Nursing Care on Types of Strokes PDF

1. Types of Stroke: Pathophysiology and Clinical Manifestations Ischaemic Stroke Pathophysiology: Occurs when a blood clot or blockage (thrombus or embolus) reduces blood flow to the brain, causing cell death due to lack of oxygen. Clinical Manifestations: Sudden weakness, faci...

1. Types of Stroke: Pathophysiology and Clinical Manifestations Ischaemic Stroke Pathophysiology: Occurs when a blood clot or blockage (thrombus or embolus) reduces blood flow to the brain, causing cell death due to lack of oxygen. Clinical Manifestations: Sudden weakness, facial droop, slurred speech, vision problems, dizziness, difficulty walking. Haemorrhagic Stroke Pathophysiology: Caused by the rupture of a blood vessel in the brain, leading to bleeding and increased pressure on brain tissue. Clinical Manifestations: Severe headache, nausea, vomiting, loss of consciousness, seizures, weakness, or numbness. Transient Ischaemic Attack (TIA) Pathophysiology: Temporary blockage of blood flow to the brain, often called a “mini-stroke,” but no permanent damage occurs. Clinical Manifestations: Same as a stroke but symptoms resolve within 24 hours. 2. Comprehensive Nursing History and Focused Physical Assessment for Stroke Patients Primary Survey (ABCDE) A – Airway: Ensure airway patency. B – Breathing: Check respiratory rate, effort, and oxygen saturation. C – Circulation: Assess blood pressure, heart rate, and peripheral perfusion. D – Disability: Assess neurological status (Glasgow Coma Scale, pupil response, limb strength). E – Exposure: Expose the patient to check for injuries or skin changes. Secondary Survey History Taking (AMPLE): Allergies Medications Past medical history Last meal Events leading to the condition Focused Physical Assessment: Assess cranial nerves, speech, facial symmetry, limb movement, coordination, and sensation. 3. Diagnostic Tests and Investigations for Stroke CT Scan (Non-contrast): First-line test to differentiate between ischaemic and haemorrhagic stroke. MRI: Provides more detailed imaging of brain tissue, especially in early stroke. Carotid Ultrasound: Assesses blood flow and blockages in the carotid arteries. ECG: Identifies any cardiac issues, such as atrial fibrillation, that may cause emboli.  Blood Tests: To check glucose levels, electrolyte imbalances, clotting factors, and lipid profiles. 4. Recognising Clinical Cues for Deterioration in Stroke Patients Sudden decline in consciousness or responsiveness. Increasing weakness or paralysis (especially on one side). Worsening speech or communication difficulties. Severe headache, nausea, or vomiting. Changes in pupil size or reactivity. Altered respiratory patterns or signs of aspiration. Seizures or signs of increased intracranial pressure. 5. Developing a Therapeutic Plan of Care for Stroke Patients Assessment Findings: Review diagnostic results, neurological assessments, and monitor vital signs. Clinical Reasoning Cycle: 1. Consider the Patient Situation: Gather information from history and physical exams. 2. Collect Cues and Information: Recognise neurological signs, imaging results, and labs. 3. Process Information: Analyse findings (e.g., CT scan confirms ischaemic stroke). 4. Identify Problems: Prioritise patient’s needs (e.g., airway protection, BP control). 5. Establish Goals: Reduce brain damage, restore circulation, prevent complications. 6. Take Action: Administer medications (e.g., thrombolytics), monitor closely. 7. Evaluate Outcomes: Assess for improvements in neurological function, reduce risk of further complications. 6. Collaborative Management Strategies in Acute Care Setting Early Interventions: Ischaemic Stroke: Administer thrombolytics (e.g., tPA) within 3-4.5 hours of symptom onset. Haemorrhagic Stroke: Blood pressure management, reversal of anticoagulation, possible surgery. Team Roles: Neurologist: Oversees diagnostic decisions and treatment plan. Registered Nurse: Monitors vital signs, neurological status, administers medication, and provides patient education. Physiotherapist: Focuses on rehabilitation and motor function recovery. Speech Therapist: Assesses and helps with swallowing and speech recovery. 7. Pharmacological Agents and Polypharmacy Considerations in Stroke Care Medications:  Thrombolytics: Used in ischaemic stroke to dissolve blood clots. Anticoagulants (e.g., warfarin, heparin): To prevent clot formation, particularly for those with atrial fibrillation. Antiplatelets (e.g., aspirin, clopidogrel): To prevent platelets from clumping together. Antihypertensives: To control blood pressure and reduce the risk of haemorrhagic stroke. Statins: Lower cholesterol to reduce future stroke risk. Polypharmacy: Increased risk of drug interactions, side effects, and adherence challenges. Nurses need to monitor for adverse effects, drug effectiveness, and patient education on proper medication use. 1. Pathophysiology of Stroke Key Concepts: Stroke Types: o Ischemic Stroke (85% of strokes): Results from a blood clot that blocks blood flow to a part of the brain, causing ischemia and, potentially, tissue death. § Thrombotic Stroke: Clot forms within the brain's arteries. § Embolic Stroke: Clot forms elsewhere (e.g., heart) and travels to the brain. o Hemorrhagic Stroke (15% of strokes): Occurs when a blood vessel ruptures, leading to bleeding in or around the brain. § Intracerebral Hemorrhage: Bleeding within brain tissue. § Subarachnoid Hemorrhage: Bleeding in the space between the brain and skull. Pathophysiological Mechanism: o Brain requires continuous blood flow (750–1000 mL/minute) to supply oxygen and glucose to neurons. o Cerebral Autoregulation: Maintains stable blood flow despite BP changes. o Ischemic Cascade: Disrupted blood flow → metabolic disruption within 30 seconds → neuronal metabolism ceases in 2 minutes → irreversible cell death in 5 minutes. Warning Signs of Stroke: Sudden numbness, confusion, trouble speaking, visual disturbances, severe headache. Transient Ischemic Attack (TIA): "Mini-stroke," often precedes ischemic strokes; brief symptoms without permanent damage, but should be treated as a medical emergency. What is a Stroke? Stroke occurs when blood supply to the brain is interrupted, either by a blockage (ischemic stroke) or bleeding (hemorrhagic stroke). This causes brain cells to die, leading to loss of function like movement, sensation, and emotions, depending on the affected brain area.  Risk Factors for Stroke Non-modifiable (cannot change): Age (risk doubles every decade after 55) Gender (more common in men, more deaths in women) Family history Modifiable (can change): High blood pressure Smoking Heart disease High cholesterol Excessive alcohol consumption Obesity Lack of exercise Poor diet Sleep apnoea Types of Stroke Ischemic Stroke: Most common (85% of strokes), caused by a blockage in a brain artery. Transient Ischemic Attack (TIA): A “mini stroke” that lasts less than 24 hours. It’s a warning sign. Hemorrhagic Stroke: Occurs when there’s bleeding in or around the brain (15% of strokes). Intracerebral: Bleeding within the brain tissue. Subarachnoid: Bleeding between the brain and skull. Symptoms of Stroke Impaired motor skills: Difficulty moving, walking, or using limbs. Speech issues: Trouble speaking or understanding speech. Swallowing issues: Trouble eating or drinking. Emotional changes: Mood swings or confusion. Sensory issues: Loss of feeling, especially on one side of the body. Warning Signs of Stroke Sudden weakness or numbness, especially on one side of the body. Trouble speaking or understanding speech. Sudden trouble seeing in one or both eyes. Sudden severe headache with no known cause. Diagnostic Tests CT Scan/MRI: To confirm the type of stroke (ischemic vs hemorrhagic) and locate the damage. Blood Tests: To check cholesterol and glucose levels. Carotid Ultrasound: To check blood flow in the neck arteries. Treatment Ischemic Stroke: Thrombolysis (clot-busting drugs) or Embolectomy (clot removal). Antiplatelet or anticoagulant drugs to prevent further clots. Hemorrhagic Stroke: Control bleeding and blood pressure. Surgery to remove blood or repair blood vessels.  