Endocrine Disorders: Focus on Diabetes Mellitus Revision PDF

**Endocrine Disorders: Focus on Diabetes Mellitus** **Session Objectives** - **Understand the function of the pancreas**: - The pancreas plays a crucial role in **glucose regulation**. - **Discuss the causes, pathophysiology, and clinical manifestations of diabetes mellitus**:...

**Endocrine Disorders: Focus on Diabetes Mellitus** **Session Objectives** - **Understand the function of the pancreas**: - The pancreas plays a crucial role in **glucose regulation**. - **Discuss the causes, pathophysiology, and clinical manifestations of diabetes mellitus**: - **Type 1 Diabetes Mellitus**: - An autoimmune condition leading to the destruction of insulin-producing beta cells in the pancreas. - Results in **absolute insulin deficiency**. - **Type 2 Diabetes Mellitus**: - Characterized by insulin resistance and relative insulin deficiency. - Often associated with obesity and lifestyle factors. - **Compare and contrast the pathophysiology and management of Type 1 and Type 2 diabetes mellitus**: - **Pathophysiology**: - Type 1: Autoimmune destruction of beta cells. - Type 2: Insulin resistance and progressive beta-cell dysfunction. - **Management**: - Type 1: Requires **insulin therapy** for survival. - Type 2: Managed through lifestyle modifications, oral medications, and possibly insulin. **Endocrine System Overview** - The **endocrine pancreas** is integral to the regulation of blood glucose levels. - It secretes hormones such as **insulin** and **glucagon** to maintain homeostasis. Type 1 diabetes mellitus is characterised as an autoimmune condition cause absolute **insulin deficiency** due to beta cell destruction Management of T1DM requires insulin therapy for **insulin supplementation** T2DM is typically managed through lifestyle changes, oral medication, and possibly **supplemental insulin** T2DM differs from type 1 in that it involves insulin resistance and **relative deficiency**, often linked to **obesity** and **lifestyle** The function of the pancreas in relation to diabetes mellitus is to regulate glucose levels by secreting hormones like **insulin** and glucagon The primary function of the pancreas is to **monitor BGL and release regulatory hormones (insulin and glucagon)** T1DM is characterized by **an autoimmune destruction of insulin-producing beta cells** **Insulin resistance and relative insulin deficiency** is a key feature of T2DM T1DM **requires insulin therapy for survival** Management of T2DM differs from type 1 as it **involves dietary and lifestyle changes** Glucagon **maintains blood glucose levels during fasting** **Elevated BGLs** are a notable clinical manifestation of diabetes mellitus **Glucose, Insulin, and Diabetes Mellitus** **Glucose and Insulin in Metabolism** - **Glucose**: A primary energy source for the body, crucial for cellular metabolism. - **Insulin**: A hormone produced by the pancreas that regulates blood glucose levels by facilitating the uptake of glucose into cells. **Normal Blood Glucose Levels** - **Fasting Blood Glucose Level (BGL) Range**: - Normal range is **4 - 6 mmol/L**. **Diabetes Mellitus** - **Definition**: - A group of metabolic diseases characterized by **hyperglycemia** due to defects in **insulin secretion**, **insulin action**, or both. - **Chronic Nature**: - Diabetes is a **chronic and progressive disease** that can lead to severe long-term complications if poorly managed. **Complications of Poorly Managed Diabetes** - **Cardiovascular Disease (CV Disease)** - **Kidney Failure** - **Blindness** - **Depression** **Types of Diabetes Mellitus** 1. **Type 1 Diabetes**: - Results from **beta cell destruction** leading to severe or absolute insulin deficiency. - Characterized by **chronic hyperglycemia**. 2. **Type 2 Diabetes**: - Caused by **insulin resistance** at target tissues and a relative insulin deficiency. - Also characterized by **hyperglycemia**. 3. **Gestational Diabetes**: - Development of **glucose intolerance** during pregnancy. - Constitutes **10% of diabetes cases**. **Prevalence of Diabetes Types** - **Type 1 Diabetes**: Constitutes **approximately 10%** of cases. - **Type 2 Diabetes**: Constitutes **approximately 85%** of cases. - **Risk of Progression**: Individuals with gestational diabetes have a risk of progression to type 2 diabetes of up to **60%**. Gestational diabetes constitutes of approximately **10%** of diabetes cases Diabetes mellitus is characterized by **elevated BGLs** from defects in insulin secretion Normal fasting BGLs range from **4-6mmol/L** Glucose serves as a primary **energy source** crucial for cellular metabolism T1DM is characterized by **autoimmune destruction of beta cells** leading to insulin deficiency Diabetes mellitus is considered **a chronic and progressive disease** **Cardiovascular disease** is associated with poor management of diabetes mellitus T2DM is caused by **insulin resistance and relative insulin deficiency** **Glucose intolerance during pregnancy** characterizes gestational diabetes **T2DM** makes up 85% of diabetes cases The risk of progression to T2DM for individuals with gestational diabetes is **approximately 60%** **Epidemiology and Causes of Diabetes** **Global Epidemiology** - **Prevalence**: Approximately **422 million adults** worldwide are affected by diabetes (WHO, 2021). - **Mortality**: Diabetes is the **seventh leading cause** of death and morbidity globally (WHO, 2021). **Epidemiology in Australia** - **Prevalence**: More than **1.2 million Australians** have diabetes (AIHW, 2020). - **Mortality Impact**: Diabetes accounted for **10% of all deaths** in Australia in 2017 (AIHW, 2018). **Populations at Risk** - **Indigenous Australians**: **One in five** Aboriginal and Torres Strait Islander (ATSI) individuals over **25 years** have diabetes (Sainsbury et al, 2018). - **Rapid Growth**: The prevalence of diabetes is increasing rapidly in **low- and middle-income countries** (WHO, 2019). - **At-Risk Groups**: Higher rates of diabetes are observed in specific population groups, including: - **Pacific Islanders** - **Southeast Asians** - **Middle Eastern populations** - **Southern and Eastern Europeans** - **Contributing Factors**: - **Obesity** - Living in **remote or rural communities** **Causes of Diabetes** **Type 1 Diabetes** - **Mechanism**: Characterized by **autoimmune destruction** of the **beta cells** in the pancreas. - **Destruction Level**: **80-90%** of beta cells are destroyed before acute symptoms manifest. - **Contributing Factors**: - **Genetic susceptibility** - **Environmental factors**: Includes exposure to certain **drugs** and **viruses** that may trigger the autoimmune response. **Other Forms of Diabetes** - **Idiopathic Diabetes**: Involves beta cell destruction without an autoimmune response. - **Non-immune Mediated Diabetes**: Can occur secondary to other conditions, such as **pancreatitis**. The global prevalence of diabetes according to WHO is approximately **422 million** in 2021 In 2017, **10%** of all deaths in Australia were attributed to diabetes The populations that have higher rates of diabetes