Patho Exam 4 Study Guide PDF

**[Patho Exam 4 Study Guide ]** **Systole** - Systole refers to the phase of the heartbeat where the heart muscle contracts and pumps blood out of the chambers into the arteries. In the context of the cardiac cycle, systole is the period of ventricular contraction, forcing blood into...

**[Patho Exam 4 Study Guide ]** **Systole** - Systole refers to the phase of the heartbeat where the heart muscle contracts and pumps blood out of the chambers into the arteries. In the context of the cardiac cycle, systole is the period of ventricular contraction, forcing blood into the pulmonary artery (from the right ventricle) and the aorta (from the left ventricle). It\'s the opposite of diastole, the relaxation phase where the heart chambers fill with blood. **Diastole** - Diastole is the phase of the heartbeat when the heart muscle relaxes and allows the chambers (atria and ventricles) to fill with blood. It\'s the period between contractions, in contrast to systole, the contraction phase. During diastole, the atria first contracts to fill the ventricles, followed by a period of ventricular relaxation and filling before the next heartbeat cycle begins. **Endocardium** - The endocardium is the innermost layer of the heart wall. It\'s a thin, smooth membrane that lines the chambers of the heart and covers the heart valves. Its smooth surface minimizes friction as blood flows through the heart. The endocardium is continuous with the lining of the blood vessels that connect to the heart. It plays a crucial role in maintaining the efficient flow of blood. **Myocardium** - The myocardium is the thick middle layer of the heart wall, composed primarily of cardiac muscle tissue. This layer is responsible for the heart\'s powerful contractions that pump blood throughout the body. The myocardium\'s thickness varies depending on the chamber; the left ventricle, responsible for pumping blood to the entire body, has the thickest myocardium. The coordinated contraction of the myocardium is essential for the circulatory system\'s function **Pericardium** - The pericardium\'s functions include protecting the heart, preventing overstretching, and anchoring it within the mediastinum. The pericardium is a double-walled sac that surrounds and protects the heart. It consists of two main layers: - **The fibrous pericardium:** - The outer layer, a tough, inelastic sac that protects the heart and anchors it to surrounding structures. - **The serous pericardium:** - The inner layer, composed of two layers itself: the parietal layer (lining the fibrous pericardium) and the visceral layer (adhering directly to the heart\'s surface, also known as the epicardium). Between these two serous layers is the pericardial cavity, containing a small amount of pericardial fluid that lubricates the heart\'s movement and minimizes friction during contractions. **Sympathetic nervous system** - The sympathetic nervous system is one of the two main divisions of the autonomic nervous system. It\'s often referred to as the \"fight-or-flight\" system because it prepares the body for stressful or emergency situations. These effects are mediated by the release of neurotransmitters, primarily norepinephrine, at the target organs. The sympathetic nervous system\'s actions are generally catabolic (breaking down stored energy) and increase overall metabolic activity. It works in a complementary way with the parasympathetic nervous system to maintain homeostasis. It does this by triggering a cascade of physiological changes, including: - **Increased heart rate and contractility:** - This increases blood flow to muscles and other vital organs. - **Increased blood pressure:** - Due to vasoconstriction (narrowing of blood vessels) in non-essential areas and vasodilation (widening) in muscles. - **Bronchodilation:** - Opening of airways to increase oxygen intake. - **Increased blood glucose levels:** - Providing energy for muscles. - **Pupil dilation:** - Enhancing vision. - **Reduced digestive activity:** - Blood flow is diverted away from the digestive system to more crucial areas. **Sympathetic Nervous System Effects on the Heart** - The sympathetic nervous system has significant effects on the heart, primarily increasing its activity to meet the body\'s demands during stress or exertion. These combined effects lead to an overall increase in