Disorders of Blood Flow and Blood Pressure Regulation

Vocabulary practice flashcards covering arterial and venous pathology, dyslipidemia, atherosclerosis, vasculitis, aneurysms, and blood pressure regulation.

Ischemia

Reduction in blood flow insufficient to meet the oxygen demands of tissues.

Injury (Vascular)

Reversible tissue damage resulting from impaired blood flow.

Infarction

Irreversible tissue damage with necrosis resulting from an absence or severe restriction of blood flow.

Tunica Adventitia

The outer layer of an artery wall.

Tunica Media

The middle layer of an artery wall, composed mainly of vascular smooth muscle cells.

Tunica Intima

The innermost layer of an artery wall, lined by endothelial cells.

Endothelial Cells

Vascular cells involved in platelet adhesion, blood clotting, blood flow modulation, hormone metabolism, immune/inflammatory response, and cell growth.

Endothelial Dysfunction

Potentially reversible changes in endothelial function occurring in response to environmental stimuli, representing a systemic alteration in maintaining vascular tone, permeability, inflammation, and hemostatic balance.

Nitric Oxide and Prostaglandins

Normal antithrombotic and vasodilatory substances synthesized by healthy vascular endothelium.

Inflammatory Inducers of Endothelial Dysfunction

Products that cause endothelial inflammation, including cytokines, bacteria, viruses, hemodynamic stresses, lipid products, and hypoxia.

Endothelial Dysfunction in Diabetes

A pathophysiologic cascade starting with oxidative stress leading to endothelial dysfunction, which promotes atherosclerosis, nephropathy, retinopathy, and cardiovascular disease.

Endothelial Dysfunction in Sepsis

Inflammatory endothelial injury leading to capillary leak, vasodilation, microvascular thrombosis, tissue hypoperfusion, and organ dysfunction.

Triglycerides

Lipids used primarily in energy metabolism.

Phospholipids

Important structural constituents of lipoproteins, blood clotting components, the myelin sheath, and cell membranes.

Cholesterol

A lipid substance whose chemical activity is similar to other lipid substances and is implicated in plaque formation.

Hyperlipidemia

Elevated levels of triglycerides, phospholipids, or cholesterol in the blood, serving as a major cause of atherosclerosis.

Very-Low-Density Lipoprotein (VLDL)

A class of lipoprotein that carries large amounts of triglycerides.

Low-Density Lipoprotein (LDL)

The main carrier of cholesterol in the blood, commonly referred to as bad cholesterol.

High-Density Lipoprotein (HDL)

A lipoprotein consisting of 50% protein synthesized and released by the liver, commonly referred to as good cholesterol.

Monocytes and Macrophages (Lipid Scavengers)

Scavenger cells whose removal of LDL from plasma correlates with plasma cholesterol levels and can lead to foam cell formation in the arterial wall.

Foam Cells

Lipoprotein-laden macrophages created when macrophages take up excess oxidized LDL in the arterial wall.

LDL-C vs Total Cholesterol

LDL-C measures the specific amount of cholesterol carried by LDL (the major atherogenic lipoprotein entering arterial walls), making it more directly useful than total cholesterol for lipid-lowering treatment decisions.

Reverse Cholesterol Transport

The process by which HDL facilitates the clearance of cholesterol from atheromatous plaques and transports it back to the liver for excretion in bile.

Factors Increasing HDL

Regular exercise and moderate alcohol consumption.

Factors Decreasing HDL

Smoking and diabetes mellitus.

Primary Hypercholesterolemia

Elevated cholesterol levels caused by an independent genetic basis, such as familial hypercholesterolemia.

Secondary Hypercholesterolemia

Elevated cholesterol levels associated with health and lifestyle factors such as nutrition, excess calorie intake, saturated fats, cholesterol, obesity, and diabetes mellitus.

Heterozygous Familial Hypercholesterolemia (HeFH) Risk

Historical state in which approximately 30–50% of untreated individuals experienced a coronary event by age 60; statin therapy reduces this coronary risk by 75–80%.