Medications to prevent seizures and manage hypertension. Complications of Stroke Impaired Mobility: Difficulty walking, need for rehabilitation. Dysphagia (difficulty swallowing): Can lead to malnutrition or aspiration. Cognitive Issues: Memory loss or difficulty concentrating. Emotional and Psychological Effects: Depression or anxiety after stroke. Nursing Considerations Monitor vital signs: Check blood pressure, oxygen levels, and temperature. Assess swallowing: Check for signs of difficulty swallowing to prevent choking. Rehabilitation: Encourage physical, speech, and occupational therapy to regain independence. Prevent complications: Regular movement to prevent blood clots, use of compression stockings, and managing skin care. 2. Pharmacology for Stroke Management Ischemic Stroke Treatment: Thrombolytic Therapy (e.g., Alteplase): To dissolve blood clots if administered within 4.5 hours of symptom onset. Antiplatelet and Anticoagulant Therapy: Prevent further clot formation. o Aspirin (initial treatment) for long-term prevention. o Warfarin or DOACs (Direct Oral Anticoagulants) for patients with atrial fibrillation. Statins: Lower cholesterol levels to reduce stroke risk. Hemorrhagic Stroke Treatment: Blood Pressure Control: Avoid excessive BP elevation (SBP ~140 mmHg). Surgical Intervention: For large bleeds or aneurysms (e.g., clipping, coiling). Seizure Prophylaxis: Given in some cases to prevent post-stroke seizures. 3. Clinical Manifestations and Linking to Pathophysiology Manifestations Based on Brain Area Affected: Motor and Sensory Impairments: Paralysis or weakness on one side (contralateral to lesion). Language and Cognitive Deficits: o Left Brain Stroke: Affects language and analytical abilities; leads to aphasia (inability to speak). o Right Brain Stroke: Leads to spatial-perceptual deficits, impulsivity. Other Impairments: Swallowing (dysphagia), bladder/bowel dysfunction, emotional changes, memory deficits. Linking Manifestations to Risk Factors: Hypertension: Major cause of both ischemic and hemorrhagic strokes due to vessel damage. Heart Disease (e.g., atrial fibrillation): Increases embolic stroke risk by promoting clot formation. Diabetes, Smoking, High Cholesterol: Promote atherosclerosis, increasing risk of thrombotic stroke. 4. Risk Factor Management and Prevention Lifestyle Modifications: Promote regular exercise, healthy diet, limit alcohol intake, avoid smoking. Medical Management: Blood pressure control, cholesterol management, antiplatelet therapy for those with a history of TIAs or high cardiovascular risk. Patient Education: Emphasize FAST (Face, Arms, Speech, Time) for early detection and prompt intervention. 5. Diagnostic Investigations Key Imaging and Tests: Non-contrast CT Scan: First-line imaging to differentiate between ischemic and hemorrhagic stroke. MRI: Provides detailed images of brain tissue damage and ischemic areas. CTA (CT Angiography) or MRA (Magnetic Resonance Angiography): Visualize blood vessels. Other Tests: Carotid ultrasound (detects atherosclerosis), cardiac imaging (for embolic sources), blood tests (glucose, coagulation profile). 6. Assessment, Diagnosis, and Interventions Nursing and Medical Interventions: Airway, Breathing, Circulation (ABCs): Prioritize airway and hemodynamic stability. Monitoring and Managing Neurological Status: Frequent assessments to track progression or improvement. BP Control: Critical to maintain within safe limits for both ischemic and hemorrhagic stroke patients. Thrombolysis (for ischemic strokes only): Administered if indicated, with close monitoring for bleeding. Rehabilitation and Long-term Care: Physical and Occupational Therapy: Improve mobility and self-care ability. Speech Therapy: For patients with aphasia or dysphagia. Psychosocial Support: Address emotional impacts, promote coping strategies. Nursing Management of ischemic chest pain MINUTES MEAN MYOCARDIUM ASSESS & position PQRST & Vital signs commence O2 if required, establish IV access 12 lead ECG Nitroglycerin (GTN) +/- Morphine, Aspirin Escalation of care, Cardiac biomarkers, Cardiac monitoring, bed rest If STE present prepare for angiogram and transfer to coronary care unit Treatment ACS- REPERFUSION STEMI: Primary Percutaneous Coronary Intervention (PCI): Angioplasty, drug-eluting stent (DES) thrombectomy > may need CABGS Goal open blocked artery within 90min of onset of symptoms Advantages Complications Nursing care pre and post angiogram Thrombolytics: Considered if PCI not available Not recommended > 12hours after onset of symptoms Ideally within 3 hours symptom onset Contraindications Treatment ACS- Reperfusion Unstable Angina/NSTEMI Relieve pain (nitrates and morphine), Antiplatelet Anticoagulant angiography once stabilised Chronic Kidney Disease (CKD) Study Notes What is CKD? Chronic Kidney Disease (CKD) is a long-term condition where kidney function slowly worsens over time. It is often caused by diabetes or hypertension. CKD is defined by a Glomerular Filtration Rate (GFR) of less than 60 mL/min for at least 3 months. GFR measures how well the kidneys are filtering waste from the blood. A GFR below 60 indicates kidney dysfunction. Kidney Function Overview Kidneys filter blood to remove waste and excess fluids, regulate blood pressure, balance pH, and maintain electrolytes (such as sodium and potassium). Nephrons are the functional units inside the kidneys that filter blood and produce urine. GFR is the most important test to measure kidney function. Normal GFR is 100- 120 mL/min, and a lower GFR indicates reduced kidney function. Causes & Risk Factors Main causes of CKD: o Diabetes: High blood glucose damages kidney blood vessels, leading to reduced kidney function (called diabetic nephropathy). o Hypertension: High blood pressure damages the blood vessels in the kidneys, reducing blood flow and filtering ability. o Glomerular diseases: Conditions like glomerulonephritis (inflammation of the kidney's filtering units) or polycystic kidney disease (genetic disorder that causes cysts to form in the kidneys) can also cause kidney damage. Risk factors: o Modifiable: Obesity, smoking, poor control of diabetes or high blood pressure, use of nephrotoxic drugs (e.g., NSAIDs). o Non-modifiable: Older age, family history of kidney disease, genetic predisposition. Chronic Kidney Disease (CKD) Study Notes What is CKD?  Chronic Kidney Disease (CKD) is a long-term condition where kidney function gradually declines, usually due to diabetes or hypertension. Defined by a Glomerular Filtration Rate (GFR) of less than 60 mL/min for at least 3 months. Kidney Function Overview Kidneys filter blood, remove waste, regulate blood pressure, pH, and electrolytes. Nephrons are the functional units that filter blood and produce urine. GFR is a key measure of kidney function. Normal range is 100-120 mL/min. Causes & Risk Factors Main causes: o Diabetes: High blood glucose damages kidney blood vessels, leading to decreased kidney function. o Hypertension: High blood pressure thickens kidney blood vessels, reducing blood flow and triggering further kidney damage. o Glomerular diseases: Conditions like glomerulonephritis (inflammation of the kidney's filtering units) and polycystic kidney disease (PKD) (genetic condition causing cysts to form in the kidneys) contribute to kidney damage. Risk factors: o Modifiable: Obesity, smoking, uncontrolled diabetes, nephrotoxic drugs (e.g., NSAIDs). o Non-modifiable: Age (over 60), genetics, family history of kidney disease. Stages of CKD 1. Stage 1: Normal kidney function, slight damage. 