production of mucus, which can block the airflow in the lungs.
- Emphysema: Involves damage to the alveoli (air sacs) in the lungs, leading to overinflation and reduced elasticity of the lungs, making it difficult for the lungs to exchange oxygen and carbon dioxide effectively.
- Airway Hyperresponsiveness and Inflammation: Continuous exposure to irritants causes an inflammatory response in the lungs, leading to narrowing of the airways and decreased airflow.
- Airflow Limitation: The combination of inflammation, mucous hypersecretion, and structural changes in the lung tissue contribute to restricted airflow, which is not fully reversible even with treatment.
### Clinical Signs: - Dyspnea (Shortness of Breath): Typically progressive, worsens with exercise, and manifests during daily activities in advanced stages.
- Chronic Cough: May be intermittent and may be unproductive or productive of sputum.
- Sputum Production: Characteristic of chronic bronchitis, the sputum can be clear, white, yellow, or greenish.
- Wheezing: A whistling sound when breathing, especially during exhalation.
- Chest Tightness: A sensation of pressure or tightness in the chest.
- Frequent Respiratory Infections: Individuals with COPD are more susceptible to colds, the flu, and pneumonia.
- Fatigue: Due to decreased oxygen levels in the body.
- Weight Loss and Muscle Wasting: In advanced stages, due to the increased energy requirement for breathing and decreased food intake related to breathlessness during eating.
### Diagnostics: - Spirometry: The primary diagnostic test for COPD. It measures the amount of air a person can expel from the lungs and how quickly it can be expelled, identifying obstruction in the airways.
- Chest X-Ray: Can show emphysema one of the main components of COPD, as well as rule out other lung conditions.
- CT Scan: Provides detailed images of the lungs, can help identify emphysema and check for other lung conditions.
- Arterial Blood Gas Analysis: Measures how well the lungs are moving oxygen into the blood and removing carbon dioxide from the blood.
- Pulmonary Function Tests (PFTs): Additional tests to assess the overall function of the lungs.
- Alpha-1 Antitrypsin Deficiency Testing: Since COPD can be caused by a genetic condition leading to deficiency of alpha-1 antitrypsin, a protein that protects the lungs.
- Bronchial asthma. Definition. Etiology and pathogenesis (concept of predisposing factors, causative factors and triggers). Pathogenesis of extrinsic and intrinsic asthma. Classification.
Bronchial asthma, commonly known as asthma, is a chronic inflammatory disease of the airways that causes episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or early in the morning. These episodes are often associated with widespread but variable airflow obstruction within the lungs that is often reversible either spontaneously or with treatment.
Etiology and Pathogenesis:
- Predisposing Factors: These include genetic predisposition to atopy, which is the hereditary tendency to develop allergic diseases such as asthma, eczema, and hay fever. A family history of asthma or allergies can significantly increase the risk of developing asthma.
- Causative Factors: Allergens are the most common causative factors of extrinsic (allergic) asthma. This type includes pollen, dust mites, molds, pet dander, and pest droppings. Intrinsic (non-allergic) asthma, however, isn’t triggered by allergens and its causes are less clear but may include respiratory infections, stress, exercise, cold air, and other non-allergic factors.
- Triggers: Triggers are those factors that can worsen asthma or induce an acute attack. These can include respiratory infections, exercise, cold air, tobacco smoke, emotional stress, and exposure to chemical irritants or industrial dusts.
–The pathogenesis of asthma involves inflammation and hyper-responsiveness of the airways, leading to obstruction and symptoms. For extrinsic asthma, exposure to specific allergens can lead to an immune response that causes airway inflammation, mucus production, and bronchospasm. Intrinsic asthma’s pathogenesis, while involving some similar pathways of inflammation and hyper-responsiveness, does not rely on allergen exposure and may be more related to nonspecific airway irritability.
–Classification:—————
Asthma is classified based on frequency of symptoms, forced expiratory volume in one second (FEV1), and peak expiratory flow rate (PEFR). The common classifications include:
1. Intermittent Asthma: Symptoms less than 2 days per week and night waking less than 2 times per month; normal FEV1 between exacerbations and PEFR variability of less than 20%.
2. Mild Persistent Asthma: Symptoms more than 2 days per week but not daily and night waking 3-4 times per month; FEV1 is greater than or equal to 80% of normal and PEFR variability is 20-30%.
3. Moderate Persistent Asthma: Daily symptoms and night waking more than once a week but not nightly; FEV1 is between 60% and 80% of normal and PEFR variability is greater than 30%.
4. Severe Persistent Asthma: Continual symptoms throughout the day, frequent night waking; FEV1 is less than 60% of normal and PEFR variability is greater than 30%.
- Bronchial asthma. Diagnosis of the disease in the presence of typical and atypical attacks
(respiratory discomfort). Specific diagnostics
Diagnosing bronchial asthma, particularly between typical and atypical attacks, involves a comprehensive evaluation that considers a patient’s medical history, physical examination, and specific diagnostic tests. Both typical and atypical asthma presentations require careful assessment due to the variability in how asthma symptoms present.
### Typical Attacks
Typical asthma attacks are characterized by episodes of wheezing, shortness of breath, chest tightness, and coughing, especially at night or early in the morning. These symptoms often vary in intensity and frequency from person to person.
