Study Notes – Overview of Common Diseases and Pathophysiology. Cardiovascular System

1. Congestive Heart Failure (CHF)

• Definition: Heart unable to pump blood efficiently → fluid buildup (“congestion”).

• Types:

  • Left-sided failure: Blood backs up into lungs → pulmonary edema (crackles, dyspnea).

  • Right-sided failure: Blood backs up into body → systemic edema (leg swelling).

• Key Pathophysiology: Inadequate forward flow → backward pressure → venous congestion.

• Treatment: Diuretics, ACE inhibitors, beta blockers, oxygen therapy, fluid/salt restriction.

2. Cardiac Arrest

• Definition: Sudden cessation of effective heart function due to electrical failure.

• Cause: SA node or AV node stops firing → no electrical conduction.

• Treatment: CPR + AED (defibrillator) to restart SA node rhythm.

• Mnemonic: “AED for Arrest → Electrical restart.”

3. Hypertension (High Blood Pressure)

• Definition: Sustained elevation of arterial pressure.

• Causes: Atherosclerosis (narrowed arteries), stress, obesity, poor diet, inactivity.

• Effects on Organs:

  • Kidneys: Chronic pressure damages nephrons → CKD/AKI, proteinuria.

  • Brain: Can cause strokes (ischemic or hemorrhagic).

  • Heart: Leads to LV hypertrophy, MI, heart failure.

• Treatment: Lifestyle modification, antihypertensive meds (ACE inhibitors, ARBs, diuretics, beta blockers).

II. Neurological Conditions

4. Stroke

• Ischemic Stroke: Blocked artery → reduced brain perfusion → neuron death.

  • Cause: Clot or plaque buildup.

  • Treatment: Clot busters (tPA) within time window.

• Hemorrhagic Stroke: Artery rupture → brain bleed.

  • Cause: Chronic hypertension, aneurysm.

  • Treatment: Clot-promoting agents; surgical intervention.

5. Myocardial Infarction (MI)

• Definition: Ischemic necrosis of heart muscle due to coronary artery blockage.

• Cause: Atherosclerosis, plaque rupture, thrombosis.

• Symptoms: Chest pain (radiating to left arm/jaw), diaphoresis, nausea.

• Treatment: Aspirin, nitroglycerin, thrombolytics, PCI/stent.

• Mnemonic: “MONA” – Morphine, Oxygen, Nitrates, Aspirin.

III. Pulmonary (Respiratory) System

6. COPD (Chronic Obstructive Pulmonary Disease)

• Definition: Irreversible airflow limitation (includes chronic bronchitis, emphysema).

• Cause: Smoking, air pollution, long-term toxin exposure.

• Pathophysiology: Inflammation → fibrosis → alveolar wall destruction → ↓ gas exchange.

• Complication: Respiratory acidosis due to CO₂ retention.

• Treatment: Stop smoking, bronchodilators, corticosteroids, oxygen.

7. Asthma

• Definition: Reversible airway narrowing from smooth muscle constriction.

• Triggers: Exercise, allergens, cold air, stress.

• Treatment:

  • Albuterol (β₂-agonist): Bronchodilator.

  • Epinephrine: For severe cases (anaphylaxis).

  • Inhaled corticosteroids: Reduce inflammation.

8. Pulmonary Embolism (PE)

• Definition: Obstruction of pulmonary artery by a clot (often from DVT).

• Pathophysiology: Clot travels via venous system → heart → pulmonary arteries → ↓ oxygenation.

• Symptoms: Sudden dyspnea, chest pain, tachycardia, hypoxia.

• Treatment: Anticoagulants, thrombolytics, embolectomy (if severe).

IV. Neurological (Degenerative) Disorders

9. Alzheimer’s Disease

• Cause:

  • Amyloid plaques (extracellular).

  • Tau protein tangles (intraneuronal).

• Effect: Neuron compression and death → memory loss, cognitive decline.

