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Blood Vessel Disease Flip Cards
Blood Vessel Disease Flip Cards
Arterial Diseases
Atherosclerosis
Arterial Disease
Atherosclerosis
What Goes Wrong:
Buildup of fatty plaques (atheroma) in arterial walls, narrowing the lumenThe inside space of a hollow organ or structure. and creating turbulent blood flow. LDL cholesterolA lipid molecule that is a key component of cell membranes and a precursor for bile acids and steroi deposits in tunica intimaThe innermost layer of a blood vessel, consisting of endothelium and a thin connective tissue layer. → inflammatory response → fibrous cap formation → vessel narrowing and stiffening.
Resistance Factors Affected:
Diameter (↓ lumen), turbulenceIrregular, chaotic blood flow that increases resistance and can contribute to clot formation. (↑ resistanceThe opposition to airflow in the respiratory tract, influenced by airway diameter.), vessel elasticity (↓ complianceThe ease with which the lungs expand and contract during breathing.)
Common Locations:
Coronary arteriesBlood vessels that carry oxygenated blood away from the heart (except pulmonary arteries, which carr, carotid arteries, aorta, peripheral leg arteries
Signs & Symptoms:
Often asymptomatic until severe; may cause angina, intermittent claudication, or stroke depending on location
Risk Factors:
High LDL, smoking, hypertension, diabetes, sedentary lifestyle
Why It Matters:
Leading cause of heart attacks and strokes; creates permanent structural changes that increase BP and resistance
Arteriosclerosis
(Arterial Stiffening)
(Arterial Stiffening)
Arterial Disease
Arteriosclerosis
What Goes Wrong:
“Hardening of the arteries” – loss of arterial elasticity due to calcium deposits, collagenA structural protein in the dermis that provides strength and elasticity. buildup, or aging. Elastic arteries lose ability to stretch and recoil → can’t dampen pressureThe force exerted by gases in the respiratory system, affecting airflow and gas exchange. spikes from heartbeats → sustained high systolic pressure.
Resistance Factors Affected:
Vessel compliance (↓), systolic pressure (↑ dramatically), pulse pressureThe difference between systolic and diastolic blood pressure, indicating the force of each heartbeat widens
Versus Atherosclerosis:
Atherosclerosis = plaque buildup; arteriosclerosis = stiffening (can coexist)
Signs & Symptoms:
Isolated systolic hypertension (high systolic, normal diastolic), visible/palpable tortuous temporal arteries
Common In:
Elderly patients (age-related), chronic kidney disease patients (calcificationThe hardening of tissues due to calcium salt deposition.)
Why It Matters:
Increases cardiac workload, causes left ventricular hypertrophy, raises stroke risk even when diastolic is normal
Aneurysm
Arterial Disease
Aneurysm
What Goes Wrong:
Abnormal dilation/bulging of arterial wall due to weakness in the vessel structure. Weakness in tunica mediaThe middle layer of a blood vessel, composed of smooth muscle and elastic tissue, responsible for va (often from chronic hypertension, genetic defects, or atherosclerosis) → vessel balloons outward → risk of rupture.
Types:
Fusiform (entire circumference bulges), saccular (one side bulges out like a balloon)
Resistance Factors Affected:
Changes local blood flow patterns, may create turbulence, reduces effective pressure delivery
Signs & Symptoms:
Often asymptomatic until rupture; abdominal aortic aneurysm may cause pulsating abdominal mass; cerebral aneurysm may cause severe headache if ruptures
Dangerous Locations:
Aorta (especially abdominal), cerebral arteries (subarachnoid hemorrhage), popliteal artery
Why It Matters:
Rupture is often fatal; requires surgical intervention when large enough; screening recommended for high-risk patients
Peripheral Artery Disease (PAD)
Arterial Disease
Peripheral Artery Disease
What Goes Wrong:
Atherosclerosis specifically affecting peripheral arteries, most commonly in the legs, reducing blood flow to extremities. Plaque buildup in femoral, popliteal, or tibial arteries → reduced perfusion to leg muscles and tissues → ischemia during exercise or at rest.
Resistance Factors Affected:
Diameter (↓ from plaques), length (peripheral vessels already have high resistance), turbulence (↑)
Signs & Symptoms:
Intermittent claudication (leg pain with walking that resolves with rest), cool extremities, weak/absent pulses, poor wound healing, pallorAn unusual paleness of the skin due to reduced blood flow.An unusual paleness of the skin due to red on elevation
Progression:
Mild PAD → claudication → rest pain → critical limb ischemia → gangrene/amputation if untreated
Risk Factors:
Smoking (biggest), diabetes, hypertension, high cholesterol, age >65
Why It Matters:
Marker for systemic atherosclerosis (coronary/cerebral); significantly increases heart attack and stroke risk; can lead to limb loss
Venous Diseases
Varicose Veins
Venous Disease
Varicose Veins
What Goes Wrong:
Enlarged, twisted, superficialNear the surface of the body. veinsBlood vessels that return deoxygenated blood to the heart (except pulmonary veins, which carry oxyge (usually in legs) caused by valve failure and venous pooling. Venous valves become incompetent → blood flows backward (reflux) → increased venous pressure → vein walls stretch and become tortuous.