### Atypical Attacks
Atypical presentations might not include the classic symptoms of wheezing or shortness of breath. Instead, patients might experience cough as the sole symptom (cough variant asthma), chest pain without clear wheezing, or difficulty breathing triggered by exercise (exercise-induced bronchoconstriction).
### Specific Diagnostics
The diagnosis of asthma, including distinguishing between typical and atypical presentations, often involves a combination of the following specific diagnostic tools:
1. Spirometry: This is the most common pulmonary function test used to assess how well the lungs work by measuring how much air one can inhale, how much air one can exhale, and how quickly one can exhale. Spirometry is crucial for diagnosing asthma and can help monitor the severity of the disease over time.
2. Peak Expiratory Flow Rate (PEFR): Measured by a peak flow meter, PEFR indicates the maximum speed of expiration. Fluctuations in PEFR over time can suggest asthma variability, supporting the diagnosis.
3. Bronchial Provocation Tests: Tests such as the methacholine challenge involve exposing the patient to an aerosolized agent that causes airway narrowing in sensitive individuals, helping to identify hyperreactivity in the airways.
4. Fractional exhaled nitric oxide (FeNO) Test: This measures the level of nitric oxide in the breath, which can be higher in people with asthma due to airway inflammation.
5. Chest X-ray or High-resolution CT Scan: Although not diagnostic for asthma, imaging studies can be used to exclude other conditions that might mimic or complicate asthma.
6. Allergy Testing: Since allergens are common triggers for asthma, skin prick tests or blood tests for specific IgE antibodies can help identify specific allergic triggers for individuals with allergic asthma.
- Differential diagnosis of bronchial asthma.
- Chronic Obstructive Pulmonary Disease (COPD): Though COPD and asthma both involve airflow obstruction, COPD is usually associated with a history of smoking and presents in older adults, whereas asthma typically starts in childhood. Spirometry after bronchodilator administration can help distinguish between the two, as asthma shows a significant reversible component.
- Gastroesophageal Reflux Disease (GERD): GERD can cause a chronic cough and mimic asthma. It may also worsen asthma and needs to be considered, especially in asthmatic patients who have symptoms after eating or when lying down.
- Heart Failure: Left ventricular heart failure can lead to pulmonary edema and cause wheezing (cardiac asthma), particularly in older patients. Clinical history, examination, and investigations like echocardiography can differentiate it from bronchial asthma.
- Vocal Cord Dysfunction (VCD): VCD involves inappropriate vocal cord closure during inhalation, often presenting with wheezing or stridor that may be mistaken for asthma. However, VCD doesn’t respond to asthma medications, and laryngoscopy can diagnose it.
- Allergic Rhinitis and Sinusitis: These conditions can produce symptoms such as cough and wheeze due to post-nasal drip, often coexisting with asthma. Differentiating them involves clinical evaluation and, sometimes, imaging studies.
- Foreign Body Aspiration: Especially relevant in children, foreign body aspiration can cause sudden onset of coughing, wheezing, or unilateral reduced breath sounds and requires an urgent evaluation.
- Bronchiectasis: Chronic productive cough, recurrent respiratory infections, and localized wheezes or crackles may suggest bronchiectasis, differentiated from asthma by high-resolution CT scan.
- Pulmonary Embolism (PE): PE can cause sudden shortness of breath and chest pain, mimicking an acute asthma attack. Risk factors, clinical signs, and diagnostic tests like D-dimer levels and CT pulmonary angiography can help in diagnosis.
- Cystic Fibrosis (CF): In children and young adults, recurrent respiratory infections, chronic cough with thick sputum, and failure to thrive might suggest CF. Sweat chloride test and genetic testing can confirm the diagnosis.
-
Infections: Respiratory infections such as bronchitis, pneumonia, and tuberculosis can cause symptoms similar to asthma. Clinical history, examination, and investigations like chest X-ray can help differentiate these conditions.
When diagnosing asthma, it’s vital to conduct a thorough patient history and physical examination, supplemented by p
- Treatment of bronchial asthma. Stepwise scheme of treatment of the disease. Other methods of treatment. Features of treatment of extrinsic and intrinsic asthma.
Stepwise Scheme of Treatment:
Step 1: Intermittent Asthma
- Short-acting beta-agonists (SABA) as needed (e.g., Salbutamol or Albuterol)
Step 2: Mild Persistent Asthma
- Low-dose inhaled corticosteroids (ICS) (e.g., Beclometasone, Budesonide)
- Leukotriene receptor antagonists (LTRAs) may be used as an alternative (e.g., Montelukast)
Step 3: Moderate Persistent Asthma
- Low-dose ICS plus a long-acting beta-agonist (LABA) (e.g., Fluticasone/Salmeterol, Budesonide/Formoterol)
- or Medium-dose ICS
Step 4: Severe Persistent Asthma
- Medium-dose ICS plus LABA
- Consideration of other treatments like tiotropium (a long-acting muscarinic antagonist), leukotriene modifiers, theophylline, or using biologic therapies for patients with allergic asthma and severe symptoms despite high-dose ICS and LABA
- Oral corticosteroids for short term
Step 5: Severe Asthma
- High-dose ICS plus LABA
- Add-on treatments as needed (e.g., biologic therapies like Omalizumab for allergic asthma, Mepolizumab for eosinophilic asthma)
- Oral corticosteroids for chronic management if necessary, although minimizing their use through alternative treatments is preferred due to side effects
### Other Methods of Treatment:
- Biologic Therapies: Target specific pathways or cells involved in the inflammatory process. For allergic asthma, Omalizumab, an anti-IgE antibody, is used. Other biologics target interleukins involved in the eosinophilic inflammation pathway (e.g., Benralizumab, Reslizumab).