cardiac output (the amount of blood pumped by the heart per minute), providing more oxygen and nutrients to the body\'s tissues during periods of increased activity or stress. The opposite effects occur with parasympathetic stimulation. These effects are mediated by the release of norepinephrine onto the heart muscle (myocardium) and specialized conducting cells: - **Increased Heart Rate (Chronotropic Effect):** - Norepinephrine increases the rate of spontaneous depolarization in the sinoatrial (SA) node, the heart\'s natural pacemaker, leading to a faster heart rate. - **Increased Force of Contraction (Inotropic Effect):** - Norepinephrine increases the contractility of the heart muscle, making each contraction more forceful and increasing the amount of blood pumped with each beat (stroke volume). This is achieved by increasing calcium influx into cardiac myocytes. - **Increased Conduction Velocity (Dromotropic Effect):** - Norepinephrine speeds up the conduction of electrical impulses through the heart, particularly in the atrioventricular (AV) node, thus facilitating faster transmission of the heartbeat signal. **Pulmonary Circulation V. Systemic Circulation** - Pulmonary and systemic circulation are the two main circuits of the circulatory system, working together to deliver oxygenated blood to the body\'s tissues and remove waste products like carbon dioxide. In essence, pulmonary circulation is a short loop focusing on gas exchange in the lungs, while systemic circulation is a much longer loop supplying the entire body. Both are crucial for maintaining life. - **Pulmonary Circulation** - **Pathway** - Right ventricle → pulmonary artery → lungs → pulmonary veins → left atrium. - **Purpose:** - To oxygenate blood. Deoxygenated blood from the body is pumped to the lungs where it releases carbon dioxide and picks up oxygen - **Pressure:** - Low pressure system. The pulmonary arteries and veins have thinner walls than their systemic counterparts because the blood is not pumped against as much resistance. - **Blood Oxygenation:** - Blood is deoxygenated at the beginning of the circuit and oxygenated at the end. - **Systemic Circulation:** - **Pathway:** - Left ventricle → aorta → body tissues → vena cava → right atrium. - **Purpose:** - To deliver oxygenated blood and nutrients to the body\'s tissues and remove waste products. - **Pressure:** - High-pressure system. The left ventricle must pump blood with greater force to overcome the resistance of the extensive network of systemic vessels. - **Blood Oxygenation:** - Blood is oxygenated at the beginning of the circuit and deoxygenated at the end. **Preload V. afterload** - **Preload** - Volume of blood the heart pumps out - **Afterload** - The pressure that must be generated to pump the blood out of the heart **Cardiac output** - The amount of blood that the heart pumps each minute - **Cardiac output (CO)** = Stroke volume (SV) x Heart rate (HR) - **Stroke volume:** amount of blood pumped with each beat - **Heart rate:** number of times the heart beats each minute **Baroreceptors** - Stretch sensitive receptors - Monitors blood pressure - In carotid sinus (regulate head/neck BP) and aortic arch (regulate body BP) **Arteries** - Thick-walled vessels with large amounts of elastic fibers - To keep up with the pressure exerted during systole - Stretch during cardiac systole and recoil during diastole **Arterioles** - Resistance vessels for circulatory system - Acts as control valves where blood is released as it moves into the capillaries **Capillaries** - Connect arterial and venous segments - Fluids/electrolytes/gases/cell waste move across endothelium by diffusion/filtration/pinocytosis - Interstitial fluid exchange - Controlled by hydrostatic and osmotic pressures **Veins** - Use valves to prevent backflow - Not as muscular **Frank- Starling Law** - The greater the volume of blood before each contraction, the greater the volume of blood ejected from the heart **Disorders of the Cardiovascular System** - Dyslipidemia - **Risk factors** - Family history/genetics - Poor diet - Obesity - Sedentary lifestyle - Comorbidities - Diabetes - Hypothyroidism - Chronic kidney disease - Age - Medications - Alcohol consumption - **Pathophysiology** - Increased LDL levels - Leads to accumulation of cholesterol in arterial walls \--\> promotes atherosclerosis - Decreased