Pathology Exam 3 PDF

Dyslipidemia: imbalance in triglycerides, phospholipids, and cholesterol Etiology and Pathogenesis: Factors that raise blood lipid: nutrition, genetics, medications, comorbid conditions, metabolic disease - Primary dyslipidemia vs secondary dyslipidemia - Dyslipidemia is characteri...

Dyslipidemia: imbalance in triglycerides, phospholipids, and cholesterol Etiology and Pathogenesis: Factors that raise blood lipid: nutrition, genetics, medications, comorbid conditions, metabolic disease - Primary dyslipidemia vs secondary dyslipidemia - Dyslipidemia is characterized by increase triglycerides, increase total blood cholesterol, increase LDL and cholesterol and decrease HDL cholesterol Family hypercholesterolemia: autosomal dominant disorder - Xanthomas (cholesterol deposits) along the tendon and atherosclerosis Secondary dyslipidemia: causes include dietary factors, obesity, metabolic changes associated with type 2 Diabetes mellitus Obesity - Elevate triglycerides, LDL and decreased HDL - Insulin resistance leads to a further increase in blood lipid levels Type 2 DM - Develop a state of insulin resistance along with metabolic alternatives (metabolic syndrome- know the conditions) Other systemic disorders can elevate lipids Medications can also increase lipid levels Diagnostic Tests: Lipid panel (total cholesterol, LDL, HDL, triglycerides). Atherosclerosis: hardening of the arteries - Formation of fibrofatty lesions - Intimal lining of large sized arteries - Intimal lining of medium sized arteries Etiology and risk factors: Hypercholesterolemia: can be modified by dietary, lifestyle changes and medications - Elevations in LDL cholesterol Additional risk factors - Age, family history of heart disease, male sex at time of birth - Hypertension, DM  - Female sex at time of birth – after menopause increase risk - Physical inactivity, stressful life patterns, blood levels of C-reactive protein (CRP), serum homocysteine levels Pathogenesis: types of lesions: fatty streak, fibrous atheromatous plaque, complicated lesions Clinical manifestations: depends on the vessel involved and extent of vessel obstruction - Narrowing of the vessel - Production of ischemia - Hemorrhage or rupture - Thrombosis - Formation of emboli - Aneurysm formation Vessel size: Large vessels: thrombus formation, weakening of the vessel wall Medium sized arteries: ischemia and infarction Diagnostic Tests: Angiography, ultrasound, CT scan, MRI. Peripheral Artery Disease (atherosclerotic occlusive disease)- Etiology: cigarette smoking and diabete mellitus Clinical manifestation: Symptoms gradual Intermittent claudication - Calf pain - Vague aching feeling - Numbness - Other signs - Pulses, temperature- weak or missing pulse, lower temp in one leg over the other - Limb color due to position - Ischemic pain – muscle cramps in hips and legs when walking that stops when resting - Necrosis - due to lack of oxygen Diagnosis: Inspection Sings of chronic low-grade ischemia Palpation Doppler ultrasound Ultrasound imaging Magnetic Resonance Imaging (MRI) arteriography Invasive contrast angiography Treatment: Goals of treatment - Decrease cardiovascular risk - Reduce symptoms - Antiplatelet agents Treatment: - Statin - Walking : improves blood flow to the legs which develops new, smaller vessels that can alleviate pain and discomfort caused by restricted blood supply to the muscles allowing them to walk further distances without leg pain - Percutaneous or surgical vascular intervention Aneurysms: Local dilation or outpouching of a vessel wall or cardiac chamber - Arteries and veins - Most common site: aorta True aneurysms - Weakening of all three layers of wall False aneurysms - Extravascular hematoma that communicates with the intravascular space Aorta most susceptible, especially abdominal - Causes include atherosclerosis, hypertension - Can lead to aortic dissection or rupture Berry: location (TRue) - Usually located in a bifurcated area Fusiform: involved the