- Bronchial Thermoplasty: A procedure for severe asthma not controlled with inhaled steroids and long-acting bronchodilators. It uses thermal energy to reduce the muscle mass surrounding the airways, decreasing the ability of these airways to constrict.
### Features of Treatment in Extrinsic and Intrinsic Asthma:
- Extrinsic Asthma: Treatment focuses on controlling allergic inflammation. This may include regular use of ICS, avoidance of known allergens, and possibly immunotherapy (allergy shots) if specific allergens are identified and are contributing significantly to asthma symptoms.
- Intrinsic Asthma: Since this type isn’t triggered by allergens, treatment focuses more on controlling airway inflammation with ICS and bronchodilators. It might not respond as well to allergy-specific treatments like immunotherapy.
- Chronic lung abscess. Etiology, pathogenesis, clinic, diagnosis, treatment, prevention.
A lung abscess is a localized area filled with pus within the lung tissue, resulting from a bacterial infection. It often arises due to aspiration pneumonia, where bacteria are inhaled into the lungs from the mouth or throat, especially in individuals with decreased levels of consciousness or altered swallowing mechanisms. Lung abscesses can also develop from a complication of existing lung diseases, septic emboli, or through direct invasion by bacteria in cases of chest trauma or following surgery.
Etiology:
- Bacterial Infections: The most common cause. Anaerobic bacteria from the mouth or throat, such as Fusobacterium, Prevotella, and Peptostreptococcus, are frequently involved. Aerobic bacteria, such as Staphylococcus aureus and Klebsiella pneumoniae, can also cause lung abscesses.
- Aspiration: Especially in individuals with impaired consciousness, dysphagia (difficulty swallowing), or those who regurgitate stomach contents.
- Obstruction: Blockage of the airways due to a tumor or foreign body can lead to abscess formation.
- Septic Embolism: Infections elsewhere in the body can lead to the dissemination of bacteria through the bloodstream to the lungs.
### Pathogenesis:
The development of a lung abscess typically follows aspiration of infectious organisms into the lung, leading to localized infection and necrosis of lung tissue. The immune system’s response to this infection leads to the formation of an abscess cavity, which fills with pus.
### Clinical Presentation (Clinic):
Symptoms of a lung abscess can be acute or chronic, including: - Persistent cough, often producing foul-smelling or bloody sputum
- Fever, chills, and night sweats
- Fatigue and weight loss
- Shortness of breath and pleuritic chest pain
### Diagnosis - Chest X-ray: Shows a cavity often with an air-fluid level within the lung parenchyma.
- CT Scan: Provides a more detailed picture, clarifying the extent of the abscess and its relation to surrounding structures.
- Sputum Culture: Identifies the causative pathogen.
- Blood Tests: Increased white blood cell count indicates infection; blood cultures may identify the causative organism in cases of septic embolism.
### Treatment: - Antibiotics: The cornerstone of treatment, selecting based on the results of sputum cultures. For anaerobic infections, the typical regimen includes Clindamycin or a combination of β-lactam and β-lactamase inhibitors. In cases involving aerobic bacteria, treatment may involve more specific antibiotics targeting the identified pathogen.
- Percutaneous Drainage: Considered when the abscess is large or does not respond to antibiotic therapy alone.
- Surgery: Rarely needed, but may be considered if there is a failure of other treatments, suspected malignancy, or significant hemoptysis.
### Prevention: - Proper oral hygiene to decrease the risk associated with aspiration of oral pathogens.
- Avoidance of alcohol and drugs that can depress consciousness and swallowing reflexes.
- Vaccination and timely treatment of respiratory infections to prevent complications.
- Management of underlying conditions that may predispose to lung abscess formation, such as gastroesophageal reflux disease (GERD) or conditions causing dysphagia.
- Atherosclerosis. Etiology and pathogenesis. Features of clinical picture and dependence on
the predominant localisation.
Atherosclerosis is a chronic inflammatory condition characterized by the thickening and hardening of the arterial walls due to the accumulation of fatty deposits, cholesterol, calcium, and other substances, known collectively as plaque. This process can lead to reduced or blocked blood flow, potentially resulting in various cardiovascular diseases depending on the arteries affected.
### Etiology:
The exact cause of atherosclerosis is complex and multifactorial. Risk factors include:
- Genetics: Family history of cardiovascular disease increases risk.
- Unhealthy Diet: High intake of saturated fats, trans fats, and cholesterol.
- High Blood Pressure (Hypertension): Damages the arterial wall over time.
- High Cholesterol Levels: Particularly high low-density lipoprotein (LDL) cholesterol.
- Smoking: Contributes to the formation and acceleration of atheromatous plaques.
- Diabetes Mellitus: Especially poorly controlled, leads to damage of the arterial wall.
- Obesity: Often associated with diabetes, hypertension, and high lipid levels.
- Physical Inactivity: Contributes to conditions like hypertension, obesity, and diabetes.
- Age: The risk increases with age as the arteries naturally become less flexible.