Resistance Factors Affected:
Venous return (↓), venous pressure in legs (↑), capillary hydrostatic pressureThe force exerted by a fluid, such as the pressure of blood pushing against the walls of capillaries (↑ leading to edemaExcess fluid in interstitial spaces.)
Signs & Symptoms:
Visible bulging, rope-like veins under skinThe body’s largest organ, providing protection and regulation.; aching, heaviness in legs; worse with prolonged standing; ankle edema; skin changes (venous stasis dermatitis)
Risk Factors:
Prolonged standing, pregnancy, obesity, family history, age, female sex
Complications:
Venous stasis ulcers (especially medial malleolusLarge inner ankle bump at distal tibia.), superficial thrombophlebitis, bleeding if injured
Why It Matters:
Affects quality of life; can progress to chronic venous insufficiency; requires lifestyle modifications and sometimes surgical intervention
Deep Vein Thrombosis (DVT)
Venous Disease
Deep Vein Thrombosis
What Goes Wrong:
Blood clot formation in deepAway from the surface of the body. veins, most commonly in legs, that obstructs venous return. Virchow’s Triad: (1) venous stasis, (2) endothelial injury, (3) hypercoagulability → thrombus forms → blocks venous flow → backup of blood/pressure.
Resistance Factors Affected:
Venous diameter (↓ from obstruction), venous return severely impaired, pressure proximalCloser to the point of attachment or origin. to clot (↑)
Signs & Symptoms:
Unilateral leg swelling, warmth, redness, pain (especially in calf), Homan’s sign (unreliable); may be asymptomatic
Risk Factors:
Immobility (surgery, long flights), malignancy, pregnancy, oral contraceptives, smoking, inherited clotting disorders
Danger:
Pulmonary embolism (PE) – clot breaks off and travels to lungs, potentially fatal
Why It Matters:
Medical emergency requiring immediate anticoagulation; can be fatal if embolizes to lungs; post-thrombotic syndrome causes chronic leg problems
Chronic Venous Insufficiency
Venous Disease
Chronic Venous Insufficiency
What Goes Wrong:
Long-term condition where leg veins fail to efficiently return blood to the heart, causing chronic venous congestion. Valve dysfunction or venous obstruction → chronic elevated venous pressure → capillary hypertension → fluid/protein leak into tissues → inflammation and fibrosis.
Resistance Factors Affected:
Venous return (chronically ↓), capillary hydrostatic pressure (↑), impaired filtrationThe process by which fluid moves out of capillaries into surrounding tissues due to hydrostatic pre/reabsorption balance
Signs & Symptoms:
Persistent leg edema, aching/heaviness, skin hyperpigmentation (hemosiderin deposits), lipodermatosclerosis (hard, woody skin), venous ulcers
Common Causes:
Post-DVT syndrome, chronic varicose veins, congenital valve abnormalities
Venous Ulcers:
Typically at medialToward the midline of the body malleolus; shallow, irregular borders; minimal pain; surrounded by stasis dermatitis
Why It Matters:
Significantly impairs quality of life; venous ulcers difficult to heal and frequently recur; requires lifelong management with compression therapy
Hypertensive Disorders
Essential (Primary) Hypertension
Hypertensive Disorder
Essential Hypertension
What Goes Wrong:
Chronically elevated blood pressure (≥130/80 mmHg) with no identifiable single cause; accounts for 90-95% of all hypertension cases. Multifactorial: genetic predisposition + environmental factors → increased peripheral resistance → sustained elevated BP → vascular remodeling perpetuates hypertension.
Resistance Factors Affected:
All three: diameter (↓ from chronic vasoconstrictionThe narrowing of blood vessels due to contraction of smooth muscle, increasing blood pressure and re/arterial remodeling), length (↑ with obesity), viscosityThe thickness or resistance to flow in a fluid, such as blood. (may ↑)
Signs & Symptoms:
“Silent killer” – usually asymptomatic until complications develop; occasional headaches, dizziness, or nosebleeds in severe cases
Risk Factors:
Family history, age, obesity, high sodium(Na⁺): Major ECF cation; important for fluid balance, nerve function. diet, physical inactivity, excessive alcohol, stress, sleep apnea
End-Organ Damage:
Left ventricular hypertrophy/heart failure, stroke, chronic kidney disease, retinopathy, aortic aneurysm
Why It Matters:
Leading modifiable risk factor for cardiovascular disease worldwide; requires lifelong management with lifestyle changes and often medication
Preeclampsia
Hypertensive Disorder
Preeclampsia
What Goes Wrong:
Pregnancy-specific hypertensive disorder (BP ≥140/90 after 20 weeks) with proteinuria and/or end-organ dysfunction. Abnormal placental developmentThe process of growth and differentiation. → poor spiral artery remodeling → placental ischemia → release of anti-angiogenic factors → widespread endothelial dysfunction and vasospasm.