enter circumference (TR) Saccular- extends over part of the circumference of the vessel (TRue) Dissecting- tear (False) Diagnostic Tests: Ultrasound, CT scan, MRI. Aortic aneurysm: involve any part of the aorta (true) Etiology: atherosclerosis, degeneration of the vessel media, hypertension, males >age 50 who smoke Clinical manifestation: Asymptomatic, Substernal, back and neck pain, Hoarseness – indicated the aortic aneurysm could compress laryngeal nerve which controls vocal cords , Difficulty swallowing – indicated aortic aneurysm can occur in the aneurysm compresses esophagus or nearby structures , Distended neck veins and edema of the face and neck – indicate can suggest serious condition such as superior vena cava syndrome- which happens when aneurysm compresses the vein Abdominal aortic aneurysm: Below the level of the renal artery - Involve bifurcation of the aorta and proximal end of the common iliac arteries. - Palpable (larger than 4 cm) - Lower back pain that radiates to the posterior aspect of legs – puts pressure on nearby structures such as the nerves that innervate lower back and legs, referred pain leading in discomfort to areas distant from the source, inflammation may cause pain - Complication - rupture Diagnosis and treatment: - Ultrasonography - Echocardiography - CT scan, MRI - surgical repair Diagnostic Tests: Ultrasound, CT scan, MRI. Aortic Dissection- Acute, life-threatening condition - Bleeding into the vessel wall with l longitudinal tearing - Occurs without evidence of previous vessel dilation - Most common site - Ascending aorta - Second most common site - Thoracic aorta - Distal to the origin of the subclavian artery Etiology and pathogenesis: Conditions that weaken or degenerate the elastic and smooth muscle layers of the aorta - Most common in 40 – 60-year-old - Risk factors - Hypertension - Degeneration of the medial layer of the vessel - Connective tissue disease – Marfan syndrome - Occur during pregnancy - Congenital defects of the aortic valve and aortic coarctation  - Complications of cardiac surgery or catheterization Clinical manifestation: - Abrupt presence of excruciating pain - Described as tearing or ripping - Anterior chest – dissection of the ascending aorta - Back pain – dissection of the descending aorta - Dissection disrupts - Symptoms of occlusion of blood vessels that supply the brain - Heart failure – Aortic valve is involved Diagnosis and Treatment: - History and physical - Vascular imaging- CT, and MRI - Treatment depends on acute or chronic - Medical or surgical - Diagnostic Tests: CT angiography, MRI, chest X-ray. Disease of the Veins Varicose veins - A vein in which blood has pooled - Distended, tortuous, and palpable veins - Caused by trauma or gradual venous distention Risk factors: - Age - Female gender - Family history - Obesity - Pregnancy - Deep vein thrombosis - Prior leg injury Disease of the veins : Thrombus formation in veins  - Obstruction of venous flow leading to increased venous pressure - Thrombus: attached to vessel wall - Thromboembolus: detached Factors promoting thrombosis (Triad of Virchow) 1. Venous stasis 2. Venous endothelial damage 3. Hypercoagulable states Other (cancer, orthopedic surgery/trauma, heart failure, immobility) Hypertension : Consistent elevation of systemic arterial blood pressure - Sustained systolic blood pressure of 130 mm Hg or greater or a diastolic pressure of 80 mm Hg or greater Primary: tissue wall is thick, decrease perfusion, greater pressure is needed to pump blood - Essential or idiopathic hypertension - Genetic and environmental factors - Affects 92% to 95% of individuals with hypertension Risk factors: - Family history - Diet (high sodium, low potassium, calcium, magnesium) - Tobacco and alcohol consumption - Obesity and glucose intolerance Secondary: Caused by a systemic disease process that raises peripheral vascular resistance or cardiac output - Renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary tumors, and drugs - Complicated hypertension: chronic hypertensive damage to blood vessels and tissues leading to target organ damage in the heart, kidney brains and eyes - Brain: stroke, confusion, headache, convulsion - Retina of eye: hypertensive retinopathy - Heart: heart attack, heart failure - Blood: elevate sugar levels - Kidneys: chronic renal failure - Myocardial hypertrophy Hypertensive crisis: rapid progressive hypertension  - Systolic pressure> 180 mm Hg and/or diastolic pressure is usually >120 mm Hg - Lifethreathing - Diagnostic Tests: Blood pressure measurement, ambulatory blood pressure monitoring. Hypotension: orthostatic (postural hypotension) - Decrease in both systolic and diastolic blood pressure upon standing - Lack of normal blood pressure compensation in response to gravitational changes on the circulation - Acute orthostatic hypotension - Chronic orthostatic hypotension Thrombus formation: Blood clot that remains attached to the vessel wall - Risk factors include intimal injury/inflammation, obstruction of flow, pooling (stasis) - Thromboembolus - Arterial thrombi Systolic: measured between when the heart contracts Diastolic: is measure between beats when the heart relaxes Embolism: Bolus of matter that is circulating in the bloodstream - Dislodged thrombus - Air bubble - Amniotic fluid - Aggregate of fat - Bacteria - Cancer cells - Foreign substance Intermittent chest pain after exercise- atherosclerotic plaque progression Coronary Artery Disease: any vascular disorder that narrows or occludes the coronary arteries leading to myocardial ischemia - Atherosclerosis is the most common cause: primary cause of heart disease in US Conventional (major) risk factors: - Nonmodifiable - Increased age - Family history - Male gender or female gender postmenopause - Modifiable - Dyslipidemia  - Hypertension - Cigarette smoking - Diabetes mellitus and insulin resistance - Obesity/sedentary lifestyle - Atherogenic diet Nontraditional risk factors: markers of inflammation and thrombosis: High density C reactive protein, troponin - Adipokines - Chronic kidney disease - Air pollution and ionizing radiation - Certain medication - Microbiome Transient myocardial ischemia: local temporary deprivation of the coronary blood supply - Stable angina - Prinzmetal angina - Silent ischemia and mental stress induced ischemia Acute coronary syndromes : Unstable angina - Results from reversible myocardial ischemia - Myocardial infarction Diagnostic Tests: Stress test, coronary angiography, ECG. Myocardial Infarction: extended obstruction of the myocardial blood supply causing myocyte necrosis - STEMI or nonSTEMI - STEMi: complete blockage of coronary artery leading to significant portion of the heart muscle being deprived of oxygen, ST segment elevation immediate intervention: angioplasty, thrombolytic therapy: chest pain, shortness of breath, sweating - NSTEMI: partial blockage of coronary artery which may lead to heart muscle damage: does not show ST segment elevation, but has ST segment depression or T wave inversions: management may involve medications, close monitoring and potential angiography: some may not have chest pain, fatigue and nausea - Subendocardial or transmural infarction - Subendocardial infarction: partial thickness damage, ST segment depression better prognosis - Transmural- full thickness damage usually happens from a thrombosis that blocks blood flow, ST segment elevation , worse prognosis - Structural changes: myocardial stunning, hibernating myocardium, myocardial remodeling Manifestations:  - Sudden severe chest pain; may radiate - Nausea, vomiting - Diaphoresis - Dyspnea Complications: sudden cardiac arrest to ischemia, left ventricular dysfunction and electrical instability Diagnostic Tests: ECG changes, troponin levels, cardiac biomarkers. Disorders of pericardium: Inflammation of the pericardium: sac surrounds heart and roots of great vessel: Cushions and prevent friction - acute pericarditis - Pericardial effusion : accumulation