• Treatment: Cholinesterase inhibitors (donepezil), supportive care.

10. Parkinson’s Disease

• Cause: Low dopamine in basal nuclei → loss of motor control.

• Symptoms: Tremors, rigidity, bradykinesia, shuffling gait.

• Treatment: Levodopa + Carbidopa (dopamine precursor).

V. Renal and Urinary System

11. Rhabdomyolysis

• Definition: Breakdown of skeletal muscle releasing creatine phosphokinase (CPK).

• Cause: Overexertion, crush injury, heat stroke, prolonged immobilization.

• Pathophysiology: CPK and myoglobin clog renal tubules → ↓ filtration rate → AKI.

• Symptoms: Muscle pain, dark urine, fatigue.

• Treatment: Aggressive IV fluids, monitor kidney function.

12. Urinary Tract Infection (UTI)

• Definition: Bacterial infection (commonly E. coli) of urinary tract.

• Symptoms: Burning, frequency, urgency, cloudy urine.

• Treatment: Antibiotics, hydration, cranberry supplements (natural antibacterial).

13. Kidney Stones (Nephrolithiasis)

• Definition: Crystals (calcium oxalate, uric acid) formed in kidneys.

• Cause: Dehydration, high soda intake, high oxalate diet.

• Symptoms: Flank pain, hematuria, nausea.

• Treatment: Hydration, pain control, lithotripsy if large.

• Prevention: Increased fluids, dietary modification.