### Pathogenesis:
The development of atherosclerosis involves:
1. Endothelial Injury: Caused by factors like hypertension, smoking, hyperlipidemia, and diabetes, leading to a dysfunction in the endothelial lining of arteries.
2. Lipid Accumulation: LDL cholesterol under the endothelium gets oxidized, triggering an inflammatory response.
3. Inflammation: Attracts leukocytes (especially monocytes, which become macrophages) that attempt to phagocytose the oxidized LDL, forming foam cells and fatty streaks on the arterial walls.
4. Plaque Formation: Foam cells, together with smooth muscle cell proliferation, collagen, and extracellular matrix, contribute to atheroma (plaque) development. A fibrous cap develops over the plaque.
5. Plaque Progression and Complications: Plaques can become unstable, rupture, and form a thrombus, potentially leading to acute cardiovascular events.
### Clinical Picture and Dependence on Predominant Localization:
Coronary Arteries:
- Can lead to coronary artery disease (CAD), angina pectoris, myocardial infarction, and sudden cardiac death.
Carotid Arteries:
- Plaques in these arteries can cause transient ischemic attacks (TIAs) or strokes.
Peripheral Arteries:
- Atherosclerosis in the legs and arms can lead to peripheral artery disease (PAD), characterized by pain and fatigue in the limbs, particularly during exercise.
Aorta:
- Plaque in the aorta can lead to aneurysms and chronic kidney disease if renal arteries are affected.
### Features:
The clinical manifestations of atherosclerosis depend on the specific arteries involved and the extent of obstructed blood flow. Initially, atherosclerosis might be asymptomatic until significant artery narrowing or a plaque rupture occurs, leading to various complications like chest pain, stroke, or leg pain during exertion. The risk and severity of symptoms can be significantly influenced by lifestyle factors, management of comorbid conditions, and genetic predisposition.
- Atherosclerosis. Treatment and prophylaxis
Treatment and prevention of atherosclerosis aim to reduce risk factors, slow the progression of the disease, and prevent cardiovascular events such as heart attack and stroke. Management involves a combination of lifestyle modifications and medications.
### Lifestyle Modifications:
1. Diet: Adopting a heart-healthy diet low in saturated fats, trans fats, cholesterol, and sodium while rich in fruits, vegetables, whole grains, and omega-3 fatty acids.
2. Exercise: Regular physical activity, aiming for at least 150 minutes of moderate-intensity aerobic exercise per week.
3. Weight Management: Achieving and maintaining a healthy weight.
4. Smoking Cessation: Quitting smoking and avoiding secondhand smoke.
5. Alcohol: Limiting alcohol intake.
### Medications:
The choice of medication often depends on the individual’s overall risk of cardiovascular disease, existing conditions like hypertension or diabetes, and the presence of specific symptoms or complications associated with atherosclerosis.
1. Statins: Reduce LDL cholesterol and have a protective effect against cardiovascular events.
- Examples: Atorvastatin, Simvastatin, Rosuvastatin
2. Antiplatelets: Prevent the formation of blood clots that can block arteries.
- Aspirin (usually in low doses for prophylactic use) or Clopidogrel for those who are aspirin intolerant.
3. Angiotensin-converting enzyme (ACE) inhibitors: Lower blood pressure and have protective effects on the heart and kidneys.
- Examples: Lisinopril, Enalapril
4. Angiotensin II Receptor Blockers (ARBs): Also lower blood pressure and protect the heart and kidneys, used as an alternative to ACE inhibitors.
- Examples: Losartan, Valsartan
5. Beta-blockers: Reduce blood pressure and heart rate, can be beneficial post-myocardial infarction.
- Examples: Metoprolol, Atenolol
6. Calcium Channel Blockers: Lower blood pressure and reduce the workload on the heart.
- Examples: Amlodipine, Diltiazem
7. Antihypertensives: Various other medications may be used to control high blood pressure.
8. Antidiabetic medications: Control blood sugar in patients with diabetes, as high blood sugar levels can exacerbate atherosclerosis.
- Examples: Metformin, insulin, and SGLT2 inhibitors (e.g., Empagliflozin)
### Prophylaxis (Prevention):
Preventative measures focus on controlling risk factors:
- Regular health check-ups for monitoring blood pressure, cholesterol levels, and blood sugar.
- Lifestyle modifications as mentioned above.
- Vaccinations as appropriate (e.g., influenza vaccine, as influenza can be a risk factor for myocardial infarction in vulnerable individuals).
- Coronary heart disease: definition, social significance, risk factors, classification, formulation
of diagnosis.
Coronary heart disease (CHD), also known as coronary artery disease (CAD), is a condition characterized by the narrowing or blockage of the coronary arteries, the blood vessels that supply oxygen and nutrients to the heart muscle. This primarily results from atherosclerosis, the buildup of plaque within the arterial walls, leading to reduced blood flow to the heart. It can manifest as various clinical conditions, including angina pectoris, myocardial infarction (heart attack), and sudden cardiac death.
### Social Significance:
CHD holds significant social and healthcare implications due to its prevalence, morbidity, mortality, and the economic burden it imposes. It is one of the leading causes of death globally. The high prevalence of CHD contributes to substantial healthcare costs, including long-term management of chronic conditions, hospitalizations for acute events, and the need for surgeries or procedures like coronary artery bypass grafting (CABG) or percutaneous coronary intervention (PCI). Furthermore, CHD impacts patients’ quality of life, leading to disability and limiting daily activities.
