Chapter 9 - Blood Vessels Flashcards
Hypertensive Vascular Disease
Normal 120/80 Prehypertension: 120/80 to 139/89 Hypertension: 140/90 or greater Stage I: <160/100 Stage 2: >160/100 Hypertensive "urgency": 180/110 Hypertensive "emergency": 220/140
Pathogenesis: interaction of genetic, environmental and demographic factors
Causes: essential (idiopathic) - majority, secondary - 5%
Essential (idiopathic) hypertension mechanism
complex, multifactorial disorder
environmental factors affect variables controlling blood pressure in a genetically predisposed individual
increased blood volume and increased peripheral resistance contribute to elevated BP
Secondary Hypertension causes
Renal: Acute glomerulonephritis, chronic renal disease, polycystic disease (kidney has cysts), renal artery stenosis, renal vasculitis, renin-producing tumors
Endocrine: adrenocortical hypofunction, pheochromocytoma, acromegaly, hypothyroidism, hyperthryoidism, pregnancy-induced
Cardiovascular: cortication of aorta, polyarteritis nodosa, increased intravascular volume, increased cardiac output, rigidity of aorta
Neurologic: psychogenic, increased intracranial pressure, sleep apnea, acute stress
Hyaline arteriolosclerosis
hyaline accumulates in the wall of small arteries and arterioles, producing the thickening of their walls and narrowing of the lumen.
major morphology of benign nephrosclerosis - glomerular arterioles damage and renal impairment
Hyperplastic Arteriosclerosis
thickened concentric smooth muscle cell layer and thickened, duplicated basement membrane
most prominent in the kidney and can lead to ischemia and acute renal failure
“onion-skin”
Aneurysm
localized abnormal dilation of a blood vessel or heart
atherosclerotic aneurysms most common in abdominal aorta
Smokers over 60 years old particularly at risk
Aortic dissection
separation of the layers within the aortic wall
tears in the intimal layer result in the propagation of dissection secondary to blood entering the intima-media space
Mortality is high and risk factors include arterial hypertension (major cause) and connective tissue disorder (Marfan’s predisposing factor)
Vasculitis
inflammation of the walls of vessels and may involve any artery or vein
caused by direct invasion of walls by infectious pathogens, immune-mediated (immune complex) inflammation
Direct Infection vasculitis
Bacterial - Neisseria meningitidis
Rickettsial - Rocky Mountain Spotted fever
Fungal
Viral
Immune-mediated vasculitis
drug hypersensitivity - antigen-antibody complex deposition
viral infections - hepatitis B (antigen-antibody deposition)
Blood Vessel Vasculitis
- Giant cell arteritis
- Polymyalgia rheumatica
- Takayasu arteritis
- Kawasaki disease
- Granulomatosis with polyangiitis
- Thromboangiitis obliterans
Giant cell (temporal) arteritis
most common of vasculitides
involves small and larger arteries principally of head (temporal, vertebral, ophthalmic and other extracranial arteries)
nodular thickenings of vessels with reduction of lumen, may be granulomatous, etiology unknown
Symptoms: fever, fatigue, masseter muscle claudication common, lingual musculature claudication, transient to complete vision loss (opthalmic artery involvement and retinal ischemia)
Polymyalgia Rheumatica
closely related to giant cell arteritis
pain, weakness, stiffness more pronounced in neck and shoulders, spreading to hips
50% of pts with GCA also have this
15-20% of pts with PR develop GCA
Takayasu Arteritis “Aortic Arch Syndrome”
common in females <40 (asians)
Granulomatous vasculitis involving proximal aorta and branches
markedly weak pulse in arms (pulseless disease of females)
blindness may result and substantial morbidity with unknown etiology
Kawasaki Disease
acute, febrile illness of infancy & childhood (80% < 4 yrs) (common in asians)
arteritis involving vessels of all sizes, Coronary artery involvement is most significant feature (Leading cause of ACQUIRED heart disease in children)
red, racked lips; strawberry tongue; palatal erosions; oral erythema; cervical lymph node enlargement; mucocutaneous lymph node syndrome
Granulomatosis with Polyangiitis (Wegener Granulomatosis)
Autoimmune necrotizing vasculitis, acute necrotizing granulomatous vasculitis of upper respiratory tract and/or lungs, renal disease (glomerulonephritis)