of fluid slowly over time: can progress to circulatory shock and cardiac arrest - Symptoms: chest pain, shortness of breath, compression of near structures - allows pericardium to stretch out to accommodate bigger volumes of fluid without compressing heart - Tamponade - Cardiac tamponade: compresses heart - Constrictive pericarditis Due to viral infection, uremia, autoimmune disease, after trauma Associated with severe chest pain Becks triad: low blood pressure, muffled heart sounds, distended jugular veins Cardiomyopathies: Types Disorders of myocardium: - Cardiomyopathies: describes a variety of issues that result from disease of myocardium Develops to compensate for underlying disease such as hypertension or valve disease→ secondary cardiomyopathy can develop by itself: primary cardiomyopathy - dilated cardiomyopathy - Dilated and impaired construction of one or both ventricles - Ischemia, valvular, infectious (viral, chagas, HIV, lyme) , toxic (alcohol, cocaine, methamphetamine, chemotherapy), genetic, idiopathic - Hypertrophic cardiomyopathy: hypertrophic myocardium, autosomal dominant, leading cause of sudden cardiac death in young athletes - Hypertrophic obstructive cardiomyopathy (asymmetric septal hypertrophic cardiomyopathy) - Hypertensive (valvular) hypertrophic cardiomyopathy - Restrictive cardiomyopathy: walls of ventricles become still but not necessarily thickened - Impaired diastolic filling, preserved systolic function, infiltrative (amyloid,sarcoid), storage (hemochromatosis,fabry), endomyocardial fibrosis Diagnostic Tests: Echocardiogram, MRI, genetic testing. Valvular heart disease: Mitral Stenosis : narrowing of valvular orifice dastole, does not open all the way - Difficult fillwing in left ventricle - Increase in left atrium pressure - Increase venous pressure and pulmonary artery pressure - Decreased cardiac output - Pulmonary hypertension need to push blood to valve Etiology Rheumatic Fever: Most common cause, often following streptococcal throat infection. Calcific Degeneration: Common in elderly patients. Congenital Defects: Such as parachute mitral valve. Other Causes: Tumors, infective endocarditis, or fibrosis. Pathogenesis Narrowing of the mitral valve orifice leads to obstruction of blood flow from the left atrium to the left ventricle during diastole. Increased pressure in the left atrium can result in atrial dilation and potential atrial fibrillation.  Elevated pulmonary pressures may develop, leading to pulmonary congestion. Signs/Symptoms/Clinical Presentation Dyspnea: Most common symptom due to pulmonary congestion. Palpitations: From atrial fibrillation. Fatigue: Due to reduced cardiac output. Hemoptysis: Coughing up blood from pulmonary congestion. Signs: Loud S1, opening snap, diastolic murmur best heard at the apex. Diagnostic Tests Echocardiogram: Most important for assessing mitral valve morphology and hemodynamics. Electrocardiogram (ECG): May show atrial fibrillation or left atrial enlargement. Chest X-ray: Can show left atrial enlargement and pulmonary congestion. Cardiac Catheterization: In select cases to assess severity. Mitral Regurgitation systole: does not close all the way Etiology Degenerative (Myxomatous Degeneration): Most common cause, especially in older adults. Rheumatic Heart Disease: Can lead to valve damage. Ischemic Heart Disease: Damage from myocardial infarction affecting the papillary muscles. Endocarditis: Infection leading to valve dysfunction. Congenital Malformations: Such as cleft mitral valve. Pathogenesis Incomplete closure of the mitral valve during systole causes backflow of blood into the left atrium. This leads to volume overload of the left atrium and ventricle, resulting in dilation and hypertrophy over time. Increased left atrial pressure can cause pulmonary congestion and atrial fibrillation. Signs/Symptoms/Clinical Presentation Dyspnea: Due to pulmonary congestion. Fatigue: From decreased cardiac output. Palpitations: Due to atrial fibrillation. Signs: Holosystolic (or pansystolic) murmur best heard at the apex, often with a radiation to the left axilla, and may have a laterally displaced apex beat. Diagnostic Tests Echocardiogram: Key for evaluating valve structure, function, and regurgitant volume. Electrocardiogram (ECG): May show left atrial enlargement or atrial fibrillation. Chest X-ray: May reveal left atrial enlargement and pulmonary congestion. Cardiac MRI: In some cases, for detailed assessment. Summary Mitral Stenosis: Primarily causes obstruction during diastole; often presents with exertional dyspnea and loud S1. Mitral Regurgitation: Causes volume overload during systole; often presents with holosystolic murmur and can lead to heart failure. Heart Failure: heart is unable to generate adequate cardiac output - Inadequate perfusion of tissues - Increased diastolic filling pressure of left ventricle - Pulmonary capillary pressure increases Congestive heart failure: enlarged heart, fluid around lungs,bloated stomach, swollen and cyanotic legs and feet pulmonary congestion and pressure, low organ perfusion and hypoxia Left heart failure: - Usually caused by hypertension, coronary artery disease and valvular disease - Tachycardia, fatigue, cyanosis, exertional dyspnea, pulmonary congestion: cough, crackles, pink tinged sputum, tachypnea Systolic heart failure:The left ventricle is too weak to pump blood out to the body during a heartbeat. This is also known as heart failure with reduced ejection fraction (HFrEF). Diastolic heart failure: The left ventricle is stiff and can't relax between heartbeats, making it difficult to fill with blood. This is also known as heart failure with preserved ejection fraction (HFpEF) Systolic heart failure: - Ejection fraction less than 40% - inability of the heart to generate adequate cardiac output to perfuse tissues - Stroke volume: contractility, preload, afterload - Disruptions decrease cardiac output - Falling cardiac output ng progressively worsens heart failure - More volume in left ventricle, decreased ejection fraction - Manifestations: Dyspnea, orthopnea, cough of frothy sputum, fatigue, decreased urine output, and edema - Pulmonary edema, hypotension/hypertension, S3 gallop Diastolic heart failure: pulmonary congestion despite normal stroke volume and cardiac outpu - Major causes include hypertension incidence myocardial hypertrophy and myocardial ischemia induced ventricular remodeling - Decreased compliance of left ventricle - Abnormal diastolic relaxation - Manifestation: dyspnea on exertion-fatigue, pulmonary edema may develop overtime S4 galop Right heart failure: - Inability of right ventricle to provide adequate blood flow at a normal venous pressure - Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation - Most commonly caused by a diffuse hypoxic pulmonary disease - Can be caused by left ventricular failure, right MI or pulmonary hypertension - Right ventricle cannot empty completely - May be secondary to pulmonary problems (COPD) - Symptoms Peripheral edema, ascites, enlarged liver and spleen, JVD< weight gain, increased peripheral venous pressure High output failure: inability of the heart to supply the body with blood-borne nutrients despite adequate blood volume and normal or elevated myocardial contractility - Causes include anemia, hyperthyroidism, septicemia, and beriberi Heart failure diagnostic tests: Echocardiogram, BNP levels, chest X-ray Infective Endocarditis: Inflammation of the endocardium Agents: Bacteria Viruses Fungi Rickettsiae Parasites Pathogenesis Damaged (prepared) endocardium Blood-borne microorganism adherence Proliferation of the microorganism (vegetations) Infection of the endocardium: bacterial or fungal infection of the endocardial lining of the heart valves - Microbe→ bloodstream - 4 heart chambers: 2 atria, 2 ventricles - Heart valves: 2 atrioventricular: mitral or bicuspid(L) prevents blood from returning to atria - 2 semilunar: aortic (L), pulmonary (R): prevent blood from