2. Stage 2: Mild decrease in kidney function. 3. Stage 3: Moderate decrease in kidney function. 4. Stage 4: Severe decrease, preparing for dialysis. 5. Stage 5: End-stage kidney failure, requires dialysis or transplant. Symptoms Early symptoms: Often none. As it progresses: o Polyuria (frequent urination) and nocturia (nighttime urination). o Edema (swelling), fatigue, nausea, loss of appetite. o Uremia: Toxin buildup causing mental confusion, lethargy, and asterixis (hand tremor). o High blood pressure. Diagnosis of CKD 1. Blood Tests: o Elevated creatinine and BUN levels indicate impaired kidney function because the kidneys can’t remove these waste products effectively. o Decreased GFR shows the kidneys' decreased ability to filter blood. 2. Urinalysis:  o Presence of protein, blood, or glucose in the urine suggests kidney damage, as the kidneys can’t retain these substances. 3. Imaging: o Ultrasound or X-rays help assess the kidney’s structure, detecting abnormalities like cysts or blockages. 4. Biopsy: o A kidney biopsy helps determine the cause of kidney damage, such as glomerulonephritis, polycystic kidney disease, or other conditions. Identifying the cause helps direct treatment. Treatment Stage 1 & 2: Control underlying risk factors (e.g., blood pressure, blood sugar), use ACE inhibitors or ARBs. Stage 3: Correct blood abnormalities (e.g., anemia, electrolytes), manage bone health. Stage 4: Prepare for dialysis or kidney transplant. Stage 5 (End-stage Renal Disease - ESRD): Initiate dialysis or consider a kidney transplant. Nursing Care Monitor: Fluid balance, lab results, vitals, and weight. Signs of fluid overload: Rapid pulse, hypertension, lung crackles. Electrolyte imbalances: Monitor and correct sodium, potassium, calcium levels. Dialysis care: Assess vascular access for infection or clotting. Psychosocial support: Address anxiety, depression, and coping strategies. Client Education Lifestyle changes: Low-sodium, low-potassium diet, fluid restriction. Medications: Avoid nephrotoxic drugs, take prescribed medications as directed. Monitor: Daily weight, report changes in urine output or swelling. Follow-up: Regular doctor visits to monitor kidney function and adjust treatments. Summary CKD is a progressive disease that leads to kidney function loss. Early stages may have few symptoms, but later stages cause fluid retention, toxin buildup, and multi-system complications. Treatment focuses on symptom management, controlling underlying conditions, and preparing for dialysis or transplant when necessary. ] Defining Chronic Kidney Disease Chronic kidney disease is defined as a decline in renal function, usually for greater than or equal to 3 months, resulting in a decrease in the glomerular filtration rate (GFR). GFR is a key measure of renal function and is used to stage the severity of CKD. #### Causes of Chronic Kidney Disease Hypertension is a common cause of CKD, leading to glomerulosclerosis and a decrease in GFR. Diabetes, particularly diabetic nephropathy, is the leading cause of CKD. Glomerulonephritis, caused by autoimmune or infectious processes, can also lead to CKD. Polycystic kidney disease can cause CKD through compression of renal vessels and impaired tubular function. Overuse of non-steroidal anti-inflammatory drugs (NSAIDs) can also contribute to CKD. #### Pathophysiology of CKD Hypertension can lead to thickening of the vessel walls (hyaline arteriosclerosis), reduced oxygen delivery, and subsequent fibrosis and glomerulosclerosis. In diabetes, non-enzymatic glycation of proteins and lipids can cause inflammation and arteriolar sclerosis, leading to hyperfiltration and glomerulosclerosis. In glomerulonephritis, immune complexes can deposit in the glomerular basement membrane, causing inflammation and increased permeability, ultimately leading to glomerulosclerosis. #### Clinical Manifestations of CKD Electrolyte abnormalities, including hyperkalemia, hyperphosphatemia, and hypocalcemia, are common in CKD. Fluid imbalances, such as volume overload, can lead to pulmonary edema, hypertension, and peripheral edema. Accumulation of waste products, like urea, can cause uremic complications, including encephalopathy, pericarditis, and platelet dysfunction. Hormonal imbalances, such as decreased erythropoietin and secondary hyperparathyroidism, can lead to anemia and bone disease. #### Diagnosis and Treatment of CKD Diagnosis of CKD is based on a history of at least 3 months of kidney injury, as evidenced by a decreased GFR and/or increased albuminuria. Treatment focuses on addressing the underlying causes, such as controlling hypertension and diabetes, and managing the complications of CKD. In advanced CKD, dialysis or kidney transplantation may become necessary if medical therapies are no longer effective. Osteoarthritis (OA) OA is a degenerative joint disease, and its management often includes a combination of non-pharmacological and pharmacological treatments to relieve pain and inflammation. 1. Medications for OA: Analgesics (Pain Relief): o Paracetamol – An analgesic for pain relief. o NSAIDs (Non-Steroidal Anti-Inflammatory Drugs): § Ibuprofen (Brand name: Nurofen) § Diclofenac (Brand name: Voltaren) § Meloxicam (Brand name: Mobic) § These reduce inflammation and provide pain relief. Corticosteroids (for inflammation control): o Prednisolone – A systemic corticosteroid for severe flare-ups. o Triamcinolone – Can be injected into the joint for localized inflammation control. COX-2 Inhibitors (for pain relief with reduced GI side effects): o Celecoxib (Brand name: Celebrex) Classes of Medications for OA: Analgesics (e.g., Paracetamol) NSAIDs (e.g., Ibuprofen, Diclofenac) Corticosteroids (e.g., Prednisolone, Triamcinolone) COX-2 Inhibitors (e.g., Celecoxib) Rheumatoid Arthritis (RA) RA is an autoimmune condition, and its treatment typically involves medications that address inflammation and the underlying immune response. 2. Medications for RA: Disease-Modifying Anti-Rheumatic Drugs (DMARDs): o Methotrexate (Brand name: Rheumatrex) – The most commonly prescribed DMARD. o Sulfasalazine (Brand name: Salazopyrin) – Often used in combination with other DMARDs. o Leflunomide (Brand name: Arava) – Another DMARD used to slow disease progression. Biologic DMARDs: o Etanercept (Brand name: Enbrel) – A TNF-alpha inhibitor. o Adalimumab (Brand name: Humira) – A TNF-alpha inhibitor. o Rituximab (Brand name: Rituxan) – A B-cell depleting agent used in severe RA. NSAIDs for pain and inflammation control: o Ibuprofen (Brand name: Nurofen) o Diclofenac (Brand name: Voltaren) Corticosteroids (for acute flare-ups): o Prednisolone – Oral or injectable corticosteroid. Classes of Medications for RA: DMARDs (e.g., Methotrexate, Sulfasalazine, Leflunomide) Biologic DMARDs (e.g., Etanercept, Adalimumab, Rituximab) NSAIDs (e.g., Ibuprofen, Diclofenac) Corticosteroids (e.g., Prednisolone) Systemic Lupus Erythematosus (SLE) SLE is an autoimmune disease that can affect multiple organs, and management typically includes immunosuppressive and anti-inflammatory therapies. 