### Risk Factors:
Risk factors for CHD are divided into modifiable and non-modifiable categories.
- Modifiable Risk Factors:
- Hyperlipidemia (elevated levels of cholesterol and triglycerides)
- Hypertension
- Smoking
- Diabetes mellitus
- Obesity
- Sedentary lifestyle
- Unhealthy diet
- Excessive alcohol consumption
- Non-Modifiable Risk Factors:
- Age (risk increases with age)
- Gender (higher risk in men and post-menopausal women)
- Family history of CHD
- Genetic predisposition
### Classification:
CHD is classified based on its pathophysiology, clinical presentation, and the results of diagnostic tests. Common classifications include:
1- Stable Angina: Chest pain or discomfort that usually occurs with effort or stress and follows a predictable pattern.
2- Unstable Angina: A more serious condition where chest pain occurs more frequently, even at rest, and with increasing severity.
3- Myocardial Infarction (Heart Attack): Occurs when blood flow to a part of the heart is blocked for an extended period, causing damage or death to part of the heart muscle.
4- Sudden Cardiac Death: Results from an abrupt loss of heart function.
### Formulation of Diagnosis:
The diagnosis of CHD typically involves a combination of clinical assessment, imaging tests, and laboratory investigations:
- Clinical Assessment: Includes a thorough history and physical examination, focusing on cardiovascular risk factors and symptoms.
- Electrocardiogram (ECG): Detects heart rhythm, signs of ischemia, or evidence of a previous or ongoing heart attack.
- Echocardiography: Assesses heart function and structure.
- Exercise Stress Test: Evaluates how the heart responds to physical activity.
- Coronary Angiography: A specialized X-ray test that uses contrast dyes to visualize blood flow through the coronary arteries.
- Blood Tests: Assess levels of cardiac biomarkers (e.g., troponins), lipids, and other factors.
- CHD: stable angina pectoris. Clinical singes, diagnosis, classification, treatment, prevention
Stable angina pectoris is a clinical syndrome characterized by chest pain or discomfort that typically occurs with effort or emotional stress and is relieved by rest or nitroglycerin. It signifies a mismatch between the oxygen demand of the heart muscle and the oxygen supply due to narrowed coronary arteries, usually resulting from atherosclerosis.
Clinical Signs:
- Chest pain or discomfort described often as pressure, squeezing, fullness, or pain.
- Pain may radiate to arms, shoulder, neck, jaw, or back.
- Dyspnea or shortness of breath.
- Indigestion or heartburn-like sensation.
- Symptoms usually last a short period and are relieved by rest or nitroglycerin.
Diagnosis:
The diagnosis of stable angina involves a combination of clinical evaluation, imaging tests, and other diagnostic procedures:
- Clinical history and physical examination are essential for identifying the characteristic features of angina.
- Electrocardiogram (ECG) may show abnormalities, particularly during pain or stress testing.
- Exercise stress test (Treadmill test) to detect ischemia and evaluate functional cardiovascular capacity.
- Echocardiography can assess cardiac function.
- Coronary angiography is the gold standard for delineating the coronary anatomy and the extent of coronary artery disease.
### Classification:
Stable angina is often classified according to the Canadian Cardiovascular Society grading system based on the severity and limitation it imposes on physical activity:
- Grade I: Angina only during strenuous or prolonged physical activity.
- Grade II: Slight limitation, with angina occurring on walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, under emotional stress, or only during the first few hours after awakening.
- Grade III: Marked limitation of ordinary physical activity, with angina occurring on walking one to two blocks on the level or climbing one flight of stairs at a normal pace.
- Grade IV: Inability to carry on any physical activity without discomfort – anginal symptoms may be present at rest.
### Treatment:
Treatment aims to reduce the frequency of angina attacks and prevent CHD complications. It includes lifestyle modifications, medications, and potentially revascularization procedures.
- Lifestyle Modifications: Such as smoking cessation, regular physical activity, weight management, and healthy diet.
- Medications:
- Nitroglycerin: For immediate relief of angina symptoms.
- Beta-blockers: e.g., Atenolol, Metoprolol, to reduce heart rate and cardiac workload.
- Calcium Channel Blockers: e.g., Amlodipine, Diltiazem, to relax and widen blood vessels, improving blood flow.
- ACE Inhibitors: e.g., Ramipril, Lisinopril, particularly beneficial for patients with high blood pressure or heart failure.
- Antiplatelet agents: e.g., Aspirin, Clopidogrel, to prevent blood clots.
- Statins: e.g., Atorvastatin, Simvastatin, to lower cholesterol and stabilize plaques.
- Revascularization Procedures: Such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) for selected patients.
### Prevention:
Preventing stable angina involves managing risk factors for CHD:
- Adhering to a heart-healthy lifestyle.
- Regular physical activity.
- Maintaining healthy blood pressure, cholesterol, and glucose levels.
- Avoiding tobacco products and limiting alcohol intake.
- Periodic health screenings for early identification and management of risk factors.
- CHD: unstable angina pectoris. Etiology, pathogenesis, classification, clinical singes,
diagnosis, treatment. The concept of acute coronary syndrome.