include **pacific islanders, southeast Asians, middle eastern populations, and southern and eastern Europeans** The contributing factors to T1DM include **genetic susceptibility and environmental factors** such as exposure to certain drugs and viruses T1DM is characterised by **autoimmune destruction** of beta cells in the pancreas Globally, diabetes mellitus is the **7^th^ leading cause of death** Mor than **1.2 million Australians** have diabetes **1 in 5** ATSI people over 25 have diabetes in Australia Roughly **80-90% of beta cells** are autoimmune destructed before T1DM acute symptoms occur Idiopathic diabetes is defined by **beta cell destruction without an autoimmune response** Non-immune mediated diabetes is **secondary to other conditions like pancreatitis** **Pathophysiology and Management of Type 1 Diabetes Mellitus** **Pathophysiology of Type 1 Diabetes Mellitus** - **Genetic Factors**: - **HLA-linked genes** play a significant role in the predisposition to Type 1 DM. - **Viral Infections**: - Certain viral infections can contribute to the damage of beta cells in the pancreas. - **Beta Cell Damage**: - Other factors can lead to damage of beta cells, resulting in an **immune response** against these cells. - **Consequences of Beta Cell Destruction**: - **Lack of Insulin Release**: This leads to **hyperglycemia**. - **GLUT-4 Activation**: GLUT-4 transporters are not activated, preventing glucose uptake by cells. - **Liver Glucose Release**: The liver continues to release glucose into the bloodstream. - **Glucagon Release**: Increased glucagon levels further exacerbate hyperglycemia. **Clinical Manifestations** - **Initial Signs and Symptoms**: - **Polyphagia**: Increased hunger. - **Polyuria**: Increased urination. - **Polydipsia**: Increased thirst. - **Weight Loss**: Unintentional weight loss. - **Fatigue**: General tiredness. - **Confusion**: Altered mental status. - **Late Signs and Symptoms**: - **Nausea and Vomiting**: Gastrointestinal distress. - **Abdominal Pain**: Discomfort in the abdominal area. - **Tachycardia**: Increased heart rate. - **Tachypnea**: Rapid breathing. - **Ketonic Breath**: Fruity odor due to ketone bodies. - **Metabolic Acidosis**: Acid-base imbalance due to ketone accumulation. - **Seizures**: Neurological disturbances. - **Coma**: Severe alteration in consciousness. - **Blurred Vision**: Visual disturbances. **Treatment of Type 1 Diabetes Mellitus** - **Insulin Therapy**: - Insulin is the **only treatment option** for Type 1 DM. - It is a **protein-based molecule** that mimics physiological insulin levels. - **Insulin Regimen**: - Patients are placed on an insulin regimen tailored to their **age** and **lifestyle needs**. - Insulin preparations vary from **ultra-short** to **long-acting** formulations. - The **basal-bolus regimen** is often used for optimal insulin delivery. - **Mechanism of Action**: - Insulin facilitates glucose uptake and utilization in the body. - **Drug Interactions**: - Certain medications, such as **corticosteroids** and **ACE inhibitors**, can impact glycemic control and should be monitored. The consequence of **beta cell destruction** in T1DM is a lack of **insulin release**, which leads to **hyperglycaemia** and inadequate **glucose uptake** The primary treatment for T1DM is **supplemental insulin therapy**, which is the only treatment option for this condition Insulin **facilitates** glucose **uptake** and utilization in the body for the management of T1DM The primary genetic factors influencing T1DM are **HLA-linked genes**, which significantly predispose individuals to **T1DM** Common initial manifestation of T1DM include **polyphagia, polyuria, polydipsia**, weight loss, fatigue and confusion Viral infections **damage beta cells in the pancreas** -\> can lead to T1DM **Session Objectives** - **Understanding of Respiratory System**: - Gain a comprehensive understanding of the **anatomy** and **physiology** of the respiratory system. - **Regulation of Ventilation and Respiration**: - Explain the mechanisms involved in the regulation of **ventilation** and **respiration**. - **Lung Volumes and Spirometry**: - Understand the significance of measuring **lung volumes** and the clinical applications of **spirometry**. **Respiratory Anatomy** - **Key Structures to Identify**: - **Trachea**: The windpipe that conducts air to the lungs. - **Right and Left Main Bronchus**: The primary air passages that branch from the trachea into each lung. - **Mediastinum**: The central compartment of the thoracic cavity, containing the heart and other structures. - **Diaphragm**: The primary muscle involved in respiration, separating the thoracic and abdominal cavities. - **Visceral Pleura**: The membrane covering the lungs. - **Parietal Pleura**: The membrane lining the thoracic cavity. - **Pleural Space/Cavity**: The space between the visceral and parietal pleura, containing pleural fluid. - **Lung Bases**: The lower portions of the lungs. - **Lung Apices**: The uppermost portions of the lungs. The primary function of the diaphragm in the respiratory system is to facilitate **respiration** by separating the thoracic and abdominal cavities Spirometry plays a crucial role in **respiratory health** by measuring lung volumes for clinical assessment of respiratory function The primary air passages branching from the trachea are the **right** and **left** man bronchus The pleural space in the respiratory system is significant because it contains **pleural fluid**, which allows lung expansion and contraction during breathing The **mediastinum** compartment of the thoracic cavity contains the heart The **diaphragm** is primarily involved in breathing **Respiratory Anatomy and Regulation** **Respiratory Anatomy** - **Lung Apex**: The topmost part of the lung, important for understanding lung structure. - **Right Main Bronchus**: The bronchus that leads to the right lung; wider and more vertical than the left. - **Left Main Bronchus**: The bronchus that leads to the left lung; narrower and more horizontal. - **Trachea**: The windpipe that connects the larynx to the bronchi, allowing air passage to the lungs. - **Mediastinum**: The central compartment of the thoracic cavity, containing the heart, great vessels, and other structures. - **Diaphragm**: The primary muscle of respiration, separating the thoracic cavity from the abdominal cavity. - **Visceral Pleura**: The membrane covering the lungs, providing a smooth surface for lung movement. - **Parietal Pleura**: The membrane lining the thoracic cavity, providing protection and support to the lungs. - **Pleural Space/Cavity**: The space between the visceral and parietal pleura, containing pleural fluid to reduce friction during breathing. - **Lung Bases**: The lower parts of the lungs, where gas exchange occurs. **Regulation of Respiration** - **Purpose**: To maintain normal levels of *PO2* (partial pressure of oxygen) and *PCO2* (partial pressure of carbon dioxide) in arterial blood. **Central Controller** - **Respiratory Centre**: Located in the brain, specifically in the brain stem (pons and medulla) and the cerebral