9.4 Vascular Pathology & Hypertension

9.4 Vascular Pathology & Hypertension

Quick Answer: Most hypertension is primary (complex renal sodium handling, RAAS, SNS, vascular stiffness). Secondary hypertension has a findable driver—renovascular RAAS activation or endocrine hormone excess. Aneurysms are pathologic dilations; dissections are wall separations after intimal tear. Vasculitis is classified by vessel size and immune pattern (including ANCA). DVT/PE follow Virchow’s triad. Shock is sorted by hemodynamics: volume, pump, vasodilation, or obstruction.

Hypertension: Primary vs Secondary Mechanisms

Blood pressure ≈ cardiac output × systemic vascular resistance. Chronic hypertension damages vessels (hyaline arteriolosclerosis, hyperplastic “onion-skin” arteriolosclerosis in malignant ranges), accelerates atherosclerosis, and drives left ventricular hypertrophy and HFpEF risk.

Primary (essential) hypertension accounts for most adult cases. Mechanisms intertwine: genetic set-points for renal sodium excretion, inappropriate RAAS activity for the volume status, increased sympathetic tone, endothelial dysfunction with reduced NO, obesity-related insulin resistance and sleep apnea, and age-related arterial stiffening raising systolic pressure. The final common path is elevated SVR and/or volume with adverse vascular remodeling.

Secondary hypertension should be considered with abrupt onset, young age, resistant BP, or clue-rich phenotypes:

Malignant hypertension features extreme BP with acute end-organ injury (encephalopathy, papilledema, thrombotic microangiopathy, hyperplastic arteriolosclerosis). Mechanism questions emphasize fibrinoid necrosis of arterioles and loss of autoregulation.

Vessel Wall Layers and Aortic Disease

Arteries have three layers:

1. Intima — endothelium + basement membrane; atherosclerosis begins here.
2. Media — smooth muscle and elastic lamellae (especially elastic arteries); strength against pulse pressure.
3. Adventitia — connective tissue, vasa vasorum, nerves.

Aortic aneurysm is pathologic dilation (all wall layers intact but remodeled). Abdominal aortic aneurysm (AAA) associates with atherosclerosis, smoking, age, male sex—risk of rupture rises with diameter. Thoracic aneurysms associate with hypertension, bicuspid aortic valve, Marfan (fibrillin-1 / TGF-β pathway), Loeys–Dietz, syphilis historically (vaso vasorum endarteritis). Pathophysiology of rupture is wall stress (Laplace: larger radius → higher wall tension).

Aortic dissection begins with an intimal tear allowing blood to enter a false lumen within the media, propagating antegrade/retrograde. Predispositions: hypertension (most common), connective tissue disorders, bicuspid aortic valve, cocaine, trauma. Stanford A involves the ascending aorta (surgical emergency physiology: can occlude coronaries, cause tamponade, severe AR). Stanford B begins distal to left subclavian (often managed medically for BP/shear unless complications). False lumen can obstruct branch vessels causing stroke, mesenteric ischemia, renal infarction, or limb ischemia.

Vasculitis: High-Yield Patterns

Vasculitis is vessel-wall inflammation causing stenosis, aneurysm, rupture, or thrombosis. Classify by vessel size and immune markers.

Large-Vessel

• Giant cell (temporal) arteritis: older adults; branches of carotid (temporal artery headache, jaw claudication, risk of blindness from ophthalmic artery involvement); association with polymyalgia rheumatica; granulomatous inflammation of medium/large arteries.
• Takayasu arteritis: “pulseless disease” in younger females; granulomatous large-vessel vasculitis of aortic arch and branches → stenoses, asymmetric BP, claudication of upper extremities.

Medium-Vessel

• Polyarteritis nodosa (PAN): segmental transmural necrotizing inflammation of medium muscular arteries; microaneurysms (renal, mesenteric); spares lungs typically; association with hepatitis B in a subset; not ANCA-associated.
• Kawasaki disease: childhood medium-vessel vasculitis; mucocutaneous lymph node syndrome; critical risk of coronary artery aneurysms and thrombosis—pathophysiology of delayed coronary complications is board-critical.

Small-Vessel (ANCA-Associated and Immune Complex)

Buerger disease (thromboangiitis obliterans) affects small/medium arteries and veins in heavy tobacco users—segmental thrombosis and inflammation, claudication, Raynaud, autoamputation risk; smoking cessation is the mechanistic therapy concept.

ANCA-associated vasculitides damage vessels via neutrophil activation, NETosis, and endothelial injury rather than bulky immune-complex deposits (pauci-immune glomerulonephritis). HSP is the prototype small-vessel IgA immune-complex vasculitis after triggers in children.

DVT and PE: Virchow Triad

Virchow triad: (1) stasis (immobility, heart failure, venous compression), (2) endothelial injury (trauma, surgery, prior DVT), (3) hypercoagulability (factor V Leiden, antithrombin/protein C/S deficiency, antiphospholipid syndrome, cancer, pregnancy, OCP/estrogen). Deep vein thrombi, often calf or proximal leg veins, propagate and can embolize through right heart to pulmonary arteries.

Pulmonary embolism increases dead space (ventilated but underperfused lung), causes V/Q mismatch, hypoxemia, and acute pulmonary hypertension that can precipitate right ventricular failure (obstructive/cardiogenic overlap shock in massive PE). Paradoxical embolism requires right-to-left communication (PFO/ASD) when right pressures rise.

Shock Types: Hemodynamic Overview

Shock is inadequate tissue perfusion. Classify by the dominant lesion in the CO–SVR–preload circuit:

Hypovolemic shock: loss of circulating volume → low preload → low SV/CO; baroreflex tachycardia and vasoconstriction raise SVR; cool, clammy skin.

Cardiogenic shock: pump failure → low CO with high filling pressures; pulmonary edema common; compensatory SVR rise worsens afterload.

Distributive shock: pathologic vasodilation (inflammatory mediators in sepsis; histamine in anaphylaxis; loss of sympathetic tone in neurogenic) → low SVR; septic physiology may show high CO early with warm skin before myocardial depression.

Obstructive shock: mechanical obstruction to venous return or pulmonary flow (tamponade equalizes diastolic pressures and impairs filling; tension pneumothorax kinks venous return; massive PE blocks RV output).

Mixed pictures occur (septic cardiomyopathy; PE with RV ischemia). For CBSE, match the stem’s volume status, neck veins, skin temperature, and precipitant to the table rather than memorizing drug protocols.

Synthesis for Exam Stems

Hypertension items ask whether RAAS is appropriately or autonomously activated. Aortic items ask dilation versus dissection plane and branch compromise. Vasculitis items give age, vessel size, lung/kidney involvement, and ANCA flavor. Thrombosis items name which Virchow limb is dominant. Shock items give a hemodynamic fingerprint. Link vessel wall biology across all of these: intima starts atherosclerosis and dissection tears; media determines aneurysm and large-vessel vasculitis targets; lumen thrombosis unifies PE and many vasculitic occlusions.

Section mastery means you can explain BP as CO × SVR with secondary drivers, label aneurysm versus dissection, assign each vasculitis to size/ANCA/organ pattern, apply Virchow’s triad, and sort shock into four hemodynamic buckets.