Unstable angina pectoris represents a critical and unpredictable condition characterized by new-onset angina, angina that occurs at rest or with minimal exertion, or angina of increasing severity or frequency. It falls under the umbrella of acute coronary syndrome (ACS), which also includes myocardial infarction (MI). Unstable angina is distinguished from MI primarily by the absence of detectable levels of cardiac biomarkers, indicative of heart muscle damage, which are present in MI.
The primary cause of unstable angina is disruption of an atherosclerotic plaque in a coronary artery, leading to partial or transient complete occlusion of the vessel by a thrombus (blood clot). This results in reduced blood flow to the myocardium (heart muscle), causing ischemia (insufficient oxygen) and anginal pain. Risk factors for plaque disruption include high blood cholesterol levels, smoking, high blood pressure, diabetes, and a sedentary lifestyle.
### Classification:
Unstable angina is part of the acute coronary syndrome and is classified based on clinical presentation, ECG findings, and cardiac biomarker levels. It can be considered a condition between stable angina and myocardial infarction.
### Clinical Signs:
- New onset of severe angina or a significant change in the pattern of previously stable angina.
- Angina that occurs at rest or with minimal exertion.
- Angina lasting longer than 20 minutes.
- Angina that is not relieved by rest or nitroglycerin.
- Possible accompanying symptoms such as dyspnea, diaphoresis (sweating), nausea, or lightheadedness.
### Diagnosis:
The diagnosis of unstable angina involves clinical assessment, ECG, and blood tests to detect cardiac biomarkers:
- Electrocardiogram (ECG) may show new or worsening ischemic changes, such as ST-segment depression or transient ST-segment elevation.
- Blood Tests: Cardiac biomarkers (e.g., troponins) are used to differentiate unstable angina from myocardial infarction. In unstable angina, these markers remain within their normal range.
- Coronary Angiography may be performed to identify the specific coronary artery lesions and guide further treatment.
### Treatment:
Immediate treatment focuses on relieving ischemia, preventing myocardial damage, and reducing the risk of MI.
- Medications:
- Antiplatelet Agents: Aspirin and clopidogrel to prevent thrombus formation.
- Anticoagulants: Such as heparin or low molecular weight heparin to prevent further clot formation.
- Nitrates: To relieve chest pain and improve coronary blood flow.
- Beta-blockers: To reduce myocardial oxygen demand by lowering heart rate and blood pressure.
- ACE Inhibitors: Especially in patients with certain risk factors like hypertension, diabetes, or heart failure.
- Statins: To stabilize plaques and reduce cholesterol levels.
- Revascularization Procedures: Such as percutaneous coronary intervention (PCI) with stent placement or coronary artery bypass grafting (CABG) may be indicated based on the results of coronary angiography.
- Myocardial infarction. Etiology, pathogenesis, classification, clinical singes, diagnosis (electrocardiographic and laboratory changes).
Myocardial infarction (MI), commonly known as a heart attack, is a medical condition that occurs when blood flow to a part of the heart muscle is abruptly cut off, causing tissue damage or death to that part of the heart muscle due to lack of oxygen. This is most often caused by obstruction of the coronary arteries due to plaque rupture and subsequent thrombus (blood clot) formation.
### Etiology:
The primary cause of MI is coronary artery disease (CAD), resulting from:
- Atherosclerosis: Buildup of fatty plaques in the coronary arteries.
- Plaque rupture: Leading to thrombosis and artery occlusion.
- Spasm of a coronary artery.
Other contributing factors include high blood pressure, high cholesterol levels, smoking, diabetes, obesity, sedentary lifestyle, and genetic predisposition.
### Pathogenesis:
The basis of MI is the prolonged ischemia (lack of oxygen) and subsequent necrosis (death) of myocardial (heart muscle) tissue. This process begins with the rupture of an atherosclerotic plaque, followed by platelet aggregation and thrombus formation, resulting in complete or partial occlusion of a coronary artery.
Classification:
MI can be classified based on ECG findings and blood biomarkers:
- ST-segment elevation MI (STEMI): Characterized by elevation in the ST segment on ECG, indicating a full thickness (transmural) myocardial injury.
- Non-ST-segment elevation MI (NSTEMI): Involves non-transmural myocardial injury, with no ST-segment elevation but may have ST-segment depression or T-wave inversion.
### Clinical Signs:
- Severe chest pain, often radiating to the left arm, shoulder, neck, jaw, or back. The pain is typically not relieved by rest or nitroglycerin.
- Sweating (diaphoresis), nausea, vomiting, breathlessness (dyspnea), and anxiety.
- Sometimes, especially in the elderly, women, or people with diabetes, the presentation can be atypical, such as sudden onset of shortness of breath, fainting (syncope), or confusion.
### Diagnosis:
#### Electrocardiographic Changes:
- STEMI: Elevation of the ST segment in consecutive ECG leads corresponding to the area of the heart affected.
- NSTEMI: There might be ST-segment depression, T-wave inversion, or sometimes no changes.
#### Laboratory Changes:
- Cardiac biomarkers are central to diagnosing MI. Troponins (I and T), which are proteins released into the blood from damaged heart muscle, are the most sensitive and specific markers.
- Creatine kinase-MB (CK-MB) is also used but is less specific than troponins.
- Myoglobin is an early marker but lacks specificity.
- Myocardial infarction: clinical singes, diagnosis and treatment. Outcomes of myocardial
infarction.