cortex, responsible for initiating and regulating the breathing process. **Effectors** - **Mechanical Regulation**: Involves the respiratory muscles, including: - **Diaphragm**: The main muscle for inhalation. - **Accessory Muscles**: Additional muscles that assist in breathing, especially during exertion. **Sensors** - **Chemical Regulation**: Involves chemoreceptors that monitor the chemical composition of blood: - **Chemoreceptors**: - **Central Chemoreceptors**: Sensitive to changes in pH of cerebrospinal fluid (CSF) and can maintain normal *PaCO2* levels. - **Peripheral Chemoreceptors**: Monitor arterial blood gases. - **Function**: - Chemoreceptors detect changes in *pH*, *PaCO2*, and *PaO2* of arterial blood. - If alveolar ventilation is inadequate, *PaCO2* rises, leading to increased *H+* concentration, which decreases pH. - This regulation helps maintain homeostasis in respiratory function. Central **chemoreceptors** monitor the **pH** of cerebrospinal fluid, while peripheral ones monitor **arterial blood gases** The right main bronchus if **wider** and more **vertical** compared with the left main bronchus, which is narrower and more horizontal The diaphragm is the primary muscle responsible for **inhalation** in **respiration** The respiratory centre is in the **brain stem** and the **cerebral cortex** The purpose of respiratory regulation is to maintain normal levels of **PO2** and **PCO2** in arterial blood. **Overview of Asthma** - **Asthma** is a chronic respiratory condition characterized by: - **Inflammation** of the airways. - **Bronchoconstriction**, leading to difficulty in breathing. - **Hyper-responsiveness** to various stimuli. **Pathophysiology of Asthma** - The pathophysiological mechanisms involved in asthma include: - **Airway Inflammation**: Caused by allergens, irritants, and infections. - **Bronchial Hyperreactivity**: Increased sensitivity of the airways to various stimuli. - **Airway Remodeling**: Structural changes in the airways due to chronic inflammation. **Clinical Manifestations** - Common symptoms of asthma include: - **Wheezing**: A high-pitched whistling sound during breathing. - **Shortness of Breath**: Difficulty in breathing, especially during physical activity. - **Chest Tightness**: A feeling of pressure or constriction in the chest. - **Coughing**: Often worse at night or early morning. **Diagnosis** - Diagnosis of asthma typically involves: - **Patient History**: Assessment of symptoms and triggers. - **Physical Examination**: Observing respiratory function. - **Pulmonary Function Tests**: Measuring airflow and lung capacity. **Management and Treatment** - Management strategies for asthma include: - **Medications**: - **Bronchodilators**: To relieve bronchospasm. - **Anti-inflammatory agents**: To reduce airway inflammation. - **Avoidance of Triggers**: Identifying and minimizing exposure to allergens and irritants. - **Patient Education**: Teaching patients about asthma management and action plans. **Conclusion** - Understanding asthma is crucial for effective nursing care and management of patients with respiratory disorders. **Airway inflammation, bronchial hyperactivity,** and **airway remodelling** are key mechanisms that contribute to the pathophysiology of **asthma** Common clinical manifestations of asthma include **wheezing, SOB,** chest tightness, and **coughing** Asthma is characterized by **airway inflammation, bronchoconstriction,** and **hyper-responsiveness** Asthma is typically diagnosed through patient **history,** physical **examination,** and pulmonary function **tests** Main management strategies for asthma include **medication,** avoidance of **triggers,** and patient **education** **Inflammation of the airways** causes bronchoconstriction in asthma Airway remodelling in asthma is a result of **chronic inflammation of the airways** **Exposure to pathogens** is a common trigger for patients with asthma Asthma is commonly diagnosed by **respiratory function tests** **Bronchodilators** are commonly used to relieve bronchospasms **Pathophysiology of Asthma** **Initial Exposure to Allergen** - **Allergen Exposure**: The process begins with the initial exposure to an allergen (antigen). - **Production of Specific IgE Antibodies**: The immune system produces **specific IgE antibodies** to target the allergen or foreign substance. - **Minimal Signs and Symptoms**: During this phase, there may be minimal signs and symptoms present. - **Binding to Mast Cells**: Once produced, these specific IgE antibodies bind to **mast cells** located within the lung tissue. **Re-exposure to Allergen** - **IgE Activation**: Upon re-exposure to the allergen, it binds to the previously formed IgE antibodies. - **Mast Cell Rupture**: This binding activates the IgE, leading to the rupture of the mast cells. - **Chemical Reactions**: The rupture triggers a series of **chemical reactions** that result in the signs and symptoms of asthma. **Allergen or Irritant Exposure** - **Injury and Inflammation**: Exposure to allergens or irritants leads to injury and inflammation in the lung tissue. - **Mast Cell Degranulation**: This process involves the degranulation of mast cells within the lung tissue. **Release of Chemical Mediators** - **Chemical Mediators Released**: - **Platelet Activating Factor** - **Leukotrienes** - **Prostaglandins** - **Histamine** - **Physiological Effects**: - **Vasodilation**: Widening of blood vessels. - **Increased Vascular Permeability**: Allows fluids to leak into surrounding tissues. - **Oedema of Airways**: Swelling of the airways due to fluid accumulation. - **Mucous Production**: Increased production of mucus in the airways. - **Bronchoconstriction**: Constriction of the bronchial muscles. - **Bronchospasms**: Sudden constriction of the bronchial muscles. - **Airway Obstruction**: Resulting from the combination of these effects. **Complications of Asthma** - **Status Asthmaticus**: A severe condition that can lead to potential death. - **Characteristics**: Onset is severe and progresses rapidly despite standard therapy. - **Unresponsive to Bronchodilators**: The condition does not improve with typical bronchodilator treatments. - **Critical Care Required**: Patients may require intensive medical care. - **Other Complications**: - **Respiratory Infection** - **Respiratory Failure** - **Atelectasis**: Collapse of part or all of a lung. - **Pneumothorax**: Presence of air in the pleural space. - **Cor Pulmonale**: Right heart failure due to lung disease. The initial immune response to allergen exposure in asthma involves the production of specific **IgE antibodies** targeting the **allergen** Complications associated with asthma include **respiratory infection, respiratory failure, atelectasis,** and **pneumothorax** Status asthmaticus is a severe **asthmatic condition** that is unresponsive to **bronchodilators**, requiring intensive medical care Upon re-exposure to an allergen, **IgE antibodies** bind to the allergen, activating **mast cells** and leading to their rupture The physiological effects of chemical mediators released during asthma