Resistance Factors Affected:
Diameter (↓ from systemic vasospasm), viscosity (may ↑ from hemoconcentration), widespread increased peripheral resistance
Signs & Symptoms:
Hypertension, proteinuria, edema (especially facial/hands), severe headaches, visual changes, right upper quadrant pain, decreased platelets
Severe Features:
BP ≥160/110, severe proteinuria, HELLP syndrome (hemolysisThe rupture of red blood cells, releasing hemoglobin into the blood., elevated liverA large organ that produces bile, detoxifies blood, and stores nutrients. enzymesProteins that speed up chemical reactions in the body., low platelets), pulmonary edema, seizures (eclampsia)
Risk Factors:
First pregnancy, multiple gestation, chronic hypertension, diabetes, obesity, age >35 or <20, previous preeclampsia
Why It Matters:
Life-threatening for mother and baby; only cure is delivery; can progress rapidly to eclampsia (seizures), stroke, or maternal/fetal death
Malignant Hypertension
Hypertensive Disorder
Malignant Hypertension
What Goes Wrong:
Severe, rapidly progressive hypertension (typically >180/120 mmHg) with acute end-organ damage – a medical emergency. Extreme BP → acute vascular injury and necrosis → fibrinoid necrosis of arteriolesSmall arteries that regulate blood flow into capillaries through vasoconstriction and vasodilation → microangiopathic hemolytic anemiaAnemia caused by the destruction of red blood cells before their normal lifespan ends. → organ ischemia and failure.
Resistance Factors Affected:
Diameter (severe ↓ from vasospasm and vessel damage), turbulence (↑ from endothelial injury), acute dramatic ↑ in resistance
Signs & Symptoms:
Severe headache, visual disturbances, confusion, chest pain, dyspnea, acute kidney injury, papilledema on fundoscopy
Acute Complications:
Hypertensive encephalopathy, stroke, acute heart failure/pulmonary edema, acute renal failure, aortic dissection, MI
Triggers:
Medication non-adherence, secondary causes (renal arteryThe artery that supplies blood to the kidney. stenosis, pheochromocytoma), drug use (cocaine, amphetamines)
Why It Matters:
True hypertensive emergency requiring immediate IV antihypertensive therapy in ICU setting; untreated has 90% one-year mortality; must lower BP carefully to avoid organ hypoperfusion
Systemic Vascular Disorders
Raynaud’s Phenomenon
Systemic Vascular Disorder
Raynaud’s Phenomenon
What Goes Wrong:
Episodic vasospasm of small arteries in fingers/toes causing color changes in response to cold or stress. Exaggerated vasoconstriction response → severe reduction in blood flow to digits → tissue ischemia → characteristic tri-phasic color change.
Resistance Factors Affected:
Diameter (extreme ↓ during episodes), local peripheral resistance (↑ dramatically), flow to affected digits (↓ to nearly zero)
Signs & Symptoms:
Tri-phasic color change: (1) white/pallor from vasospasm, (2) blue/cyanosis from deoxygenation, (3) red/hyperemia upon rewarming; numbness, tingling, pain
Types:
Primary (Raynaud’s disease): idiopathic, benign. Secondary: associated with autoimmune diseases (scleroderma, lupus), medications, occupational trauma
Risk Factors:
Female sex, age 15-40, family history, living in cold climate, smoking, vibration exposure
Why It Matters:
Primary form is usually benign but uncomfortable; secondary form may indicate serious autoimmune disease and can lead to digital ulcers or gangrene
Shock
(Circulatory Failure)
(Circulatory Failure)
Systemic Vascular Disorder
Shock
What Goes Wrong:
Life-threatening condition where circulatory system fails to deliver adequate oxygen/nutrients to tissues, causing cellular dysfunction and organ failure. Inadequate tissue perfusionThe delivery of oxygen and nutrients to tissues via the blood supply. → cellular hypoxiaA deficiency of oxygen in the tissues. → anaerobicprocess that does not use oxygen metabolismThe sum of all chemical reactions in the body. → lactic acidosisA condition where blood pH falls below 7.35. → cellular injury → multiple organ dysfunction syndrome (MODS).
Types & Resistance:
Hypovolemic: ↓ blood volume (hemorrhage, dehydrationA condition in which fluid loss exceeds intake, leading to a decrease in total body water.), resistance ↑ initially. Cardiogenic: pump failure, resistance ↑. Distributive: (septic, anaphylactic, neurogenic) inappropriate vasodilationThe widening of blood vessels due to relaxation of smooth muscle, decreasing blood pressure and incr, resistance ↓. Obstructive: mechanical obstruction (PE, tamponade)
Signs & Symptoms:
Hypotension, tachycardia, altered mental status, cool/clammy skin (except distributive = warm), oliguria, weak pulses, increased lactate
Compensatory Mechanisms:
Sympathetic activation → vasoconstriction, ↑ heart rate, ↑ contractilityThe ability of muscle tissue to shorten with force.; RAAS activation → fluid retention; these eventually fail in decompensated shock
Why It Matters:
Medical emergency with high mortality; requires immediate intervention (fluids, vasopressors, treat underlying cause); demonstrates how blood vessel function is critical for life
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