returning to ventricles Findings: fever, new or changed cardiac murmur, petechial lesions of the skin, conjunctiva and oral mucosa - Characteristic physical finding: osler nodes, janeway lesions - Other: weight loss, back pain, night sweats and heart failure - Drug users - Diagnostic Tests: Blood cultures, echocardiogram Cardiogenic / Hypovolemic / Neurogenic / Anaphylactic / Septic Shock Shock: Cardiovascular system fails to perfuse the tissues adequately - Leads to impaired cellular metabolism - Impaired oxygen use - Impaired glucose use - Manifestations based on type, often include: - Feeling weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, short of breath – Hypotension, tachycardia, increased respiratory rate Types of shock:classified by cause: organs don't receive enough oxygen and nutrient Cardiogenic: heart failure : life threatening condition where heart is unable to pump enough blood to rest of body: acute hypoperfusion and hypoxia of the tissues and organs despite adequate intravascular volume in /cardiac system - Acute coronary syndrome, dysrhythmia, CHF< valvuloplasty, drug toxicity, myocarditis, myocardial contusion Hypovolemic: insufficient intravascular fluid volume - Loss of intravascular volume in cardiovascular system resulting in hypoperfusion of organs and tissues caused by blood loss or fluid loss related to certain chronic conditions or therapies - Loss of intravascular volume, less venous return, les cardiac output→ shock Neurogenic: neural alterations of vascular smooth muscle tone Imbalance between sympathetic and psychopathic stimulation - Loss of vascular sympathetic tone, unopposed parasympathetic response Anaphylactic: immunologic processes  - Septic: infection: occurs when chemicals released into the bloodstream to fight an infection trigger inflammatory responses throughout the body which an damage vital organs Risk factors - Suppression immune system - Extreme age (infants or elderly) - Procured organ- transplant - Surgical procedure - Indwelling devices - Sickness Acute Kidney Injury (AKI) Etiology Pre-renal causes: Reduced blood flow to the kidneys (e.g., dehydration, heart failure, shock). Intrinsic renal causes: Direct damage to the kidney tissue (e.g., acute tubular necrosis, glomerulonephritis). Post-renal causes: Obstruction of urine flow (e.g., kidney stones, tumors). Pathogenesis A sudden decline in renal function leads to the retention of nitrogenous waste products and disruption of fluid and electrolyte balance.  Ischemia or nephrotoxic injury can result in cellular injury, inflammation, and necrosis of renal tubules. Signs/Symptoms/Clinical Presentation Oliguria or anuria Edema Hypertension Electrolyte imbalances (e.g., hyperkalemia) Nausea and vomiting Fatigue and weakness Diagnostic Tests Serum creatinine and blood urea nitrogen (BUN) levels Urinalysis (looking for casts, protein, etc.) Imaging studies (ultrasound, CT scan) Fractional excretion of sodium (FENa) to distinguish between pre-renal and intrinsic causes Chronic Kidney Disease (CKD) Etiology Diabetes mellitus: Leading cause of CKD. Hypertension: Common contributor. Glomerulonephritis: Autoimmune or inflammatory conditions. Polycystic kidney disease: Genetic disorders. Chronic urinary tract obstruction: Long-term blockage. Pathogenesis Progressive loss of nephron function leads to reduced glomerular filtration rate (GFR). Compensatory hyperfiltration in remaining nephrons causes further injury over time. Systemic effects include alterations in fluid, electrolyte, and acid-base balance. Signs/Symptoms/Clinical Presentation Fatigue and weakness Anemia Edema (especially in lower extremities) Hypertension  Changes in urination patterns (frequency, volume) Uremic symptoms: Nausea, itching, confusion, or loss of appetite Diagnostic Tests Serum creatinine and estimated GFR (eGFR) Urinalysis (looking for proteinuria, hematuria) Imaging studies (ultrasound, CT scan) to assess kidney size and structure Kidney biopsy (in certain