HDL levels - Reduces clearance of cholesterol from the bloodstream, contributes to plaque formation - Elevated triglycerides - Associated with insulin resistance and metabolic syndrome - **Clinical Manifestations** - No symptoms until significant complications arise - Xanthomas (yellowish cholesterol-rich deposits on skin - Angina - **Diagnostics** - Lipid panel - Fasting levels are preferred - Family history assessment - C-reactive protein levels (CRP) to assess inflammation - **Management** - Lifestyle modifications - Medications - Monitoring - **Atherosclerosis** - **Risk factors** - Dyslipidemia - Smoking - Hypertension - Age - Men older than 45 - Women older than 55 - Homocysteine levels - CRP levels - HDL levels lower than 40 mg/dL - Family history of premature coronary artery disease (CAD) in first-degree relative - Obesity - Physical inactivity - **Pathophysiology** - Gradual buildup of plaques in arterial walls, leads to narrowed arteries and reduced blood flow - **Endothelial injury:** initiated by hypertension, smoking, and high cholesterol - **Lipid accumulation:** LDL infiltrates endothelium and is oxidized, this triggers an inflammatory response - **Inflammation:** monocytes migrate to site, then transform into macrophages that try to engulf the lipids, forming foam cells and contributing to plaque formation - **Plaque development:** accumulation of foam cells, smooth muscle cells, and extracellular matrix leads to plaque growth. This growth can become unstable and rupture and potentially cause a thrombosis - **Clinical Manifestations** - Asymptomatic until significant arterial blockage - Angina pectoris - Myocardial infarction - Stroke - PAD - Renal artery stenosis - **Diagnostics** - Lipid profile - Imaging (ultrasound, CTA, MRA) - Stress testing - Coronary angiography - **Management** - Lifestyle changes - Medications - Monitoring and risk assessment - **Aneurysms** - **Risk factors** - Hypertension - Smoking - Hyperlipidemia - Obesity - Sedentary lifestyle - Age - Family history - Some genetic conditions - **Pathophysiology** - An abnormal dilation of a blood vessel due to weakened vessel wall - Wall weakness: caused by hypertension, atherosclerosis, or connective tissue conditions - Increased pressure: when blood flows through weakened area, it exerts pressure causing the aneurysm to grow - Expansion and rupture: they grow over time and may eventually rupture leading to life-threatening internal bleeding - **Clinical Manifestations** - Most are asymptomatic until complications arise, symptoms vary by location - Abdominal aortic aneurysm: back pain, abdominal pain, pulsating mass in abdomen - Thoracic aortic aneurysm: chest pain, back pain, difficulty breathing - Cerebral aneurysm: severe headache, vision changes, neurological deficits (if ruptured) - Peripheral aneurysm: pain, swelling, changes in pulse in affected limb - **Diagnostics** - Physical exam - Ultrasound, CT, MRI, angiography - **Management** - Monitoring for small aneurysms that are asymptomatic - Medications to control BP to reduce risk of rupture - Surgery - **Thromboangitis obliterans (Buerger's Disease)** - **Risk factors** - Smoking - Age (20-40) - Sex (Males) - Genetics - Ethnicity (Asian and Middle East) - **Pathophysiology** - Segmental vasculitis affecting small and medium-sized arteries - Inflammation: starts with inflammation of vascular wall, leading to clot formation - Vascular occlusion: reduced blood flow to affected areas, leads to ischemia - Tissue damage: chronic ischemia leads to ulceration, necrosis, and potentially gangrene - **Clinical Manifestations** - Typically develop progressively - Claudication - Pain in limbs - Rest pain - Cold sensitivity - Skin changes - Color, hair loss, ulcerations - Gangrene - **Diagnostics** - Doppler - Angiography - Blood tests (just rules out other diseases, does not diagnose) - **Management** - Stop smoking - Medications - Surgery - Exercise therapy - **Raynaud Disease** - **Risk factors** - Genetics - Gender (women, 15-40) - Climate - Occupational factors (repetitive hand motions/vibrations) - Smoking - Those with autoimmune diseases - **Pathophysiology** - Exaggerated response of peripheral blood vessels to cold/stress leads to: - Vasoconstriction - Ischemia - Nerve dysfunction - **Clinical Manifestations** - Color changes - White from ischemia - Blue from hypoxia - Red