3. Medications for SLE: NSAIDs for pain and inflammation: o Ibuprofen (Brand name: Nurofen) o Naproxen (Brand name: Naprosyn) Antimalarial drugs (used for skin and joint symptoms): o Hydroxychloroquine (Brand name: Plaquenil) – Reduces fatigue and joint problems. Corticosteroids for exacerbations: o Prednisolone – To manage flare-ups and inflammation. o Methylprednisolone – Given as an intravenous infusion for severe flare- ups. Immunosuppressive medications for more severe cases: o Azathioprine (Brand name: Imuran) – Used to suppress the immune response. o Cyclophosphamide (Brand name: Cytoxan) – For severe, life-threatening cases. Classes of Medications for SLE: NSAIDs (e.g., Ibuprofen, Naproxen) Antimalarials (e.g., Hydroxychloroquine) Corticosteroids (e.g., Prednisolone, Methylprednisolone) Immunosuppressive Agents (e.g., Azathioprine, Cyclophosphamide) Fibromyalgia Fibromyalgia is a chronic pain syndrome, and treatment focuses on symptom management, especially pain and sleep disturbances. 4. Medications for Fibromyalgia: Analgesics for pain management: o Paracetamol (Brand name: Panadol) o Ibuprofen (Brand name: Nurofen) o Tramadol (Brand name: Ultram) – A weak opioid for moderate pain. Antidepressants for pain and sleep issues: o Amitriptyline – A tricyclic antidepressant used at low doses to help with pain and sleep. o Duloxetine (Brand name: Cymbalta) – A serotonin-norepinephrine reuptake inhibitor (SNRI) used for pain and mood improvement. Anticonvulsants for nerve pain: o Pregabalin (Brand name: Lyrica) – An anticonvulsant used for nerve pain and to improve sleep. Classes of Medications for Fibromyalgia: Analgesics (e.g., Paracetamol, Ibuprofen, Tramadol) Antidepressants (e.g., Amitriptyline, Duloxetine) Anticonvulsants (e.g., Pregabalin) Summary of Medications and Classes: Condition Medications Classes Paracetamol, NSAIDs (Ibuprofen, Analgesics, NSAIDs, COX-2 Osteoarthritis Diclofenac), COX-2 Inhibitors Inhibitors, Corticosteroids (Celecoxib), Corticosteroids Methotrexate, Sulfasalazine, Rheumatoid DMARDs, Biologic DMARDs, Etanercept, Adalimumab, Arthritis NSAIDs, Corticosteroids Prednisolone NSAIDs, Antimalarials, Systemic Lupus Hydroxychloroquine, Prednisolone, Corticosteroids, Erythematosus Azathioprine, Cyclophosphamide Immunosuppressive Paracetamol, Tramadol, Analgesics, Antidepressants, Fibromyalgia Amitriptyline, Duloxetine, Pregabalin Anticonvulsants Osteoarthritis (OA) Aetiology & Pathophysiology: OA is a degenerative joint disease often linked to aging, obesity, trauma, or mechanical stress. Cartilage degeneration and subchondral bone changes lead to pain, joint instability, and osteophyte formation. Signs & Symptoms: Joint pain worsens with activity, morning stiffness lasting less than 30 minutes, crepitus, and deformities like Heberden's and Bouchard's nodes, particularly in the knees, hips, and fingers. Medications: o Analgesics: Paracetamol. o NSAIDs: Ibuprofen, Diclofenac, Meloxicam. o COX-2 Inhibitors: Celecoxib. o Corticosteroids: Prednisolone (oral), Triamcinolone (injections). Rheumatoid Arthritis (RA) Aetiology & Pathophysiology: RA is an autoimmune disease where the immune system attacks synovial membranes, leading to inflammation, joint destruction, and deformities. Signs & Symptoms: Joint pain, swelling, and stiffness, especially in small joints. Extra-articular symptoms like fatigue, rheumatoid nodules, and cardiovascular effects may occur. Medications: o Disease-Modifying Anti-Rheumatic Drugs (DMARDs): Methotrexate, Sulfasalazine, Leflunomide. o Biologic DMARDs: Etanercept, Adalimumab, Rituximab. o NSAIDs: Ibuprofen, Diclofenac. o Corticosteroids: Prednisolone. Systemic Lupus Erythematosus (SLE) Aetiology & Pathophysiology: SLE is a systemic autoimmune disease causing inflammation in multiple organs due to the production of autoantibodies and immune complex deposition. Signs & Symptoms: Malar rash, joint pain, kidney involvement, and cardiovascular issues. Medications: o NSAIDs: Ibuprofen, Naproxen.  o Antimalarials: Hydroxychloroquine. o Corticosteroids: Prednisolone, Methylprednisolone. o Immunosuppressives: Azathioprine, Cyclophosphamide. Fibromyalgia Aetiology & Pathophysiology: Fibromyalgia is characterized by widespread musculoskeletal pain, fatigue, and disturbed sleep, with altered pain processing in the central nervous system. Signs & Symptoms: Chronic pain, sleep disturbances, and tenderness at specific points. Medications: o Analgesics: Paracetamol, Ibuprofen, Tramadol. o Antidepressants: Amitriptyline, Duloxetine. o Anticonvulsants: Pregabalin. Summary of Medications and Their Classes Condition Medications Classes Paracetamol, Ibuprofen, Analgesics, NSAIDs, COX-2 Osteoarthritis (OA) Diclofenac, Celecoxib, Inhibitors, Corticosteroids Prednisolone, Triamcinolone Methotrexate, Sulfasalazine, Rheumatoid DMARDs, Biologic DMARDs, Etanercept, Adalimumab, Arthritis (RA) NSAIDs, Corticosteroids Prednisolone Systemic Lupus Hydroxychloroquine, NSAIDs, Antimalarials, Erythematosus Prednisolone, Azathioprine, Corticosteroids, (SLE) Cyclophosphamide Immunosuppressives Paracetamol, Ibuprofen, Analgesics, Antidepressants, Fibromyalgia Tramadol, Amitriptyline, Anticonvulsants Duloxetine, Pregabalin Osteoarthritis (OA) OA is a degenerative joint disease where pain relief and inflammation control are essential. Medications: Paracetamol – Used as a first-line analgesic to reduce pain and improve quality of life in OA. It is preferred due to its mild effect and fewer side effects compared to stronger pain medications. NSAIDs (e.g., Ibuprofen, Diclofenac, Meloxicam) – These reduce inflammation and provide pain relief by inhibiting cyclooxygenase enzymes, helping to manage OA symptoms. Corticosteroids (e.g., Prednisolone, Triamcinolone) – Used for severe flare-ups to reduce inflammation quickly and effectively, often administered systemically or through joint injections for localized relief. COX-2 Inhibitors (e.g., Celecoxib) – These target the same enzymes as traditional NSAIDs but are less likely to cause gastrointestinal irritation, making them suitable for long-term use in some patients. Rheumatoid Arthritis (RA) RA is an autoimmune condition requiring medications that target inflammation and immune response. Medications: Methotrexate – A cornerstone treatment for RA, a Disease-Modifying Anti- Rheumatic Drug (DMARD) that helps slow disease progression by inhibiting the immune system's attack on the joints. Sulfasalazine – Another DMARD used to treat RA, often in combination with other medications, to help control inflammation and prevent joint damage. Etanercept, Adalimumab (Biologic DMARDs) – These biologics block TNF-alpha, a protein involved in inflammation, offering targeted treatment for severe RA unresponsive to traditional DMARDs. Prednisolone – A corticosteroid used to manage acute flare-ups by rapidly reducing inflammation and pain. Systemic Lupus Erythematosus (SLE) SLE is an autoimmune disease that requires medications to manage systemic inflammation and organ involvement. Medications: Hydroxychloroquine – Used for its anti-inflammatory and immune-modulating properties, hydroxychloroquine helps to control skin and joint symptoms of SLE and prevent flare-ups. NSAIDs (e.g., Ibuprofen, Naproxen) – Used to reduce pain and inflammation in joints and muscles affected by lupus. Prednisolone, Methylprednisolone – Corticosteroids used for managing flare- ups of inflammation and suppressing the immune system to prevent organ damage. Azathioprine, Cyclophosphamide – Immunosuppressive agents used in more severe cases of SLE to prevent organ damage by suppressing abnormal immune responses. Fibromyalgia Fibromyalgia involves widespread pain and is managed with medications that alleviate pain and improve sleep. Medications: Paracetamol, Ibuprofen – Mild analgesics used to reduce pain and improve comfort. Ibuprofen also helps with inflammation that may be contributing to muscle pain. Tramadol – A mild opioid used for moderate pain when other analgesics are insufficient. It is typically used for short-term pain relief. Amitriptyline – A