cases) for definitive diagnosis Renal Diseases: Acute Kidney Injury (AKI) Etiology Pre-renal causes: Reduced blood flow to the kidneys (e.g., dehydration, heart failure, shock). Intrinsic renal causes: Direct damage to the kidney tissue (e.g., acute tubular necrosis, glomerulonephritis). Post-renal causes: Obstruction of urine flow (e.g., kidney stones, tumors). Pathogenesis A sudden decline in renal function leads to the retention of nitrogenous waste products and disruption of fluid and electrolyte balance. Ischemia or nephrotoxic injury can result in cellular injury, inflammation, and necrosis of renal tubules. Signs/Symptoms/Clinical Presentation Oliguria or anuria Edema Hypertension Electrolyte imbalances (e.g., hyperkalemia) Nausea and vomiting Fatigue and weakness Diagnostic Tests  Serum creatinine and blood urea nitrogen (BUN) levels Urinalysis (looking for casts, protein, etc.) Imaging studies (ultrasound, CT scan) Fractional excretion of sodium (FENa) to distinguish between pre-renal and intrinsic causes Chronic Kidney Disease (CKD) Etiology Diabetes mellitus: Leading cause of CKD. Hypertension: Common contributor. Glomerulonephritis: Autoimmune or inflammatory conditions. Polycystic kidney disease: Genetic disorders. Chronic urinary tract obstruction: Long-term blockage. Pathogenesis Progressive loss of nephron function leads to reduced glomerular filtration rate (GFR). Compensatory hyperfiltration in remaining nephrons causes further injury over time. Systemic effects include alterations in fluid, electrolyte, and acid-base balance. Signs/Symptoms/Clinical Presentation Fatigue and weakness Anemia Edema (especially in lower extremities) Hypertension Changes in urination patterns (frequency, volume) Uremic symptoms: Nausea, itching, confusion, or loss of appetite Diagnostic Tests Serum creatinine and estimated GFR (eGFR) Urinalysis (looking for proteinuria, hematuria) Imaging studies (ultrasound, CT scan) to assess kidney size and structure Kidney biopsy (in certain cases) for definitive diagnosis Cardiac Disease: Dyslipidemia: imbalance in triglycerides phospholipids and cholesterol  Etiology: Genetic factors, lifestyle (diet, physical inactivity), certain diseases (diabetes, hypothyroidism). Pathogenesis: Abnormal lipid levels in blood, primarily elevated LDL and/or low HDL. Signs/Symptoms: Often asymptomatic; can lead to xanthomas(calcium deposits: Family hypercholesterolemia: autosomal dominant disorder) or pancreatitis. Diagnostic Tests: Lipid panel (total cholesterol, LDL, HDL, triglycerides). Atherosclerosis: hardening of arteries due to fibrofatty lesions Etiology: Risk factors include dyslipidemia, hypertension, smoking, diabetes, hypertension, diabetes mellitus, age, family history of heart disease, stressful life patterns, blood levels of C reactive protein, serum homocysteine levels Pathogenesis: Endothelial injury, inflammation, lipid accumulation, plaque formation. ○ Fatty streaks, plaques, and complicated lesions lead to vessel narrowing and ischemia Signs/Symptoms: Chest pain, claudication, can be asymptomatic until severe. Diagnostic Tests: Angiography, ultrasound, CT scan, MRI. Clinical manifestations: depends on the vessel involved and extent of vessel obstruction: ○ Narrowing of vessel ○ Production of ischemia ○ Hemorrhage or rupture ○ Thrombosis ○ Formation of emboli ○ Aneurysm formation Vessel size: Large vessels: thrombus formation, weakening of the vessel wall Medium sized arteries: ischemia and infarction Peripheral Artery Disease (PAD): atherosclerotic occlusive disease Etiology: Atherosclerosis, embolism, vasculitis: cigarette smoking and diabetes mellitus Pathogenesis: Narrowing of peripheral arteries leads to reduced blood flow. Signs/Symptoms: Intermittent claudication, leg pain, numbness, ulcers calf pain, numbness ○ Pulses, temperature- weak or missing pulse, lower temp in one leg over the other ○ Limb color due to position ○ Ischemic pain – muscle cramps in hips and legs when walking that stops