include **vasodilation, increased vascular permeability,** airway **oedema, mucus production,** and **bronchoconstriction** **Histamine** causes airway swelling and/or oedema **Atelectasis** involves the collapse of a part of the lung **Pathophysiology of COPD** - **Noxious Stimuli**: - Primary cause is **smoke** exposure. - **Inflammatory Response**: - Abnormal and prolonged **inflammatory response** occurs in the lungs. - **Gas Exchange and Airflow**: - **Gas trapping** leads to **hyperinflation** of the lungs. - Results in **gas exchange abnormalities** and **airflow limitation**. - **Cellular Response**: - Increased presence of **neutrophils**, **macrophages**, and **lymphocytes**. - Release of **cytokines** contributes to inflammation. - **Lung Structure Changes**: - Breakdown of **lung parenchyma** and **enlargement of air spaces**. - **Destruction of alveolar wall** and **loss of elastic recoil**. - **Symptoms**: - **Dyspnoea** (shortness of breath). - **Cough** and **hypoxaemia** (low oxygen levels). - **Hypercapnia** (elevated carbon dioxide levels). - **Cor Pulmonale**: - Development of **cor pulmonale** (right-sided heart failure) due to lung disease. - **Systemic Effects**: - Symptoms include **fatigue** and **weight loss**. - **Chronic Inflammation**: - Continuous **bronchial irritation** and inflammation. - **Hypertrophy** and **hyperplasia** of goblet cells leading to **mucous hypersecretion**. - **Bronchial oedema** and **airway remodeling** (scarring). - Increased risk of **infections**. **Clinical Manifestations of COPD** - **Chronic Productive Cough**: - Persistent cough with sputum production. - **Dyspnoea**: - Difficulty in breathing, especially during exertion. - **Tachypnoea**: - Increased respiratory rate. - **Pursed Lip Breathing**: - A technique used to ease breathing. - **Wheezing**: - A high-pitched whistling sound during breathing. - **Chest Tightness**: - Sensation of constriction in the chest. - **Hypoxaemia**: - Low levels of oxygen in the blood. - **Cyanosis**: - Bluish discoloration of the skin due to low oxygen. - **Hypercapnia**: - Elevated levels of carbon dioxide in the blood. - **Fatigue**: - Generalized tiredness and lack of energy. - **Weight Loss**: - Unintentional loss of body weight. **Complications of COPD** - **Pulmonary Hypertension (PHT)**: - Increased blood pressure in the pulmonary arteries. - **Cor Pulmonale**: - Right-sided heart failure due to lung disease. - **Ischemic Heart Disease**: - Reduced blood supply to the heart muscle. - **Heart Failure**: - The heart\'s inability to pump effectively. - **Osteoporosis**: - Decreased bone density and increased fracture risk. COPD is characterized by **persistent respiratory symptoms** and airflow limitation due to airway or alveolar abnormalities The primary cause of COPD is **tobacco smoking** COPD is projected to become the **third** leading cause of death worldwide by 2030 Risk factors such as **age, gender,** and exposure to harmful substances contribute to the likelihood and severity of **COPD** Approximately **7.5%** of Australians aged over 40 are affected by COPD Patients with COPD are at greater risk of hospitalisation due to **increased co-morbidities** Common symptoms of COPD include **dyspnoea, cough, hypoxaemia,** and **hypercapnia** The primary cause of COPD is **smoke exposure** Gas trapping in COPD results in **hyperinflation,** which causes **gas exchange abnormalities** and **airflow limitation** Chronic inflammation and airway remodelling contribute to COPD by leading to **bronchial irritation,** and increased risk of **infection** Complications that can arise from COPD include **pulmonary hypertension, cor pulmonale,** and **ischaemic heart disease** **Destruction of alveolar walls** occurs in the lungs due to COPD **Fatigue** is a common side effect of COPD **Mucous hypersecretion** occurs in response to **bronchial irritation** Cyanosis **indicates lows oxygen levels in the blood** in COPD patients **Management of COPD** **Key Aspects of COPD Management** - **Smoking Cessation** - Essential for improving lung function and overall health. - **Nicotine Replacement** - Aids in reducing withdrawal symptoms and cravings during cessation. - **Risk Factor Reduction** - Focus on eliminating or minimizing exposure to environmental and lifestyle risk factors. - **Vaccination** - **Influenza and Pneumococcal Vaccination** - Important to reduce the risk of exacerbations in COPD patients. **Pharmacological Management** - **Bronchodilators** - **Beta Agonists** - Help relax airway muscles and improve airflow. - **Antimuscarinic Drugs** - Reduce bronchoconstriction and improve lung function. - **Corticosteroids** - Used to reduce inflammation in the airways. - **Combination Therapy** - Utilizes multiple medications to enhance treatment efficacy. **Non-Pharmacological Management** - **Pulmonary Rehabilitation** - Involves exercise and self-management interventions to improve quality of life. - **Long-Term Oxygen Therapy** - For patients with severe resting chronic hypoxemia. - **Oxygen Levels** - Aim to maintain SpO2 between **88 - 92%**. - **Non-Invasive Ventilation** - **CPAP and BIPAP** - Indicated for patients with severe chronic hypercapnia. **Rationale for Maintaining SpO2 Levels** - **Respiratory Drive Mechanisms** - Major drive for respiration originates from **central and peripheral chemoreceptors**. - In COPD, CO2 retention leads to consistently elevated levels, causing central chemoreceptors to become insensitive to CO2 changes. - **Hypoxia** stimulates peripheral chemoreceptors, which trigger ventilation. - Over-oxygenation can inhibit peripheral chemoreceptor stimulation. - **PaO2 Levels** - Must be \< 60 mmHg for peripheral chemoreceptors to influence ventilation, correlating to SpO2 levels of **88 - 92%**. **Life with COPD** - **Rehabilitation, Education, and Self-Management** - Essential for improving patient outcomes and quality of life. - **Activity Limitations** - Patients may experience restrictions in daily activities. - **Economic Impact** - COPD can lead to missed work and financial strain. - **Effects on Family Routines** - The disease can disrupt family dynamics and routines. - **Psychological Effects** - Patients may experience feelings of depression and anxiety. - **Impact on Sexual Activity** - COPD can affect intimate relationships and sexual health. Bronchodilators assist in managing COPD by relaxing airway muscles which **improves airflow** and reduces bronchoconstriction COPD patients may experience feelings of **depression** and **anxiety** due to their condition The target SpO2 levels for COPD patients receiving long-term oxygen therapy is between **88-92%** Antimuscarinic drugs **reduce bronchoconstriction and enhance lung function** Corticosteroids **reduced inflammation of the airway** Non-invasive ventilation is indicated for **patients with severe chronic hypercapnia** pH is significant in ABG analysis as it measures **acidity** of blood, indicating **H+ concentration** The normal range for arterial pH is **7.35-7.45** A negative **base excess** value indicates a **HCO3 deficit,** suggesting excess acidity The initial steps to analyse an ABG include analysing the **pH,** then the **PaCO2** and **HCO3** Compensation in ABG analysis is indicated if **PaCO2** or **HCO3** moves in the opposite direction of the **pH** **Pathophysiology of Pneumonia** - **Pneumonia is an inflammatory condition of the lung primarily affecting the alveoli.