HeFH Genetics

Presence of one pathogenic FH allele, leading to typical untreated LDL-C levels of ~190–400 mg/dL (4.9–10.3 mmol/L) and premature adult-onset atherosclerosis.

Homozygous Familial Hypercholesterolemia (HoFH) Genetics

Presence of two pathogenic FH alleles, leading to typical untreated LDL-C levels >400 mg/dL (often >500 mg/dL) and early childhood onset of atherosclerosis.

Tendon Xanthomas

Common lipid deposits in HeFH and early prominent deposits in HoFH.

LDL-C Threshold $\ge 190\,m/dL$

A level of severe hypercholesterolemia where lipid-lowering therapy is recommended regardless of calculated risk, particularly important for suspected FH.

LDL-C Range $160-189\,mg/dL$

A level where lipid-lowering therapy may be appropriate even when calculated 10-year risk is low, specifically considered a reason for therapy in adults aged 30–59 years.

PREVENT-ASCVD Equations

American Heart Association risk estimation equations used for adults aged 30–79 to assess ASCVD risk.

Adult Lipid Profile Screening Guidelines

Recommended beginning at age 19 years and at least every 5 years thereafter to identify treatable ASCVD risk.

Child Lipid Screening Guidelines (Ages 9-11)

Universal screening with a lipid profile for children aged 9 to 11 years not previously tested to identify FH and other lipid disorders.

Cascade Screening in Children

Performing a single lipid profile starting at $\ge 2$ years of age in individuals with first- or second-degree relatives having premature ASCVD, severe hypercholesterolemia, or FH.

Lp(a) Measurement Guidelines

Recommended at least once in all adults for ASCVD risk assessment.

Fatty Streaks

Thin, flat yellow intimal discolorations that progressively enlarge and may be present in the first year of life as an early atherosclerotic lesion.

Fibrous Atheromatous Plaque

An atherosclerotic lesion characterized by the accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells, and formation of scar tissue.

Complicated Lesion (Atherosclerosis)

An advanced atherosclerotic lesion containing hemorrhage, ulceration, and scar tissue deposits.

Atherosclerosis Risk Factors

Hypercholesterolemia, obesity, diabetes mellitus, cigarette smoking, hypertension, family history of premature CHD, age (men $\ge 45$, women $\ge 55$), HDL $< 40\,mg/dL$, elevated CRP, elevated homocysteine, and elevated Lp(a).

Lipoprotein (a)

An altered form of LDL that acts as a risk factor for atherosclerosis and is not modified by cholesterol-lowering drugs.

Complications of Atherosclerosis

Ischemic heart disease, stroke, and peripheral vascular disease resulting from vessel narrowing, plaque rupture, thrombosis/embolism, or aneurysm.

Atherosclerosis in Large Vessels

Plaque accumulation where major complications primarily stem from thrombus formation and weakening of the vessel wall.

Atherosclerosis in Medium-Sized Arteries

Plaque accumulation where ischemia and infarction due to vessel occlusion are the primary manifestations.

Vasculitis

Inflammation of the blood vessel wall resulting in vascular injury and necrosis, affecting arteries, capillaries, or veins.

Systemic Necrotizing Vasculitides

Classified as Group I vasculitides involving widespread inflammatory necrosis of blood vessels.

Hypersensitivity Vasculitides

Classified as Group II vasculitides triggered by hypersensitivity or immune-mediated reactions.

Giant Cell (Temporal) Arteritis

A Group III large-vessel vasculitis primarily affecting head arteries in the elderly, associated with shoulder pain/stiffness, headache, temporal tenderness, and risk of blindness from ophthalmic artery involvement.

Peripheral Artery Disease (PAD)

Systemic atherosclerosis distal to the arch of the aorta, most common in men in their 60s and 70s, with smoking and diabetes mellitus as strongest risk factors.