VI. Summary Table

System	Disease	Key Problem	Main Consequence	Treatment Summary
Heart	CHF	Pump failure	Pulmonary/Systemic edema	Diuretics, ACE inhibitors
Heart	Cardiac arrest	Electrical failure	No cardiac output	CPR, AED
Circulation	Hypertension	High vascular pressure	Stroke, CKD	Antihypertensives
Brain	Stroke (Ischemic/Hemorrhagic)	Clot or rupture	Brain damage	Clot busters / Hemostatics
Heart	MI	Coronary blockage	Heart muscle death	Aspirin, Nitro, PCI
Lungs	COPD	Alveolar damage	CO₂ retention	Stop smoking, bronchodilators
Lungs	Asthma	Airway constriction	Dyspnea	Albuterol, steroids
Lungs	Pulmonary embolism	Clot in pulmonary artery	Hypoxia	Anticoagulants
Brain	Alzheimer’s	Amyloid/tau buildup	Dementia	Cholinesterase inhibitors
Brain	Parkinson’s	↓ Dopamine	Motor dysfunction	Levodopa
Kidneys	Rhabdomyolysis	Muscle breakdown → toxins	AKI	IV fluids
Urinary	UTI	Bacterial infection	Dysuria	Antibiotics
Urinary 🩸 Pathophysiology of Common Blood, Autoimmune, and Bone Diseases — Study Notes I. Blood and Red Blood Cells (RBCs) Blood = “river of life” transporting O₂ and CO₂. ~60,000 miles of blood vessels in the body. RBCs (erythrocytes): carry oxygen (O₂) to tissues and carbon dioxide (CO₂) to lungs. Hemoglobin (Hb): Iron-containing carrier protein (98% of RBC content). Composed of 2 alpha + 2 beta chains (tetrameric structure). Iron (Fe²⁺) in center binds O₂ and CO₂. “Hemoglobin = protein glob + iron (heme)” II. Anemia Definition: Low red blood cell count (RBC < 4–6 ×10¹²/L) or low hemoglobin (Hb < 130 g/L in men, <115 g/L in women). Types and Causes Iron-Deficiency Anemia ↓ Iron → ↓ Hemoglobin → ↓ RBC production. Common in women due to menstrual blood loss. Treatment: Iron-rich foods (red meat, fortified cereals) or iron supplements. Ferritin: Iron storage protein. Low ferritin = depleted iron stores → early sign of anemia. Vitamin B₁₂ Deficiency Anemia Vitamin B₁₂ (cobalamin): needed for RBC formation. RBC precursor: Hemocytoblast (blood stem cell) requires B₁₂ to mature. Intrinsic factor (IF): secreted by stomach; required for B₁₂ absorption in small intestine. ↓ IF = ↓ B₁₂ absorption → ↓ RBCs. Sickle Cell Anemia (Genetic) Mutation in β-globin gene on chromosome 11. Genotypes: HH = normal Hh = sickle cell trait (carrier, malaria-resistant) hh = sickle cell disease Pathophysiology: RBCs become crescent-shaped → obstruct capillaries → ischemia (↓ blood flow). Leads to pain crises, organ damage, fatigue due to tissue hypoxia. III. White Blood Cells (WBCs) and Immune Function Stem cells (hemocytoblasts) also form WBCs. Lymphocytes: produce antibodies (attach to antigens on pathogens). Macrophages: engulf and digest tagged pathogens. Teamwork: lymphocytes tag → macrophages destroy. IV. Infections and the Lungs Tuberculosis (TB) Cause: Mycobacterium tuberculosis (bacterium). Transmission: airborne droplets. Pathophysiology: infects alveoli → inflammation → ↓ gas exchange. Treatment: antibiotics (since bacterial). Pneumonia Definition: infection → fluid accumulation in alveoli. Causes: Bacteria (Streptococcus pneumoniae) Viruses (COVID-19) Fungi (in immunocompromised). Mechanism: Infected tissue → ↑ capillary permeability → fluid + immune cells leak into alveoli. ↓ O₂ diffusion → hypoxia. Complication: may progress to sepsis. Sepsis Definition: systemic inflammatory response from infection. Key mediator: Interleukins (IL) → trigger widespread inflammation. Consequences: Vasodilation → fluid leakage → organ hypoperfusion. Multi-organ failure, septic shock, death if untreated. Treatment: fluids, antibiotics, insulin (manage hyperglycemia). V. Autoimmune and Joint Disorders Rheumatoid Arthritis (RA) Autoimmune disease: WBCs attack synovium (joint lining). Synovial fluid: acts like “WD-40” for joints, secreted by synovial membrane. Pathophysiology: WBCs (especially lymphocytes) invade synovium → inflammation (↑ interleukins). Chronic attack erodes cartilage and bone → deformity. Treatment: immunosuppressive drugs (e.g., corticosteroids, DMARDs). Note: Progressive and irreversible damage. Gout Cause: Excess uric acid → crystal formation in joints. Uric acid: byproduct of protein and purine metabolism. Risk factors: High protein diet Alcohol Kidney disease (↓ excretion of uric acid) Obesity Pathophysiology: Crystals form in cooler areas (joints) → inflammation + pain. Common sites: big toe, ankle, knee. Treatment: Reduce purine intake (avoid red meats, alcohol). Medications: allopurinol, colchicine. VI. Clinical Summary Table Condition Cause Key Pathophysiology Main Symptoms Treatment Iron Deficiency Anemia ↓ Iron intake/loss ↓ Hemoglobin production Fatigue, pallor Iron supplements B₁₂ Deficiency ↓ Intrinsic factor or intake Impaired RBC maturation Fatigue, neuropathy B₁₂ injections Sickle Cell Anemia Genetic (β-globin mutation) Sickled RBCs → ischemia Pain crises, fatigue Hydroxyurea, transfusions Tuberculosis M. tuberculosis Lung infection Cough, weight loss Antibiotics Pneumonia Bacterial/viral infection Fluid in alveoli Fever, SOB Antibiotics/antivirals Sepsis Systemic infection Widespread inflammation Fever, hypotension IV fluids, antibiotics Rheumatoid Arthritis Autoimmune Synovial attack → joint erosion Joint pain, deformity Immunosuppressants Gout ↑ Uric acid Crystal deposition in joints Pain, swelling Allopurinol, diet changes	Kidney stones	Crystal formation	Obstruction pain	Hydration, lithotripsy