** - **It can be caused by various pathogens including bacteria, viruses, and fungi.** **Clinical Manifestations** - **Tachypnoea: Increased respiratory rate.** - **Tachycardia: Increased heart rate.** - **Dyspnoea: Difficulty in breathing.** - **Cough: Often productive, may produce sputum that is:** - ***Rusty*** - ***Green*** - ***Foul-smelling*** - **Fever: Accompanied by rigors and sweats.** - **Fatigue: Generalized weakness and tiredness.** - **Anorexia: Loss of appetite.** - **Pleuritic chest pain: Pain associated with pleurisy.** **Clinical Diagnosis** - **Full history and physical examination: Essential for initial assessment.** - **Oxygen saturation: Monitoring to assess respiratory function.** - **Sputum culture: To identify the causative organism.** - **Chest X-ray: Used to confirm the diagnosis of pneumonia.** - **Blood tests:** - ***Full Blood Count (FBC)*: May show high or low white cell count.** - ***C-reactive protein*: Typically elevated in infection.** - ***Microscopic culture and sensitivity*: To determine the appropriate antimicrobial therapy.** **Complications** - **Hypoxia: Insufficient oxygen in the tissues.** - **Respiratory acidosis: Due to impaired gas exchange.** - **Pleural empyema: Accumulation of pus in the pleural cavity.** - **Septic shock: A severe infection leading to systemic inflammation and organ failure.** - **Pleural effusion: Accumulation of fluid in the pleural space.** **Management** - **Tachypnoea and Tachycardia:** - **Administer supplemental oxygen if SpO2 \< 93%.** - **Cough and Sputum:** - **Chest physiotherapy to aid in sputum clearance.** - **Antimicrobial therapy based on culture results.** - **Fever, Rigors, and Sweats:** - **Use of antipyretics to manage fever.** - **Anorexia:** - **Intravenous fluids (IVF) to maintain hydration.** - **Pleuritic Chest Pain:** - **Provide analgesia for pain relief.** - **Fatigue:** - **Encourage group care and promote rest for recovery.** **Pneumonia** is an inflammatory condition affecting the **lungs**, particularly the **alveoli** Common clinical manifestations of pneumonia include **tachypnoea, fever, cough with sputum,** and **fatigue** Pneumonia is clinically diagnosed through a combination of **history, physical examination**, sputum culture, chest x-ray, and blood tests Management strategies for pneumonia symptoms include **supplemental oxygen, chest physiotherapy,** antipyretics, IVF, analgesia, and **promoting rest** Potential complications of pneumonia include **hypoxia, respiratory acidosis,** pleural empyema, **septic shock,** and pleural effusion **Preventers in Asthma Management** **Leukotriene Receptor Antagonists** - **Definition**: Non-steroidal preventers that act on leukotriene receptors. - **Mechanism of Action**: - Causes **bronchodilation** through direct action on bronchial muscles. - Reduces **bronchoconstriction**, **airway edema**, and **inflammation**. - **Example**: - *Montelukast* tablets. - **Adverse Effects**: - **Headaches** - **Nausea** - **Dizziness** - **Insomnia** - **Gastric upset** **Long Acting Beta Agonists (LABA)** - **Definition**: Long-acting bronchodilators not used for acute attacks. - **Mechanism of Action**: - Similar to short-acting beta agonists (SABA) but with prolonged effects. - Effects can last **up to 12 hours**. - **Role in Asthma Management**: - Controls symptoms of asthma. - **Example**: - *Salmeterol* (Serevent). - **Combination Therapy**: - Often used with corticosteroids (ICS) for effective management. - Enhances penetration of LABA into smaller airways. - Example of combination: *Fluticasone and Salmeterol* (Seretide). **Long Acting Muscarinic Antagonists (LAMA)** - **Definition**: Medications that block bronchoconstriction effects of acetylcholine. - **Mechanism of Action**: - Blocks muscarinic receptors in smooth muscles of the airway. - Leads to prolonged **bronchodilation**. - **Duration of Action**: - Lasts **12 to 24 hours**. - **Role in Asthma and COPD Management**: - Controls symptoms of both asthma and COPD. - **Combination Use**: - Can be used with LABA and ICS for optimal effects. - **Example**: - *Tiotropium* (Spiriva). Combination therapy in asthma management usually combines a **LABA** with **corticosteroids** for enhanced effectiveness and airway penetration A common example of a long-acting beta agonist (LABA) is **Salmeterol** also known as **Serevent** Long-acting muscarinic antagonists **block** the bronchoconstriction effects of **acetylcholine,** leading to prolonged bronchodilation Muscarinic receptor antagonists' function by competitively blocking the binding of **acetylcholine** to muscarinic receptors resulting in an **anticholinergic response** (reduced contraction of smooth muscle -\> prolonged bronchodilation) Leukotriene receptor antagonists are **non-steroidal preventers** that cause **bronchodilation** and reduce bronchoconstriction, airway oedema, and inflammation in asthma management The maximum duration of action for long-acting beta agonists (LABAs) can last up to **12 hours** Leukotriene receptor antagonists are classified as **non-steroidal asthma preventers** acting on Leukotriene receptors, causing **bronchodilation** through **direct action on bronchial muscles** An example of a leukotriene receptor antagonist is **Montelukast tablets** A common ADR of leukotriene receptor antagonists is **nausea** LABAs are defined as **long-term preventers** not used for acute attacks LAMAs last up to **12-24 hours** **Acute Coronary Syndrome (ACS) Overview** **Definition and Types of ACS** - **Acute Coronary Syndrome (ACS)**: A condition that arises when ischemia is prolonged and not immediately reversible. - **Types of ACS**: - **Unstable Angina**: Characterized by chest pain that is new in onset, occurs at rest, or has a worsening pattern. - **Non-ST Segment Elevation Myocardial Infarction (NSTEMI)**: Similar to unstable angina but with elevated serum cardiac markers. - **ST Segment Elevation Myocardial Infarction (STEMI)**: Results from total occlusion of a coronary artery. **Pathophysiology of ACS** - **Causes**: - **Deterioration of Stable Atherosclerotic Plaque**: Leads to the formation of a thrombus. - **Partial Occlusion**: Results in unstable angina or NSTEMI. - **Total Occlusion**: Results in STEMI. - **Mechanisms**: - **Rupture of Plaque**: Initiates the process leading to ACS. - **Platelet Aggregation**: Contributes to thrombus formation. **Clinical Presentation** - **Unstable Angina**: - **Characteristics**: - New onset chest pain. - Occurs at rest or with minimal exertion. - Increasing frequency and severity. - **Differentiation from NSTEMI**: - Unstable angina does not have elevated serum cardiac markers, while NSTEMI does. **Management** - **Immediate Action**: Patients with suspected ACS require immediate hospitalization for evaluation and treatment. Acute Coronary Syndrome (ACS) is a condition arising from **prolonged** and not immediately reversible **ischemia** **NSTEMI** is differentiated from **unstable angina** by having elevated serum cardiac markers, while unstable angina does not For suspected **ACS,** patients require immediate hospitalisation for evaluation and treatment The three types of ACS are **unstable angina, NSTEMI,** and **STEMI.