tricyclic antidepressant used in low doses to help manage pain and improve sleep quality, addressing both pain and sleep disturbances in fibromyalgia. Duloxetine (Cymbalta) – An SNRI used to treat both pain and depression associated with fibromyalgia, improving overall functioning. Pregabalin (Lyrica) – An anticonvulsant that is effective in treating nerve pain and improving sleep disturbances often experienced in fibromyalgia. Summary of Medications and Their Purposes Condition Medications Why Paracetamol, NSAIDs (Ibuprofen, Pain relief, reduce Osteoarthritis Diclofenac), COX-2 Inhibitors inflammation, control flare- (Celecoxib), Corticosteroids ups Methotrexate, Sulfasalazine, Slow disease progression, Rheumatoid Etanercept, Adalimumab, reduce immune response, Arthritis Prednisolone control flare-ups Control inflammation, Systemic Lupus Hydroxychloroquine, Prednisolone, prevent flare-ups, suppress Erythematosus Azathioprine, Cyclophosphamide abnormal immune activity Pain relief, improve sleep, Paracetamol, Tramadol, Fibromyalgia manage nerve pain and Amitriptyline, Duloxetine, Pregabalin overall symptoms ### Osteomyelitis: **Pathophysiology:** Osteomyelitis is a severe infection of the bone, often caused by Staphylococcus aureus, and can enter the body through indirect (hematogenous) or direct (open wounds) routes. The infection leads to inflammation and ischaemia, causing bone necrosis. **Clinical Manifestations:** - **Local:** Constant bone pain, swelling, tenderness, warmth, restricted movement. - **Systemic:** Fever, chills, night sweats, nausea, malaise, restlessness. **Risk Factors:** - Children and immunocompromised individuals are more at risk. - Open fractures or penetrating injuries increase susceptibility. **Diagnostic Studies:** Blood cultures, elevated WBC, ESR, MRI, CT scans. **Management:** - Antibiotics and surgery (debridement) are used to reduce mortality. --- ### Bone Tumours (Benign & Malignant): **Benign Tumour – Osteochondroma:** This benign tumour involves the overgrowth of cartilage and bone near the growth plate, typically in long bones, and is common in individuals aged 10-25. **Symptoms:** Painless mass, muscle soreness, leg or arm length discrepancies, or pressure during exercise. **Diagnosis:** X-rays, CT, and MRI confirm the presence of osteochondroma. **Treatment:** Asymptomatic tumours often don't require treatment, but symptomatic ones may need surgical resection. **Malignant Tumour – Osteosarcoma:** Osteosarcoma is a highly aggressive bone tumour, most common in children and young adults. It typically affects the distal femur, proximal humerus, and pelvis. **Symptoms:** Gradual pain and swelling around the knee, possibly after a minor injury. **Diagnosis:** Biopsy, elevated serum alkaline phosphatase, and calcium, along with imaging tests. **Treatment:** Preoperative chemotherapy and surgery (e.g., amputation or limb salvage) improve survival rates. --- ### Muscular Dystrophy (MD): **Pathophysiology:** MD is a group of genetic disorders causing progressive muscle wasting without neurological involvement. The most common form in adults is Duchenne muscular dystrophy (DMD). **Clinical Manifestations:** - Progressive muscle weakness - Difficulty walking, rising from a seated position - Enlarged calf muscles - Cardiomyopathy in some types **Diagnostic Studies:** Creatinine kinase levels, electromyogram, muscle biopsy, ECG (for cardiomyopathy). **Treatment:** There is no cure, but corticosteroids can temporarily slow progression, and physical therapy can maintain mobility. --- ### Lower Back Pain: **Acute Lower Back Pain:** Caused by trauma or stress (e.g., heavy lifting), acute lower back pain lasts up to four weeks and is often associated with muscle strain or injury. **Symptoms:** - Muscle aches, spasms - Limited range of motion - Difficulty standing straight **Diagnostic Tests:** Physical examination; MRI/CT only if trauma or systemic disease is suspected. **Chronic Lower Back Pain:** Lasts longer than three months and may result from degenerative conditions like arthritis, prior injuries, or metabolic bone diseases. **Assessment:** A thorough history and musculoskeletal assessment are key, with imaging used to rule out serious conditions like cancer. Crohn’s Disease: What is it? A type of IBD that can affect any part of the gastrointestinal (GI) tract (from the mouth to the anus). Most common areas affected are the terminal ileum (end of the small intestine) and the colon. Pathophysiology (How it works): Inflammation occurs in all layers of the intestines, which can lead to narrowing (strictures) and abnormal connections (fistulas) between organs. The inflammation is patchy, meaning some parts of the intestine are inflamed, but others are healthy. This is called skip lesions. Symptoms (What happens): Abdominal pain and cramping. Diarrhea, often with blood. Weight loss and malnutrition due to difficulty absorbing nutrients. Fatigue and mouth sores. Treatment: Corticosteroids (e.g., prednisone) to reduce inflammation. Immunosuppressants (e.g., azathioprine) to lower immune system activity. Biologics (e.g., infliximab) to target specific parts of the immune system. Surgery if necessary (for complications like fistulas or strictures). Ulcerative Colitis: What is it? A type of IBD that only affects the colon (large intestine) and rectum. Inflammation starts in the rectum and spreads up through the colon. Pathophysiology (How it works): Inflammation only affects the inner layer (mucosa) of the colon. The inflammation is continuous, not patchy. Symptoms (What happens): Bloody diarrhea, which is a key symptom. Abdominal pain, often relieved after bowel movements. Rectal bleeding and urgent bowel movements. Weight loss and fatigue. Treatment: Aminosalicylates (e.g., mesalazine) to reduce inflammation in the colon. Corticosteroids for flare-ups. Immunosuppressants to maintain remission. Biologics to control inflammation. Surgery in severe cases (to remove part of the colon). Comparison of Crohn’s Disease and Ulcerative Colitis: Feature Crohn’s Disease Ulcerative Colitis Anywhere in the GI tract (most Where it affects common in the terminal ileum Only the colon and rectum and colon) Feature Crohn’s Disease Ulcerative Colitis Type of Inflammation affects all layers of Inflammation affects only the inflammation the intestines inner lining of the colon Inflammation Patchy (areas of healthy tissue Continuous from the rectum pattern between inflamed parts) upwards Abdominal pain, diarrhea, weight Bloody diarrhea, abdominal pain, Symptoms loss, mouth sores rectal bleeding Strictures, fistulas, Complications Toxic megacolon, colon cancer malabsorption Corticosteroids, Aminosalicylates, corticosteroids, Treatment immunosuppressants, biologics, immunosuppressants, biologics, surgery surgery Summary: Crohn’s disease can affect any part of the digestive system and causes deep inflammation that can lead to serious complications like fistulas. It often requires stronger medications and sometimes surgery. Ulcerative colitis only affects the colon and rectum, and the inflammation is more superficial and continuous. It is typically managed with medications that focus on reducing inflammation in the colon. Inflammatory Bowel Disease (IBD) Definition: Inflammatory Bowel Disease (IBD) refers to a group of chronic disorders involving inflammation of the gastrointestinal (GI) tract. The two main types are Crohn's disease and ulcerative colitis, both leading to similar symptoms such as abdominal pain, diarrhea, and weight loss. Pathophysiology: In IBD, an abnormal immune response leads to inflammation in the GI tract, where the body attacks its own tissues. Crohn's disease can affect any part of the GI