Myocardial infarction (MI), commonly known as a heart attack, is a medical condition that occurs when blood flow to a part of the heart is blocked for a long enough time that part of the heart muscle is damaged or dies. It is a major component of the broader category of acute coronary syndromes.
Clinical Signs:
- Chest pain or discomfort: Often described as pressure, squeezing, fullness, or pain in the center or left side of the chest that can be mild or severe and can last for more than a few minutes or go away and come back.
- Shortness of breath: This may occur with or before chest discomfort.
- Symptoms in other areas of the upper body: Symptoms can include pain or discomfort in one or both arms, the back, neck, jaw, or stomach.
- Other possible symptoms: Breaking out in a cold sweat, nausea, lightheadedness, or feeling dizzy.
### Diagnosis:
- Electrocardiogram (ECG or EKG): The ECG can identify abnormal heart rhythms, areas of damage, and the part of the heart that’s affected. Specific patterns such as ST-segment elevation, T-wave inversion, or the presence of new Q waves can indicate a myocardial infarction.
- Laboratory tests: Blood tests are used to detect substances typically released into the blood when heart muscle has been damaged. The most common and specific markers are cardiac troponins (troponin T and troponin I).
### Treatment:
Immediate treatment is crucial for myocardial infarction and aims to restore blood flow to the heart and reduce heart muscle damage.
- Medications:
- Aspirin: Reduces blood clotting, thereby helping maintain blood flow through narrowed heart arteries.
- Thrombolytics (clot busters): Help dissolve a blood clot that’s blocking blood flow to the heart.
- Antiplatelet agents: Such as clopidogrel (Plavix) to prevent new clots.
- Anticoagulants: Like heparin, to prevent blood clots from enlarging.
- Beta-blockers: Such as atenolol or metoprolol, decrease heart rate and blood pressure, reducing the heart’s demand for oxygen.
- ACE inhibitors: Like lisinopril or enalapril, reduce the heart’s workload and can improve recovery.
- Statins: Like atorvastatin, to lower cholesterol.
- Procedures:
- Coronary angioplasty and stenting: A thin tube is threaded through a blood vessel to the blockage site in the heart, where a stent is often placed to keep the artery open.
- Coronary artery bypass surgery: Involves using blood vessels from another part of the body to bypass the blocked artery.
### Outcomes of Myocardial Infarction:
- Short-term complications can include arrhythmias, heart failure, cardiogenic shock, and in some cases, sudden death.
- Long-term outcomes vary greatly depending on the extent of the heart damage, the success of treatment, and changes in lifestyle or underlying conditions post-MI. Some people recover well, although they may need medication and to follow rehabilitation programs. Others may experience chronic heart failure or other significant heart-related disabilities.
- Rehabilitation involves structured exercise, lifestyle modification, and possibly psychological support, which plays a crucial role in recovery and reducing the risk of future cardiac events.
- Classification of CHD. Myocardial infarction: atypical forms, Differential diagnosis of myocardial infarction. Prevention of myocardial infarction.
Coronary Heart Disease (CHD), also known as coronary artery disease (CAD), involves the reduction of blood flow to the heart muscle due to the build-up of plaque in the coronary arteries. It can lead to several heart conditions, including myocardial infarction (MI), angina pectoris, heart failure, and irregular heartbeats (arrhythmias).
Classification of CHD:
CHD is classified based on the severity, symptoms, and how much they impede daily life:
1. Asymptomatic: No symptoms are apparent, but atherosclerosis is present.
2. Angina Pectoris: Classified further into stable angina (predictable pain and triggered by physical activity or stress) and unstable angina (more unpredictable, severe, and can occur at rest).
3. Myocardial Infarction (MI): Can be a STEMI (ST-elevation MI) where there is significant damage to the heart’s muscle, or a NSTEMI (non-ST-elevation MI) which typically indicates less damage.
4. Sudden Cardiac Death: Can occur as the first manifestation of CHD.
5. Chronic Heart Failure: Develops as a result of CHD where the heart’s function is inadequate to meet the body’s needs.
6. Arrhythmias: Abnormal heart rhythms occurring as a consequence of CHD.
### Myocardial Infarction: Atypical Forms
Atypical forms of MI, also known as silent myocardial infarctions or silent ischemia, lack the classic symptoms of MI. Individuals may experience minimal discomfort or symptoms such as fatigue, flu-like symptoms, or abdominal discomfort, making it difficult to diagnose without further investigation.
### Differential Diagnosis of Myocardial Infarction:
Conditions that might mimic or need to be differentiated from MI include:
- Angina pectoris.
- Peptic ulcer disease or gastritis.
- Acute pancreatitis.
- Pulmonary embolism.
- Acute pericarditis.
- Costochondritis.
- Aortic dissection.
Diagnostic tests, such as an electrocardiogram (ECG) and blood tests for cardiac biomarkers (troponins), are essential for distinguishing MI from these conditions.
### Prevention of Myocardial Infarction:
Prevention focuses on managing risk factors and making lifestyle changes to prevent the onset of CHD or to manage existing conditions.
1. Lifestyle modifications: This includes stopping smoking, adopting a healthy diet rich in fruits, vegetables, and whole grains, regular physical activity, maintaining a healthy weight, and managing stress.
2. Management of risk factors: Controlling high blood pressure, high cholesterol, and diabetes through diet, lifestyle changes, and medication as needed.