** ACS is caused by deterioration of **atherosclerotic plaque,** leading to **thrombus formation** or occlusion **Unstable angina** is a type of ACS involving chest pain at rest **Total arterial occlusion** leads to STEMI ACS process is initiated by the **rupture of an atherosclerotic plaque** Platelet aggregation contributes to **thrombus formation,** initiating the early stages of ACS Unstable angina is characterised by a **new onset chest pain with increasing severity** **Myocardial Infarction (MI)** **Overview of Myocardial Infarction** - **Definition**: Myocardial Infarction (MI) is the result of sustained **ischaemia** lasting more than **20 minutes**, leading to **irreversible myocardial cell death** (necrosis). - **Causes**: - **80% - 90%** of cases are secondary to **thrombus** formation. - **Pathophysiology**: - Ischaemia typically begins in the **subendocardium**. - **Necrosis** of the entire thickness of the myocardium occurs within **4 to 6 hours**. - Results in **loss of contractile function**. - **Types of MI**: - Can be classified as **STEMI** (ST elevation myocardial infarction) or **NSTEMI** (non-ST elevation myocardial infarction). **Clinical Manifestations of Myocardial Infarction** - **Pain**: - Characterized by **severe, immobilizing chest pain** that is not relieved by rest, position change, or nitrate administration. - Described as **heaviness, pressure, tightness, burning, constriction, or crushing**. - Pain may be **substernal, retrosternal, or epigastric** and can radiate to the **neck, jaw, or arms**. - More common in the **morning**. - Atypical presentations may occur in **women** and the **elderly**. - Patients with **cardiac neuropathy** (e.g., diabetes) may experience **no pain**. - **Other Symptoms**: - **Diaphoresis** (sweating). - **Nausea and vomiting**: Caused by reflex stimulation of the vomiting center due to severe pain and vasovagal reflex. - **Fever**: May reach up to **38°C** within the first **24 hours** due to a systemic inflammatory process resulting from myocardial cell death. **Types of Myocardial Infarction: STEMI vs. NSTEMI** - **STEMI (ST Elevation Myocardial Infarction)**: - Involves **sudden, complete occlusion** of a major coronary artery. - Results in **full thickness damage** of the heart muscle. - The heart muscle supplied by the affected artery begins to die. - **NSTEMI (Non-ST Elevation Myocardial Infarction)**: - Characterized by a **severely narrowed artery**, which is usually not completely blocked. - Leads to **partial thickness damage** of the heart muscle. - A portion of the heart muscle supplied by the affected artery starts to die. **Severity Comparison** - **Which one is the more severe form of AMI?**: STEMI is generally considered the more severe form due to the complete occlusion and full thickness damage to the heart muscle. Atypical MI presentations may occur in **women, the elderly,** or those with **cardiac neuropathy** Chest pain associated with **myocardial infarction** is characterised by being **severe** and immobilising, not relieved by rest, and can radiate to the **neck, jaw,** or arms Thrombus formation is responsible for **80-90%** of **myocardial infarction** cases Myocardial infarction results from sustained **ischemia** lasting over **20 minutes,** causing irreversible myocardial cell death STEMI involves **complete occlusion** of a coronary artery, while NSTEMI involves **severe narrowing** but not complete blockage Ischemia typically begins in the **subendocardium** in an MI Necrosis of the myocardium occurs within **4-6 hours** due to ischemia **STEMI** results in full thickness damage **Complications of Myocardial Infarction** - **Arrhythmias** - Abnormal heart rhythms that can occur post-MI, potentially leading to further complications. - **Heart Failure** - A condition where the heart is unable to pump effectively, which can result from damage caused by MI. - **Cardiogenic Shock** - A severe condition where the heart suddenly cannot pump enough blood to meet the body\'s needs, often a result of extensive heart damage. - **Papillary Muscle Dysfunction** - Impairment of the papillary muscles can lead to mitral valve insufficiency, causing further hemodynamic instability. - **Ventricular Aneurysm** - A bulge in the heart wall that can develop after an MI, potentially leading to heart failure or arrhythmias. - **Acute Pericarditis** - Inflammation of the pericardium that can occur after MI, presenting with chest pain and other symptoms. **Management, Diagnostic Tests, and Nursing Care** - **Management of MI** - Involves a combination of pharmacological and non-pharmacological interventions to restore blood flow and minimize heart damage. - **Diagnostic Tests** - Essential for confirming MI and assessing the extent of heart damage, including ECG, blood tests, and imaging studies. - **Nursing Care** - Focuses on monitoring vital signs, administering medications, and providing education to patients regarding lifestyle changes and medication adherence. Common complications that can arise after an MI include **arrythmias, heart failure,** and **cardiogenic shock** Nursing care for MI patients involves **monitoring vital signs** and **administering medications,** as well as educating patients on lifestyle changes Diagnostic tests play a crucial role in managing myocardial infarction by confirming **MI** and assessing **heart damage,** which includes methods such as **ECGs,** blood tests, and imaging studies Heart failure can result from damage caused by **MI,** impairing the heart's ability to pump effectively Cardiogenic shock is a severe condition post-**MI**, where the heart cannot pump enough blood to meet bodily needs Impairment of the papillary muscles can lead to **mitral valve insufficiency** **Ventricular aneurysm** is a bulge in heart wall that can develop after an MI, potentially leading to heart failure or arrythmias **Acute pericarditis** is characterised by inflammation of the pericardium post-MI **Pathophysiology of Atherosclerosis** - **Definition: Atherosclerosis is the major cause of Coronary Artery Disease (CAD).** - **Development:** - **Begins as soft deposits of fat that harden with age.** - **Commonly referred to as the hardening of arteries.** - **Atheromas (fatty deposits) predominantly affect the coronary arteries.** - **Characteristics:** - **Characterized by deposits of lipids within the intima of the artery.** - **Endothelial injury and inflammation are central to the development of atherosclerosis.** **Stages of Atherosclerosis Development** 1. **Fatty Streak: Initial formation of lipid deposits.