tract but typically affects the terminal ileum and colon. It presents with "skip lesions" where areas of the intestine are inflamed, with normal tissue in between. Ulcerative colitis typically affects the rectum and spreads continuously through the large intestine, affecting only the mucosal and submucosal layers. Aetiology: The exact cause is unclear, but genetic predisposition, environmental factors, and immune system dysfunction contribute to the development of IBD. Risk factors include a family history of IBD, smoking (in Crohn’s disease), and certain infections. Pharmacology Used to Treat: Corticosteroids: Used for their anti-inflammatory effects to manage flare-ups. Immunosuppressants (e.g., azathioprine): Suppress the immune response, helping to reduce inflammation. Biologics (e.g., infliximab): Target specific components of the immune system to control inflammation. Antibiotics: Can be used to treat secondary infections, particularly in Crohn's disease. Clinical Manifestations & Link to Pathophysiology: Crohn’s disease: Abdominal pain, diarrhea, malnutrition, and weight loss due to inflammation and malabsorption in affected areas of the GI tract. Ulcerative colitis: Bloody diarrhea, colicky abdominal pain, and rectal bleeding due to mucosal damage and ulcers in the colon. Risk Factor Management: Smoking cessation (particularly for Crohn’s disease). Diet modifications to reduce flare-ups and malnutrition. Medications to control inflammation and immune response. Liver Disease (Cirrhosis and Hepatitis) Cirrhosis: Definition: Cirrhosis is the advanced scarring of the liver due to long-term liver damage, often caused by chronic alcohol use, hepatitis, or fatty liver disease. Pathophysiology: In cirrhosis, liver tissue is replaced by scar tissue, impairing the liver's ability to function. The scarring disrupts blood flow through the liver and reduces its capacity to detoxify blood and produce proteins. Aetiology: Alcohol consumption: Chronic excessive drinking leads to liver injury and eventual cirrhosis. Hepatitis B and C: Chronic viral infections cause ongoing liver damage. Non-alcoholic fatty liver disease (NAFLD): Linked to obesity and metabolic syndrome. Pharmacology Used to Treat: Diuretics (e.g., spironolactone): Manage fluid retention and ascites. Beta-blockers (e.g., propranolol): Used to reduce the risk of variceal bleeding by lowering portal pressure. Lactulose: Reduces ammonia levels in the blood, preventing hepatic encephalopathy. Clinical Manifestations & Link to Pathophysiology: Jaundice: Due to impaired bilirubin metabolism. Ascites and edema: Due to portal hypertension and hypoalbuminemia. Esophageal varices: Increased pressure in the portal vein leads to varices that can rupture and bleed. Risk Factor Management: Limiting alcohol intake or complete abstinence. Management of hepatitis (antiviral drugs for Hep B or C). Regular screening for hepatocellular carcinoma. Hepatitis Definition: Hepatitis refers to inflammation of the liver, which can be acute or chronic. It is classified into types A, B, C, D, and E, with varying modes of transmission and severity. Pathophysiology: The liver becomes inflamed in response to the viral infection, which can cause liver cell damage. In chronic hepatitis, this leads to scarring and possible cirrhosis. Aetiology: Hepatitis A: Transmitted through contaminated food and water. Hepatitis B and C: Spread via blood and bodily fluids (e.g., sexual transmission, needle sharing). Hepatitis D: Occurs only in those infected with Hepatitis B. Hepatitis E: Transmitted via contaminated water. Pharmacology Used to Treat: Antiviral drugs: For chronic hepatitis B and C (e.g., interferon, direct-acting antivirals like sofosbuvir for Hep C). Supportive care: Rest, hydration, and liver-friendly diets. Clinical Manifestations & Link to Pathophysiology: Jaundice: Due to the inability of the liver to process bilirubin. Fatigue, abdominal pain, nausea: Due to inflammation and liver dysfunction. Hepatomegaly: Enlarged liver as a result of inflammation. Risk Factor Management: Vaccination (Hepatitis A and B). Avoidance of risky behaviors (e.g., safe sex, needle exchange programs). Monitoring liver function through regular screenings. Gallbladder Conditions: Cholelithiasis and Cholecystitis Cholelithiasis (Gallstones) Definition: Cholelithiasis refers to the formation of gallstones in the gallbladder. These stones can block the bile ducts, leading to pain and complications like jaundice or pancreatitis. Pathophysiology: Gallstones form when bile contains too much cholesterol or bilirubin, or when the gallbladder does not empty properly. The stones can obstruct bile flow, leading to pain and potential infection. Aetiology: Obesity and high-fat diets increase the risk of gallstone formation. Genetics: Family history of gallstones. Pregnancy: Hormonal changes increase the likelihood of stone formation. Pharmacology Used to Treat: Ursodeoxycholic acid: Can dissolve small cholesterol stones in some cases. Pain management: Analgesics to relieve biliary colic pain. Clinical Manifestations & Link to Pathophysiology: Biliary colic: Severe, intermittent pain in the upper right abdomen, often triggered by fatty meals. Jaundice: If a stone obstructs the bile duct. Nausea and vomiting: Due to obstruction and inflammation. Risk Factor Management: Weight loss and a low-fat diet. Medications to dissolve cholesterol-based stones. In some cases, surgical removal of the gallbladder (cholecystectomy). Cholecystitis Definition: Cholecystitis is the inflammation of the gallbladder, typically caused by gallstones blocking the cystic duct. Pathophysiology: Obstruction of the cystic duct leads to bile stasis, inflammation, and possible infection in the gallbladder. Aetiology: Gallstones: The most common cause of cholecystitis. Infection: Bacterial infection can occur if the bile ducts are obstructed. Pharmacology Used to Treat: Antibiotics: For bacterial infection (e.g., ceftriaxone). Pain management: Nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids. Clinical Manifestations & Link to Pathophysiology: Severe right upper abdominal pain: Due to inflammation of the gallbladder. Fever: Indicates infection. Nausea and vomiting: Due to inflammation and bile duct obstruction. Risk Factor Management: Treatment of acute episodes with antibiotics and pain management. Elective cholecystectomy (gallbladder removal) to prevent further attacks. Liver Function Tests (LFTs) Overview Liver Function Tests (LFTs) are a group of blood tests used to check how well your liver is working. These tests measure different substances in the blood that the liver produces or processes. Here's a breakdown of key components: 1. Alkaline Phosphatase (ALP): An enzyme found in the liver, bones, and placenta. Normal range: 30-120 units/L. 2. Alanine Aminotransferase (ALT): An enzyme found mainly in the liver. Normal range: 4-36 units/L. 3. Aspartate Aminotransferase (AST): Found in the liver, heart, and muscles. Normal range: 0-35 units/L. 4. Gamma-Glutamyl Transferase (GGT): An enzyme mainly in the liver. Normal range: 8-38 units/L. 5. Bilirubin: A product from the breakdown of red blood cells. It can be unconjugated (indirect) before it reaches the liver and conjugated (direct) after. Normal range: 0.3-1.0 mg/dL. When Are LFTs Done? LFTs are typically ordered when someone shows signs of liver problems, such as: Fatigue Nausea Vomiting Right upper abdominal pain Jaundice (yellowing of skin or eyes) They are also checked when monitoring people with liver diseases (like hepatitis) or those on hepatotoxic medications (e.g., acetaminophen). What Elevated LFTs Can Mean:  Hepatocellular injury (damage to liver cells): High ALT and AST levels. Biliary stasis (blockage in bile ducts): High ALP and GGT levels. Alcoholic liver disease: Typically shows a higher AST to ALT ratio (usually 2:1) and an increased GGT. Hepatitis or liver cancer: Causes damage to liver cells and increases ALT and AST. Bilirubin levels can rise if there is liver damage or excessive red blood cell breakdown, leading to jaundice. Nursing Management for Altered LFTs: 1. Collection of Sample: o A venipuncture (blood draw) is used to collect the sample. o Make sure the client fasts (if required) before the test. o Use a red-topped tube and gently invert the tube (don’t shake) to avoid altering the results. 