Intermittent Claudication

Pain with walking caused by muscle ischemia, commonly affecting the gastrocnemius muscle which has the highest oxygen consumption in the leg during walking.

Arterial Ulcers

Small, distal ulcers found below the ankle resulting from arterial insufficiency, featuring a steep "cliff edge", dry bottom, nocturnal pain when elevated, and ABI $< 0.8$.

Dependent Rubor and Lobster Foot

Signs of decreased arterial blood flow observed in limbs experiencing severe chronic arterial insufficiency.

Seven "P"s of Acute Arterial Embolism

Pistol shot (acute onset), Pallor, Polar (cold), Pulselessness, Pain, Paresthesia, and Paralysis.

Thromboangiitis Obliterans (Buerger's Disease)

An inflammatory vasculitis of medium arteries (plantar/digital vessels in foot/lower leg) triggered by tobacco, primarily affecting male smokers aged 25–40.

Raynaud's Disease

Functional disorder caused by intense vasospasm of arteries and arterioles in fingers and toes, seen in healthy young women and precipitated by cold or emotions.

Type III Hypersensitivity in Raynaud Phenomenon

Immune complex-mediated reaction where antibodies formed to circulating antigens deposit in tissues, activating complement and neutrophils to cause tissue destruction.

Aneurysm

Localized dilatation of a blood vessel classified by cause, location, and anatomical features.

True Aneurysm

A localized vessel dilatation bounded by a complete, intact vessel wall.

False Aneurysm

A localized vascular rupture leading to an extravascular hematoma that communicates with the intravascular space.

Aortic Aneurysm

Arterial dilation involving the aorta, arch, thoracoabdominal, or abdominal regions; often asymptomatic, found as a pulsating mass, and more frequent in hypertensive men over 50.

Aortic Dissection

Acute life-threatening hemorrhage into the vessel wall with longitudinal tearing/separation of the wall forming a blood-filled channel, causing excruciating tearing/ripping pain.

Marfan's Syndrome (Vascular Impact)

Connective tissue disorder associated with degeneration of the medial layer of vessel walls, serving as a risk factor for aortic dissection.

Berry Aneurysm

A small, spherical vessel dilation most often found in the Circle of Willis within cerebral circulation.

Fusiform and Saccular Aneurysms

Aneurysms characterized by gradual and progressive enlargement of the aorta, most often located in the thoracic and abdominal aorta.

Skeletal Muscle Pump

Muscular contraction surrounding deep veins that aids venous blood return against gravity despite low driving pressure and thin vessel walls.

Virchow's Triad

Three factors contributing to venous thrombosis: Vessel Wall Damage, Stasis, and Blood Coagulability (Hypercoagulability).

Causes of Venous Stasis

Bed rest, immobility, spinal cord injury, acute myocardial infarction, congestive heart failure, shock, and venous obstruction.

Factors Increasing Blood Coagulability

Genetics, stress/trauma, pregnancy, childbirth, oral contraceptives, hormone replacement, dehydration, cancer, antiphospholipid syndrome, and hyperhomocystinemia.

Causes of Vascular Trauma in DVT

Indwelling venous catheters, surgery, massive trauma/infection, fractured hip, and orthopedic surgery.

Sequential Compression Devices (SCDs)

Mechanical devices applied to legs that promote venous return in immobilized patients to prevent deep vein thrombosis.

Assessment Signs of DVT

Development of new unilateral swelling, warmth, redness, tenderness, or calf/thigh pain.

Symptoms of Pulmonary Embolism (PE)

Sudden onset of dyspnea, chest pain, tachycardia, hypoxemia, or hemoptysis requiring urgent evaluation.

Blood Pressure Formula

$$\text{BP} = \text{Cardiac Output (CO)} \times \text{Peripheral Vascular Resistance (PVR)}$$

Systolic Blood Pressure Determinants

Determined by stroke volume ejected into the aorta, velocity of ejection, and elastic properties of the aorta.

Diastolic Blood Pressure Determinants

Dependent on aortic elasticity, arteriole resistance, and competency of the aortic valve.