when resting ○ Necrosis - due to lack of oxygen Diagnostic Tests: Ankle-brachial index (ABI), Doppler ultrasound, angiography. ○ Inspection ○ Sings of chronic low-grade ischemia ○ Palpation ○ Doppler ultrasound ○ Ultrasound imaging ○ Magnetic Resonance Imaging (MRI) arteriography  ○ Invasive contrast angiography Treatment: ○ Decrease cardiovascular risk ○ Reduce symptoms ○ Antiplatelet agents ○ Statin ○ Walking : improves blood flow to the legs which develops new, smaller vessels that can alleviate pain and discomfort caused by restricted blood supply to the muscles allowing them to walk further distances without leg pain ○ Percutaneous or surgical vascular intervention Aneurysms: Types Etiology: Hypertension, atherosclerosis, genetic disorders (Marfan syndrome). Pathogenesis: Weakening of vessel wall leading to dilation. Signs/Symptoms: Often asymptomatic; may cause pain or pulsatile mass. Types: ○ Abdominal Aortic Aneurysm (AAA) ○ Thoracic Aortic Aneurysm (TAA) Diagnostic Tests: Ultrasound, CT scan, MRI. Aortic Dissection Etiology: Hypertension, connective tissue disorders, trauma. Pathogenesis: Tear in the aorta’s inner layer allowing blood to flow between layers. Signs/Symptoms: Sudden severe chest or back pain, tearing sensation, syncope. Diagnostic Tests: CT angiography, MRI, chest X-ray. Hypertension Etiology: Primary (essential) hypertension has no identifiable cause; secondary hypertension due to other conditions (e.g., kidney disease). Pathogenesis: Increased peripheral vascular resistance or cardiac output. Signs/Symptoms: Often asymptomatic; headaches, dizziness, vision changes in severe cases. Diagnostic Tests: Blood pressure measurement, ambulatory blood pressure monitoring. Coronary Artery Disease (CAD) Etiology: Atherosclerosis, risk factors include smoking, diabetes, dyslipidemia. Pathogenesis: Reduced blood flow to the myocardium due to plaque buildup. Signs/Symptoms: Angina, shortness of breath, fatigue. Diagnostic Tests: Stress test, coronary angiography, ECG. Myocardial Infarction (MI)  Etiology: CAD, thrombus formation. Pathogenesis: Ischemia due to occlusion of coronary artery leading to myocardial cell death. Signs/Symptoms: Chest pain, sweating, nausea, dyspnea. Diagnostic Tests: ECG changes, troponin levels, cardiac biomarkers. Cardiomyopathies: Types Etiology: Genetic factors, hypertension, alcohol, infections. Pathogenesis: Structural or functional abnormalities of the heart muscle. Types: ○ Dilated Cardiomyopathy ○ Hypertrophic Cardiomyopathy ○ Restrictive Cardiomyopathy Signs/Symptoms: Fatigue, heart failure signs, arrhythmias. Diagnostic Tests: Echocardiogram, MRI, genetic testing. Mitral Stenosis vs. Mitral Regurgitation Etiology: Rheumatic fever (stenosis), degenerative changes (regurgitation). Pathogenesis: ○ Stenosis: Narrowing prevents normal blood flow. ○ Regurgitation: Backflow of blood due to improper closure. Signs/Symptoms: Dyspnea, fatigue, palpitations. Diagnostic Tests: Echocardiogram, chest X-ray. Heart Failure Etiology: CAD, hypertension, cardiomyopathy. Pathogenesis: Inability of the heart to pump effectively. Signs/Symptoms: Shortness of breath, edema, fatigue. Diagnostic Tests: Echocardiogram, BNP levels, chest X-ray. Infective Endocarditis Etiology: Bacterial, fungal infections; risk factors include heart valve abnormalities. Pathogenesis: Infection of the inner heart lining, often leading to vegetations. Signs/Symptoms: Fever, murmur, petechiae, splinter hemorrhages. Diagnostic Tests: Blood cultures, echocardiogram. Types of Shock Cardiogenic Shock: Pump failure (e.g., MI). Hypovolemic Shock: Decreased blood volume (e.g., hemorrhage).  Neurogenic Shock: Loss of vascular tone (e.g., spinal injury). Anaphylactic Shock: Severe allergic reaction leading to vasodilation. Septic Shock: Infection causing systemic inflammation and vasodilation. Signs/Symptoms: Hypotension, tachycardia, altered mental status. Diagnostic Tests: Depends on type; may include blood tests, imaging, or cultures.