** 2. **Fibrous Plaque: Progression to more complex structures.** 3. **Complicated Lesion: Advanced stage with potential for serious complications.** **Management of Coronary Artery Disease (CAD)** - **Lifestyle Changes: Essential for managing CAD.** - **Pharmacological Management:** - **Lipid-lowering medication therapy:** - **Statins: Target LDL, triglycerides, and HDL levels.** - **ACE Inhibitors: Examples include ramipril and perindopril.** - **Beta Blockers: Used to manage heart rate and blood pressure.** - **Antiplatelet Therapy: Includes medications like aspirin and clopidogrel.** - **Surgical Interventions:** - **Coronary Angioplasty and Stenting: Minimally invasive procedures to open blocked arteries.** - **Coronary Bypass Surgery: Surgical procedure to improve blood flow to the heart.** **Atherosclerosis** is the major cause of **coronary artery disease (CAD)** in heart disease The development of **atherosclerosis** is characterized by fatty deposits that **harden** with age, primarily affecting **coronary arteries** The stages of atherosclerosis development include **fatty streak, fibrous plaque,** and **complicated lesion** **Beta blockers** ("lol's"**, ACE inhibitors** ("pril's")**, antiplatelet therapy,** and **statins** are types of medications used to manage **CAD** The surgical interventions available for **CAD** include coronary angioplasty, **stenting,** and **coronary bypass surgery** **Overview of Nitrates** - **Aim of Nitrates**: - **Reduce cardiac workload** - **Decrease oxygen demands** **Commonly Used Nitrates** - **Glyceryl Nitrates**: - Examples include **Anginine** and **GTN** (Glyceryl Trinitrate) - **Administration Routes**: - **Sublingual** - **Intravenous (IV)** - **Nasal spray** - **Note**: Orally inactive **Mechanism of Action** - **Metabolism**: - Nitrates are metabolized and converted to **Nitric Oxide (NO)** in the vessel walls. - **Effects of Nitric Oxide**: - **Vasodilation** of peripheral blood vessels - **Reduces Total Peripheral Resistance (TPR)** - **Decreases Preload and Afterload** - **Decreases Stroke Volume (SV)** - **Decreases Cardiac Output (CO)** - **Decreases Oxygen Demands** - **Reduces Cardiac Workload** - **Dilates Coronary Arteries**: - Increases blood flow to ischemic areas of the heart **Adverse Effects** - **Common Adverse Effects**: - **Hypotension** - **Flushing** - **Headache** - **Fainting** Common adverse effects of **nitrates** include **hypotension, flushing, headache,** and **fainting** The primary aim of using **nitrates** in angina management is to reduce cardiac workload and decrease **oxygen demands** Nitrates are metabolised and converted to **Nitrous Oxide (NO)** in the vessel walls **Nitrous Oxides** released by nitrates causes **vasodilation**, reducing total peripheral resistance, preload, afterload, and cardiac output Examples of glyceryl nitrates used for angina management include **Glyceryl Trinitrate (GTN)** and **Anginine** **Pharmacological Management of Hypertension** **Adrenergic Antagonists (Beta Blockers)** - **Definition**: Beta blockers are a class of medications that block beta-adrenergic receptors. - **Common Suffix**: *-olol* - **Location of Action**: - **Cardiac Cells**: - Increases heart rate and force of contractions. - Results in increased contractility, stroke volume (SV), cardiac output (CO), and blood pressure (BP). - **Smooth Muscle of Bronchioles and Blood Vessels**: - Causes bronchodilation. - Increases skeletal muscle excitability (can lead to tremors). - Induces vasodilation of blood vessels. - **Mechanism of Action (MoA)**: - Blocks beta receptors located in the heart and smooth muscle of bronchioles and blood vessels. - Decreases heart rate and contractility. - Reduces cardiac output, leading to decreased blood pressure and cardiac workload. - **Examples**: - *Atenolol* - *Metoprolol* - **Adverse Effects (A/E)**: - Bronchospasms (due to action on beta-2 receptors). - Bradycardia and heart block. - Hypotension. - Cold peripheries (due to vasoconstriction). - Fatigue, nightmares, and depression. **Alpha 1 Blockers** - **Definition**: Alpha 1 blockers are medications that block alpha-1 adrenergic receptors. - **Common Suffix**: *-sin* - **Mechanism of Action (MoA)**: - Blocks alpha-1 receptors on blood vessels. - Causes a decrease in total peripheral resistance through vasodilation. - Results in reduced blood pressure. - **Examples**: - *Prazosin* - **Adverse Effects (A/E)**: - Hypotension. - Headache. - Dizziness. **Additional Effects of Alpha 1 Blockers** - **Vasoconstriction**: - Alpha-1 receptors are present on all blood vessels, leading to increased blood pressure when activated. - **Pupil Dilation**: - Activation of alpha-1 receptors can cause dilation of pupils. - **Gastrointestinal (GIT) Mobility**: - Decreases GIT mobility when alpha-1 receptors are activated. **Atrial Fibrillation: Pathophysiology and ECG Characteristics** **Pathophysiology of Atrial Fibrillation (AF)** - **Abnormal Electrical Signaling**: - Signals originate from various locations in the atria rather than the **sinoatrial (SA) node**. - This results in **quivering or fibrillating** of the atria, leading to **uncoordinated atrial activity**. - **Atrial Rate**: - The atrial rate can increase significantly, ranging from **300 to 600 beats per minute (bpm)**. - **AV Node Function**: - The **atrioventricular (AV) node** is unable to filter the excessive signals from the atria. - This leads to **inadequate emptying of the atria**, causing **blood pooling**. - **Ventricular Rate**: - The ventricular rate may increase due to the excess signals passing through the AV node, potentially reaching up to **150 bpm**. - **Impact on Cardiac Output**: - The increased ventricular rate affects the **emptying of the ventricles**, resulting in: - Decreased **stroke volume (SV)**. - Decreased **cardiac output (CO)**. - **Symptoms**: - Patients may experience: - **Lightheadedness** - **Fatigue** - **Breathlessness** - **Chest pain** - Symptoms vary based on the rate of ventricular activity, severity, and duration of AF. - **Hemodynamic Changes**: - Initially, there may be **hypertension** as a compensatory mechanism. - This can progress to **hypotension** if the condition worsens. **ECG Characteristics of Atrial Fibrillation** - **Rhythm**: - The rhythm is described as **irregularly irregular**. - **R-R Intervals**: - There are **variable ventricular rates** observed in the ECG. - **P Waves**: - **P waves** are absent in AF. - **Baseline**: - The ECG shows an **undulating baseline**. - **P:QRS Ratio**: - The ratio of **P waves to QRS complexes** is many to one, indicating multiple atrial signals for each ventricular contraction. A key characteristic of an ECG in atrial fibrillation is that the rhythm is **irregularly irregular** with **absent P waves** and an undulating baseline Excess signals in atrial fibrillation can cause the ventricular rate to increase, potentially reaching up to **150bpm** The atrial rate in AF can change from **300-600** beats per minute Common symptoms of AF include **light-headedness, heart palpitations, fatigue, breathlessness,** and **chest pain** Abnormal