Pulse Pressure

The numerical difference between systolic and diastolic blood pressure, which falls during shock.

Mean Arterial Pressure (MAP)

Average blood pressure in systemic circulation calculated as $\text{MAP} = \frac{1}{3}\text{PP} + \text{DP}$, serving as a reliable indicator of tissue perfusion.

Cardiovascular Control Center

Structure located in the pons and medulla where integration with the autonomic nervous system (ANS) occurs to regulate blood pressure.

Baroreceptors

Pressure-sensitive receptors located in blood vessels and heart that respond to positional changes (e.g., lying to sitting) by increasing heart rate and inducing vasoconstriction.

Arterial Chemoreceptors

Receptors in carotids and aorta responding to oxygen, carbon dioxide, and $H^+$ changes to control ventilation and induce widespread vasoconstriction via the cardiovascular center.

Renin-Angiotensin-Aldosterone System (RAAS) Initiator

Renin secreted by kidneys in response to low BP, low ECF volume, or low extracellular sodium, converting angiotensinogen to angiotensin I.

Angiotensin II

A potent vasoconstrictor formed from angiotensin I by endothelial enzymes in lung vessels, which also stimulates aldosterone secretion from adrenal glands.

Vasopressin (ADH)

Antidiuretic hormone released from the posterior pituitary in response to decreased blood volume/pressure or increased serum osmolarity, acting as a vasoconstrictor.

Long-Term BP Regulation

Renal-mediated regulation of extracellular fluid (ECF) volume; excess ECF increases arterial pressure and water excretion rate, directly altering cardiac output and peripheral resistance.

BP Cuff Sizing Rules

Width of the cuff bladder should be at least 40% of arm circumference and length at least 80% of arm circumference.

Undercuffing vs Overcuffing

Undercuffing (cuff too small) overestimates BP; overcuffing (cuff too large) underestimates BP.

AHA BP Measurement Preparation

Avoid caffeine, exercise, smoking, and alcohol for $\ge 30\,minutes$ and empty bladder prior to measurement to prevent transient BP elevation.

AHA BP Measurement Resting Protocol

Sit quietly for $\ge 5\,minutes$ before measurement to allow sympathetic nervous system activity to settle.

Vascular Remodeling in Hypertension

Hyaline sclerosis and atherosclerosis resulting from sustained hypertension that causes a three-fold increase in coronary artery disease (CAD).

Primary (Essential) Hypertension

Sustained elevation of arterial blood pressure without evidence of other disease, accounting for 90% of cases.

Normal BP Category (AHA)

Systolic blood pressure less than 120 mmHg AND diastolic blood pressure less than 80 mmHg.

Elevated BP Category (AHA)

Systolic blood pressure 120–129 mmHg AND diastolic blood pressure less than 80 mmHg.

Stage 1 Hypertension (AHA)

Systolic blood pressure 130–139 mmHg OR diastolic blood pressure 80–89 mmHg.

Stage 2 Hypertension (AHA)

Systolic blood pressure 140 mmHg or higher OR diastolic blood pressure 90 mmHg or higher.

Hypertensive Emergency

Systolic BP higher than 180 mmHg and/or diastolic BP higher than 120 mmHg accompanied by target organ symptoms (chest pain, dyspnea, back pain, numbness, weakness, vision changes, or speaking difficulty).

Secondary Hypertension

Blood pressure elevation resulting from another underlying disorder, most commonly renal disease, pheochromocytoma, excess aldosterone, or coarctation of the aorta.

Core First-Line Antihypertensive Classes (2025 AHA/ACC)

Thiazide-type diuretics, ACE inhibitors, ARBs, and long-acting dihydropyridine calcium-channel blockers.

Orthostatic Hypotension (Postural Hypotension)

Sustained reduction in systolic BP of at least 20 mmHg or diastolic BP of at least 10 mmHg within 3 minutes of standing or head-up tilt to at least 60 degrees.