3. Medications: Use of medications such as aspirin (in certain individuals), statins to lower cholesterol, and medications to control hypertension and diabetes.
4. Regular health screenings: For blood pressure, lipid profile, and diabetes to catch and manage these conditions early.
5. Education and awareness: Understanding the signs and symptoms of heart problems to ensure early detection and treatment.
- Arterial hypertension. Definition. Social significance. Risk factors. Etiology and pathogenesis.
Arterial hypertension, commonly known as high blood pressure, is a condition characterized by the persistent elevation of blood pressure in the arteries. It is one of the most prevalent cardiovascular diseases worldwide, affecting millions of people.
Definition:
The American Heart Association and other medical organizations define hypertension as a condition where blood pressure readings consistently exceed 130 mm Hg systolic (the higher number) or 80 mm Hg diastolic (the lower number) on two or more occasions.
Social Significance:
Hypertension is a significant public health issue due to its high prevalence and the associated risks of cardiovascular, cerebrovascular, and renal diseases, which are leading causes of morbidity and mortality globally. It places a substantial burden on healthcare systems due to the cost of treatments, medications, and managing complications. Moreover, it affects the quality of life and productivity of individuals, contributing to social and economic challenges.
### Risk Factors:
There are several risk factors associated with the development of hypertension, including:
- Non-modifiable risk factors: Age, heredity, and race or ethnicity.
- Modifiable risk factors: Unhealthy diet (high in salt, saturated fats, and trans fats), physical inactivity, obesity, tobacco use, excessive alcohol consumption, and stress.
- Medical conditions: Diabetes, kidney disease, sleep apnea, and lipid abnormalities.
### Etiology:
Hypertension can be classified into two main types based on its etiology:
1. Primary (essential) hypertension: This type has no identifiable cause and develops gradually over many years. It accounts for about 90-95% of hypertension cases.
2. Secondary hypertension: This type is caused by an underlying condition. It tends to appear suddenly and cause higher blood pressure compared to primary hypertension. Causes include kidney disease, adrenal gland tumors, certain congenital heart defects, certain medications, and illegal drugs.
### Pathogenesis:
The exact mechanisms responsible for primary hypertension are not completely understood but involve a complex interaction of genetic, environmental, and physiological factors. The pathogenesis involves:
- Renin-Angiotensin-Aldosterone System (RAAS) dysfunction: Leads to inappropriate retention of salt and water by the kidneys, increased peripheral resistance, and changes in the structure of the heart and blood vessels.
- Sympathetic Nervous System Overactivity: Increases heart rate and causes the blood vessels to narrow (vasoconstriction).
- Endothelial Dysfunction: Reduces the production of vasodilators like nitric oxide, contributing to the tightening of blood vessels.
–Secondary hypertension’s pathogenesis relates directly to the underlying causes, such as kidney dysfunction affecting the body’s ability to balance fluid and salt, leading to increased blood volume and high blood pressure.
- Arterial hypertension. Classification of blood pressure levels. Criteria of risk stratification.
Division of patients according to the degree of risk. Determination of hypertensive stage.
Classification of Blood Pressure Levels:
The American Heart Association (AHA) and the American College of Cardiology (ACC) provide guidelines for blood pressure classification:
- Normal: Systolic BP less than 120 mm Hg and Diastolic BP less than 80 mm Hg.
- Elevated: Systolic BP 120-129 mm Hg and Diastolic BP less than 80 mm Hg.
- Stage 1 Hypertension: Systolic BP 130-139 mm Hg or Diastolic BP 80-89 mm Hg.
- Stage 2 Hypertension: Systolic BP at least 140 mm Hg or Diastolic BP at least 90 mm Hg.
- Hypertensive Crisis: Systolic BP over 180 mm Hg and/or Diastolic BP over 120 mm Hg.
### Criteria for Risk Stratification
Risk stratification in hypertension considers multiple factors beyond BP levels to estimate the overall risk of cardiovascular disease (CVD). These factors include: - Presence or absence of CVD or target organ damage (such as heart failure, left ventricular hypertrophy, chronic kidney disease).
- Risk factors like age (men older than 55, women older than 65), smoking, dyslipidemia, diabetes mellitus, and family history of premature CVD.
- Lifestyle factors and social determinants of health.
### Division of Patients According to the Degree of Risk:
Based on these factors, individuals with hypertension can be categorized into different risk groups: - Low Risk: No CVD, no target organ damage, and fewer than 3 primary risk factors.
- Moderate Risk: No CVD, no target organ damage, but 3 or more primary risk factors.
- High Risk: One or more of the following: CVD, target organ damage, diabetes, or stage 2 hypertension.
- Very High Risk: Advanced stages of diseases (e.g., multiple major risk factors, severe or symptomatic target organ damage, cardiovascular disease events).
### Determination of Hypertensive Stage:
Determining the hypertensive stage involves measuring BP on at least two separate occasions and evaluating for the presence of other risk factors or target organ damage. This information guides the approach to treatment, such as lifestyle modifications for lower risk stages or the addition of antihypertensive medications in higher stages, considering the overall CVD risk. - Initial Stage: Elevated or Stage 1 hypertension without other risk factors might initially require lifestyle modification.
- Advanced Stages: Stage 2 hypertension or any stage with multiple risk factors or target organ damage necessitates more aggressive interventions, including pharmacotherapy.