electrical signalling in AF is caused by signals originating from multiple locations in the **atria** instead of the **SA node** The AV node **cannot process** the number of signals from various points in the atria firing in atrial fibrillation AF can lead to **hypertension** initially Primary goal in managing atrial fibrillation is to **decrease ventricular rate** to improve cardiac output **Ventricular Fibrillation: Pathophysiology, ECG Characteristics, and Management** **Pathophysiology of Ventricular Fibrillation (VF)** - **Definition**: VF is characterized by a rapid, disorganized ventricular rhythm leading to ineffective contraction of the ventricles. - **Mechanism**: - The ventricles attempt to contract at rates of up to **500 beats per minute**. - This rapid and irregular electrical activity prevents the ventricles from contracting in a synchronized manner. - **Consequences**: - Immediate loss of **cardiac output (CO)**. - Clinical signs include: - **Absence of an audible heartbeat**. - **No pulse**. - **No ventilation**. - **Unresponsiveness**. - **Prognosis**: Cardiac arrest and death are imminent if VF is not corrected due to the lack of coordinated cardiac activity. **ECG Characteristics of Ventricular Fibrillation** - **Ventricular Rate**: Greater than **300 beats per minute**, but not measurable. - **Ventricular Rhythm**: Extremely irregular, lacking a specific pattern. - **QRS Complex**: - Irregular, undulating waves without recognizable QRS complexes. - **Absence of P waves**. **Management of Ventricular Fibrillation** - **Urgency of Treatment**: If VF is not rapidly treated, the patient will die. - **Immediate Actions**: 1. **Initiate CPR**: Begin **Cardiopulmonary Resuscitation (CPR)** and advanced cardiac life support (ACLS) immediately. - Minimize interruptions to CPR. 2. **Defibrillation**: - Should not be delayed; immediate defibrillation is critical. - Activate emergency services promptly. - Administer CPR between shocks. - Administer **adrenaline** every second cycle. - **Risks of Delay**: 1. If not revived in a timely manner, the patient may suffer irreversible brain damage due to **cerebral hypoxia**. 2. The chance of survival decreases by **7% to 10%** for every minute of delay in defibrillation. Delays in defibrillation increase the risk of **irreversible brain damage,** as survival chances decrease by between **7-10%** each minute The typical ventricular rate during VF exceeds **300bpm,** but it remains immeasurable The clinical signs indicating **VF onset** include **unconsciousness, no pulse, no audible heartbeat, no ventilation,** and **unresponsiveness** To manage **VF,** it is essential to **initiate CPR** and defibrillate without delay, while administering adrenaline every second cycle VF is characterized by **rapid, disorganised** ventricular rhythm causing **ineffective contractions** **Key Concepts in Acute Kidney Injury** **Classification of Acute Kidney Injury** - **Acute Kidney Injury (AKI)** is classified based on the underlying cause and clinical presentation. - **Prerenal AKI**: Caused by decreased blood flow to the kidneys. - **Intrinsic AKI**: Resulting from damage to the kidney tissue itself. - **Postrenal AKI**: Due to obstruction of urine flow. **Clinical Phases of Acute Kidney Injury** - **Initiation Phase**: The onset of AKI, where kidney function begins to decline. - **Maintenance Phase**: Characterized by a plateau in kidney function, often with oliguria (reduced urine output). - **Recovery Phase**: The kidneys begin to recover function, and urine output increases. **Important Considerations** - Early recognition and classification of AKI are crucial for effective management and treatment. - Monitoring of kidney function and understanding the phases of AKI can guide clinical decisions and interventions. Prerenal AKI is characterized by **decreased blood flow** to the kidneys Early recognition of **AKI** is important because it is crucial for effective management and treatment of the condition During the maintenance phase of **AKI,** kidney function **plateaus** and is often accompanied by reduced urine output (oliguria) The three classifications of AKI are **prerenal, intrinsic,** and **postrenal** based on cause and presentation During the recovery phase of AKI, the kidneys begin to regain **function** and urine output increases The primary cause of prerenal AKI is a **decrease** in blood flow to the kidneys Intrinsic AKI results from damage to the **kidney tissue** itself Postrenal AKI is primarily caused by **obstruction to urine flow** Kidney function beings to decline in the **initiation** stage of AKI The **maintenance** phase of AKI is characterised by a **plateau** in kidney function Kidneys begin to **recover** function in the **recovery** phase of AKI **Acute Kidney Injury: Pathophysiology** **Types of Acute Kidney Injury (AKI)** - **Prerenal AKI** - **Cause**: Decrease in blood volume - **Mechanism**: - Reduced renal perfusion leading to decreased glomerular filtration rate (GFR). - **Intrinsic/Intrarenal AKI** - **Cause**: Tubular damage - **Mechanisms**: - **Ischemia**: Insufficient blood flow causing cellular injury. - **Necrosis**: Cell death in renal tubules. - **Vasoconstriction**: Reduced blood flow to the kidneys. - **Decreased reabsorption of solutes**: Impaired ability to reclaim essential substances. - **Activation of inflammatory system**: - Potential for sepsis due to systemic inflammatory response. - **Nephrotoxicity**: Damage from toxic substances affecting kidney function. - **Decreased filtration, reabsorption, and secretion**: Overall decline in kidney function. - **Glomerular damage**: Injury to the glomeruli affecting filtration. - **Inflammation**: Immune response leading to further kidney injury. - **Thrombosis**: Formation of blood clots within renal vasculature. - **Interstitium damage**: Injury to the supportive tissue surrounding nephrons. - **Postrenal AKI** - **Cause**: Obstruction of the collecting system or excretion pathways. - **Mechanism**: - Can lead to **hydronephrosis**: Swelling of the kidney due to urine buildup. - Impaired urine flow resulting in increased pressure and potential kidney damage. A significant mechanism leading to intrinsic AKI is **ischemia,** which causes insufficient blood flow, resulting in **cellular injury** and tubular damage Prerenal AKI is caused by a decrease in **blood volume,** leading to reduced **renal perfusion** Postrenal AKI occurs due to **obstruction** in the **collecting system,** impairing urine flow Activation of the inflammatory system in intrinsic AKI can lead to potential **sepsis** due to **systemic response** **Hydronephrosis** is the swelling of the kidney due to **urine buildup** from obstructed flow **Reduced renal perfusion** leads to decreased GFR in prerenal AKI **Insufficient blood flow** indicates ischemia in intrinsic AKI Vasoconstriction **reduces** blood flow to the kidneys in intrinsic AKI **Acute Kidney Injury: RIFLE Classification and Clinical Phases** **RIFLE Classification** - **Risk** - **Increased creatinine**: x 1.5 - **Decreased urine output**: \