from reperfusion - Coldness/numbness - Pain or tingling - **Diagnostics** - Physical exam - Cold simulation tests - Blood tests to check for underlying autoimmune conditions - **Management** - Avoid cold and stress - Stop smoking - **Peripheral Artery Disease** - **Risk factors** - Age - Smoking - Diabetes - Hypertension - Hyperlipidemia - Obesity - Sedentary lifestyle - **Pathophysiology** - Primarily caused by atherosclerosis - Narrowed arteries: reduced blood flow to limbs - Ischemia: inadequate O2 delivery to tissues - Increased clot formation: plaque rupture can lead to thrombosis - **Clinical Manifestations** - Intermittent claudication: pain/cramping in legs during physical activity - Typically resolves with rest - Weak/absent pulse - Coldness in lower leg/foot - Changes in skin color (pale or blue tint) - Wounds/sores - Gangrene in severe cases - **Diagnostics** - Ankle-brachial index (ABI) - Doppler - Angiography - Blood tests - **Management** - Quit smoking - Exercise programs to improve circulation - Diet changes - Medications - Revascularization procedures (angioplasty or bypass surgery) - Complication management - **Varicose Veins** - **Risk factors** - Age - Gender - Family history - Obesity - Prolonged standing/sitting - History of blood clots - Hormonal influences - **Pathophysiology** - Valve failure: valves in veins that prevent backflow become weak or damaged - Increased venous pressure: blood pools in the veins causing them to stretch and bulge - Structural changes: loss of elasticity and integrity of vein wall leads to further dilation - **Clinical Manifestations** - Visible bulgin veins - Aching/heaviness - Swelling - Itching/burning - **Diagnostics** - Physical exam - Doppler ultrasound - Venography - **Management** - Weight management - Exercise to improve circulation - Avoid prolonged sitting/standing - Compression socks - Medications - Sclerotherapy - **DVT** - **Risk factors** - Prolonged immobility (long flights/car rides, surgery recovery) - Age - Previous DVT or PE - Medical conditions - Obesity - Smoking - Genetic predisposition - **Pathophysiology** - **Stasis of blood flow:** reduced circulation allows for clot formation - **Endothelial injury:** damage to blood vessel lining can trigger clotting - **Hypercoagulability:** increased tendency for blood clots - **Clinical Manifestations** - Swelling (unilateral) - Pain/tenderness - Red/discolored skin - Increased warmth - **Diagnostics** - D-dimer test - Ultrasound - venography - **Management** - Anticoagulation therapy - Compression socks - IVC filter - Lifestyle changes - **Hypertension** - **Risk factors** - Age - Family history/genetics - Dietary factors - Tabacco use - Alcohol consumption - Obesity - Chronic stress - **Pathophysiology** - Increased vascular resistance: narrowing of the blood vessels due to plaque buildup or arterial stiffness - Increased cardiac output: the heart pumps more blood and normal, happens due to stress or increased blood volume - Neurohormonal factors: activation of renin-angiotensin-aldosterone system can lead to increased blood volume and vasoconstriction - **Clinical Manifestations** - Usually asymptomatic until severe - Headaches - Dizziness/lightheadedness - Blurred vision - Nosebleeds - SOB - **Diagnostics** - BP measurement - Physical exam - Blood tests - ECG - **Management** - Lifestyle changes - Medications - Monitoring - **Orthostatic Hypotension** - **Risk factors** - Fluid deficits - Medications - Aging - Defective function of ANS - Immobility - **Pathophysiology** - Impaired autonomic reflexes: the body's inability to regulate BP properly when changing positions - Venous pooling: blood may pool in the lower extremities upon standing, leading to decreased blood flow to the heart and brain - Reduced cardiac output: failure to increase heart rate and vascular resistance when standing results in inadequate BP maintenance - **Clinical Manifestations** - Dizziness/lightheadedness - Blurred vision - Weakness/fatigue - Nausea - Fainting - **Diagnostics** - BP management - Physical exam - Tilt table test - Blood tests - **Management** - Lifestyle modifications - Adequate hydration - Medications - Gradual position changes **Normal Lab Values** - **Triglycerides** - Less than 150 mg/dL - **Total Cholesterol** - Less than 200 mg/dL - **HDL** - 60 mg/dL or above - **LDL** - Less than 100 mg/dL