2. Assess for Symptoms: o Right upper quadrant abdominal pain o Fatigue o Nausea o Jaundice o Bleeding or bruising (may indicate low clotting factors due to liver dysfunction) 3. Check Other Lab Results: o Prothrombin Time (PT) and INR if there are bleeding signs. o Albumin level if edema is present. 4. Medications: o Withhold hepatotoxic medications (e.g., acetaminophen, phenytoin) if indicated. o Administer IV fluids and other medications to treat the underlying condition. 5. Review Medications: o Ensure no medications that could affect the liver function tests (e.g., acetaminophen, allopurinol, phenobarbital). Summary: LFTs measure liver health and include tests for enzymes like ALP, ALT, AST, GGT, and bilirubin. Elevated LFTs can point to liver or bile duct problems, liver disease, or certain medications. Nursing management includes blood sample collection, symptom assessment, and reviewing medications that might impact liver function. Overview of Respiratory and Circulatory Conditions Tuberculosis (TB) Description: TB is a contagious bacterial infection caused by Mycobacterium tuberculosis that affects the lungs and can spread to other parts of the body. It's spread through airborne droplets when an infected person coughs or sneezes.  Pathophysiology: Inhaled bacteria lodge in the lung's small airways, causing inflammation and forming granulomas (small clusters of immune cells) around the bacteria. These granulomas help contain the infection, but in some cases, they break down, allowing the bacteria to spread. Management: TB is treated with a multi-drug approach (isoniazid, rifampin, ethambutol, pyrazinamide) over several months, with adherence being critical to prevent drug resistance. Symptoms: Cough, fever, weight loss, night sweats. Risk Factors: High exposure risk, lack of vaccination, or poor adherence to medication. Cystic Fibrosis (CF) Description: CF is a genetic condition that mainly affects the lungs and digestive system, causing thick, sticky mucus that blocks airways and leads to repeated infections. Pathophysiology: Due to a genetic mutation, the body produces mucus that is thicker than normal, clogging the airways and making it difficult to clear bacteria, leading to chronic lung infections and scarring over time. Management: There’s no cure, so treatment focuses on symptom control, including airway clearance techniques, mucolytics to thin mucus, antibiotics, and nutritional support. Symptoms: Chronic cough, frequent lung infections. Risk Factors: Inherited condition; early detection through genetic screening can help manage symptoms effectively. COVID-19 Description: COVID-19 is a viral infection caused by SARS-CoV-2, primarily affecting the respiratory system. It can range from mild symptoms to severe illness. Pathophysiology: The virus enters cells via ACE2 receptors, particularly in the lungs, causing inflammation. Severe cases lead to widespread inflammation that can damage lung tissue and, in some cases, affect other organs. Management: Treatment varies by severity. Mild cases may only need supportive care, while severe cases may require antivirals, corticosteroids, or anticoagulants to prevent complications. Symptoms: Fever, cough, shortness of breath, fatigue. Risk Factors: Preventive measures like mask-wearing, social distancing, vaccination, and hand hygiene are crucial. Acute Pulmonary Oedema (APO) Description: APO is a buildup of fluid in the lungs, often due to heart failure, which makes breathing difficult and reduces oxygen levels in the blood. Pathophysiology: When the heart fails to pump blood effectively, pressure builds up in the lung blood vessels, causing fluid to leak into the alveoli (air sacs), blocking normal oxygen exchange. Management: APO requires urgent treatment with diuretics to reduce fluid buildup, oxygen to aid breathing, and sometimes medications to decrease heart strain.  Symptoms: Sudden breathlessness, crackling sounds in lungs, cyanosis (blue- tinged skin). Risk Factors: Managing high blood pressure and monitoring for heart failure can help reduce risk. Pulmonary Embolism (PE) Description: PE is a blockage in a pulmonary artery, typically caused by a blood clot from another part of the body (often the legs), which can stop blood flow to part of the lung. Pathophysiology: A clot (thrombus) blocks a blood vessel in the lungs, restricting blood flow and oxygenation. This causes lung tissue to lack oxygen and can lead to serious complications if untreated. Management: PE is a medical emergency requiring anticoagulants to prevent further clots, and in severe cases, clot-busting drugs or surgery may be needed. Symptoms: Sudden chest pain, shortness of breath, hypoxia (low oxygen). Risk Factors: Preventive measures include mobility, anticoagulants for at-risk patients, and wearing compression stockings to reduce the chance of clot formation. Key Differences and Prevention Tips TB, CF, and COVID-19 primarily affect the lungs but differ in cause: TB is bacterial, CF is genetic, and COVID-19 is viral. APO and PE are circulatory in nature, with APO often resulting from heart failure and PE from blood clots obstructing the lungs. Prevention: o TB: Vaccination and avoiding exposure. o CF: Genetic screening. o COVID-19: Vaccination, hygiene, and distancing. o APO: Managing heart health and fluid intake. o PE: Preventing blood clots with mobility and compression. Perioperative Pain Management Analgesics: Used to manage surgical pain. o Opioids (e.g., morphine, fentanyl): For moderate-to-severe pain; act on CNS receptors to reduce pain perception. o NSAIDs (e.g., ibuprofen, ketorolac): Reduce inflammation and pain but monitor for bleeding risk. o Local Anesthetics (e.g., lidocaine): Block nerve conduction in a localized area. 2. Cerebrovascular Accident (CVA) / Stroke Thrombolytics (e.g., alteplase): Dissolve clots in ischemic stroke; given within a specific time window post-onset. Antiplatelets (e.g., aspirin, clopidogrel): Prevent future clots by inhibiting platelet aggregation. Antihypertensives (e.g., ACE inhibitors, beta-blockers): Lower blood pressure to reduce stroke risk. Statins (e.g., atorvastatin): Manage cholesterol to reduce recurrence risk. 3. Differential Diagnosis of Chest Pain Antiplatelets (e.g., aspirin): Prevent further clotting in suspected acute coronary syndrome (ACS). Nitrates (e.g., nitroglycerin): Dilate blood vessels to reduce chest pain in angina. Beta-Blockers (e.g., metoprolol): Decrease heart workload and oxygen demand. Calcium Channel Blockers (e.g., diltiazem): Relieve angina by relaxing blood vessels. 4. Chronic Kidney Disease (CKD) Antihypertensives (e.g., ACE inhibitors, ARBs): Control blood pressure to slow CKD progression. Diuretics (e.g., furosemide): Manage fluid retention, but use cautiously to avoid electrolyte imbalance. Phosphate Binders (e.g., calcium acetate): Reduce phosphate levels, which can build up in CKD. Erythropoiesis-Stimulating Agents (e.g., epoetin alfa): Address anemia due to decreased kidney erythropoietin production. 5. Chronic Musculoskeletal Conditions NSAIDs (e.g., ibuprofen, diclofenac): Relieve inflammation and pain in conditions like arthritis. Muscle Relaxants (e.g., baclofen): Decrease muscle spasms in neuromuscular conditions. Disease-Modifying Antirheumatic Drugs (DMARDs) (e.g., methotrexate): Slow disease progression in rheumatoid arthritis. Corticosteroids (e.g., prednisone): Reduce severe inflammation in autoimmune musculoskeletal conditions. 6. Inflammatory Bowel Disease (IBD) Aminosalicylates (e.g., mesalamine): Reduce inflammation in the intestinal lining, especially for mild to moderate cases. Corticosteroids (e.g., prednisone): Treat moderate to severe IBD flare-ups by suppressing inflammation. Immunosuppressants (e.g., azathioprine): Decrease immune response to control chronic inflammation. Biologics (e.g., infliximab): Target specific inflammatory pathways in moderate- to-severe IBD. 7. Liver Failure Diuretics (e.g., spironolactone, furosemide): Manage ascites by promoting fluid loss; spironolactone also spares potassium. Lactulose: Lowers blood ammonia levels, reducing hepatic encephalopathy symptoms. Beta-Blockers (e.g., propranolol): Prevent variceal bleeding by reducing portal hypertension.  Vitamin K and other supplements: Manage coagulation issues due to poor liver synthesis of clotting factors. 8. Respiratory Conditions Tuberculosis (TB) Antitubercular Drugs (e.g., isoniazid, rifampin): Target Mycobacterium tuberculosis; combination therapy is critical to prevent resistance. Cystic Fibrosis Mucolytics (e.g., dornase alfa): Break down thick mucus to improve airway clearance. Bronchodilators (e.g., albuterol): Open airways to ease breathing. Antibiotics: Treat chronic respiratory infections, commonly caused by Pseudomonas aeruginosa. COVID-19 Antivirals (e.g., remdesivir): Used in severe cases to reduce viral replication. Corticosteroids (e.g., dexamethasone): Reduce inflammation in severe respiratory symptoms. Anticoagulants: Prevent blood clots due to increased risk of thromboembolic events in COVID-19 patients. Acute Pulmonary Oedema (APO) Diuretics (e.g., furosemide): Rapidly remove excess fluid from the lungs. Nitrates (e.g., nitroglycerin): Reduce blood pressure and heart workload. Oxygen Therapy: Improve oxygenation in hypoxic patients. Pulmonary Embolism (PE) Anticoagulants (e.g., heparin, warfarin): Prevent clot formation and propagation. Thrombolytics (e.g., alteplase): Dissolve large clots in emergency situations. Oxygen Therapy: Address hypoxia in PE cases. 1. Antiplatelet Drugs What they do: Prevent platelets from clumping together and forming clots. Example: o Aspirin: Used for preventing heart attacks and strokes. o Clopidogrel: Often used after a heart attack or stroke to prevent further clots. 2. Anticoagulants What they do: Slow down the blood’s clotting process to prevent clot formation. Example: o Heparin: Used in hospitals to treat deep vein thrombosis (DVT) or pulmonary embolism (PE). o Warfarin: Used for long-term prevention of stroke or DVT. 3. Thrombolytics (Clot Busters) What they do: Break down existing blood clots. Example: o Alteplase: Given to patients having an acute stroke or heart attack to dissolve clots. 1. Cardiac Causes  Myocardial Infarction (MI) o Assessment: Sudden, crushing chest pain, radiating to the left arm, jaw, or back, accompanied by nausea, sweating, and shortness of breath. o Diagnosis: ECG changes (ST elevation or depression), elevated cardiac enzymes (troponins). o Interventions: Aspirin, heparin, morphine, thrombolytics (if indicated), angioplasty or CABG if needed. Angina Pectoris o Assessment: Chest pain triggered by exertion or stress, relieved by rest. o Diagnosis: ECG at rest may show no changes; stress test or coronary angiography for confirmation. o Interventions: Nitroglycerin, beta-blockers, aspirin, angioplasty or stenting in severe cases. Pericarditis o Assessment: Sharp, pleuritic chest pain worsened by lying flat, may improve with sitting up or leaning forward. o Diagnosis: ECG changes (diffuse ST elevation), elevated CRP and ESR. o Interventions: NSAIDs (e.g., ibuprofen), colchicine for recurrent cases. Aortic Dissection o Assessment: Severe, tearing chest pain that radiates to the back, often with a difference in blood pressure between arms. o Diagnosis: CT angiography or transesophageal echocardiography to visualize the dissection. o Interventions: Surgical repair or medical management with beta-blockers to control blood pressure. 2. Gastrointestinal Causes Gastroesophageal Reflux Disease (GERD) o Assessment: Burning chest pain, often after meals, worsens with lying down, associated with acid regurgitation. o Diagnosis: Endoscopy or 24-hour pH monitoring for confirmation. o Interventions: Antacids, H2 blockers (e.g., ranitidine), proton pump inhibitors (e.g., omeprazole). Esophageal Spasm o Assessment: Sudden, intense chest pain, often mistaken for angina, associated with swallowing. o Diagnosis: Esophageal manometry or barium swallow to detect spasm. o Interventions: Nitrates, calcium channel blockers for relief. Peptic Ulcer Disease (PUD) o Assessment: Burning chest pain, often worse when hungry or after meals, may have nausea or vomiting. o Diagnosis: Endoscopy to visualize ulcers. o Interventions: Proton pump inhibitors (e.g., omeprazole), antibiotics for H. pylori infection. 3. Pulmonary Causes Pulmonary Embolism (PE)  o Assessment: Sudden sharp chest pain, difficulty breathing, tachypnea, and cough. May have a history of deep vein thrombosis (DVT). o Diagnosis: CT pulmonary angiography, D-dimer test. o Interventions: Anticoagulation (e.g., heparin, warfarin), thrombolytics for massive PE. Pneumothorax o Assessment: Sudden, sharp chest pain, shortness of breath, may have history of trauma or lung disease. o Diagnosis: Chest X-ray shows air in the pleural space. o Interventions: Needle decompression or chest tube insertion. Pneumonia o Assessment: Chest pain worsened with breathing or coughing, fever, cough with sputum. o Diagnosis: Chest X-ray shows consolidation. o Interventions: Antibiotics, analgesics (e.g., paracetamol) for pain management. Pleural Effusion o Assessment: Sharp chest pain with breathing, shortness of breath, decreased breath sounds. o Diagnosis: Chest X-ray or ultrasound to detect fluid. o Interventions: Thoracentesis to drain fluid, diuretics if caused by heart failure. 4. Musculoskeletal Causes Costochondritis o Assessment: Sharp, localized chest pain that worsens with palpation of the costosternal junction. o Diagnosis: Clinical diagnosis; no imaging needed. o Interventions: NSAIDs (e.g., ibuprofen) for pain relief. Muscle Strain o Assessment: Pain related to movement, localized to chest wall muscles. o Diagnosis: Clinical diagnosis; no imaging needed. o Interventions: Analgesics (e.g., paracetamol), muscle relaxants. 5. Psychological Causes Panic Attack o Assessment: Sudden onset of chest pain, accompanied by rapid heartbeat, dizziness, and a sense of impending doom. o Diagnosis: Clinical diagnosis, often after ruling out other causes. o Interventions: Benzodiazepines (e.g., lorazepam) for acute episodes, cognitive-behavioural therapy (CBT) for ongoing management. Summary of Key Diagnostic Tools: ECG: For myocardial infarction, pericarditis, and angina. Chest X-ray: For lung-related causes (pneumonia, pneumothorax, pleural effusion). CT Pulmonary Angiography: For pulmonary embolism.  Endoscopy/Manometry: For gastrointestinal causes like GERD or esophageal spasm. Troponins and Cardiac Enzymes: To confirm myocardial infarction. Key Interventions: Aspirin and heparin for cardiac-related chest pain. Analgesics (e.g., paracetamol, ibuprofen) for musculoskeletal pain. Antibiotics for infections like pneumonia. Anticoagulants for pulmonary embolism.