PR3-ANCA (antiprotinase-3 Anti Neutrophil Cytoplasmic Antibodies) positive in about 95% of patients
Males more than females, 40 yrs is average age, 80% die in 1 year, PR3 ANCA levels used to monitor response to therapy
Thromboangiitis Obliterans (Buerger Disease)
Arteritis mainly involving the tibial and radial arteris, onset <35 yrs, ischemic changes in fingers and toes, in-step claudication, severely painful, heavy cigarette smokers
not autoimmune
Primary Raynaud Phenomenon
paroxysmal pallor/cyanosis of fingers, toes, tip of nose/ears cased by intense vasospasm of small arteries or arterioles
exaggeration of normal central and local vasomotor response to cold or emotion
usually young women
Secondary Raynaud Phenomenon
Arterial insufficiency of extremities secondary to other conditions (SLE, scleroderma, Buerger disease)
reversible arterial vasospasm, may cause ischemic necrosis of fingertips or change in nails
Monckeberg Medial Calcification
Usually not clinically significant (minimal narrowing of arterial lumen)
Older individuals, increased incidence in diabetics, incidental finding on radiograph
Atherosclerosis
disease of the arteries
characterized by the deposition of plaques of fatty material on inner walls
Fibrofatty intimal plaques called “atheromas”
fibrous cap, necrotic center
Risk Factors: advancing age, genetic derangements in lipid metabolism, hyperlipidemia, hypertension, diabetes mellitus, cigarette smoking, inflammation, hyperhomocystinemia, Lipoprotein A
Theory of Atherosclerotic Plaque Development
- endothelial injury
- endothelial dysfunction, monocyte adhesion and emigration
- smooth muscle emigration from media to intima and macrophage activation
- macrophages and smooth muscle cells engulf lipid
- smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid
Evolution of atherosclerosis
“Response to injury” theory
-oxidized LDL cholesterol, toxins as foundi n cigarette smoke, hyperglycemia, flow turbulence (Virchow’s triad), Homocystinuria (inc homocysteine level)
Role of LDL cholesterol
“BAD”
circulating LDL accumulated beneath the endothelium in the intima where it undergoes oxidation via “free radicals”
- activated macrophages (foam cells formed)
- cytotoxic to endothelial cells (inc apoptosis)
- activated macrophages secrete “free radical” compounds as well as cytokines and growth factors
- Decreased nitric oxide production by endothelial cells
Role of HDL Cholesterol
“GOOD”
“scavenger” function for LDL-C
Inhibits endothelial damage
- recycles LDL-C to liver
- levels of HDL-C <40 mg/dL associated w/ increased cardiovascular events
Clinical Complications of Atherosclerosis
myocardial infarction, gangrene (diabetics), ischemic stroke
Varicose veins
abnormally dilated tortuous veins
produced by prolonged, increased intravenous pressure with loss of vessel wall support 15-20%,
familial tendency
Clinical Problems: edema, pain and thrombosis, persistent edema leads to poor oxygenation resulting in stasis dermatitis, ulcerations of skin, poor wound healing
Thrombophlebitis/Phlebothrombosis
Thrombophlebitis: Vein inflammation (phlebitis) related to a blood clot (thrombus)
Phlebothrombosis: occurs when a blood clot (thrombosis) in a vein forms independently from the presence of inflammation in the vein
90% occur in deep leg veins
predisposing factors: congestive heart failure, malignant neoplasia, pregnancy, obesity
*First sign of phlebothrombosis may be a pulmonary embolus (bedridden pts)
Lymphangitis
inflammation or infection of lymphatic channels that occur as result of infection at a site distal to channel
most common cause in humans is Streptococcus pyogenes (Group A strep)
caused by fungus Sporothrix schenckii as well
Hemangioma
Benign vascular neoplasm, most common in skin, oral hemangiomas uncommon, but not rare
Capillary hemangioma
composed of small, capillary-sized vessels
Cavernous hemangioma
composed of larger, more “cavernous” vascular
usually do not regress, may be locally destructive
Lymphangioma
composed of benign lymphatic channels
“Cystic hygroma” (neck) - cavernous, lymphangioma, usually neck and axilla of children, Turner syndrome common
Osler-Weber-Rendu Disease (Hereditary Hemorrhagic Telangiectasia
rare AD genetic disorder, affects bv throughout body, failure of normal capillaries to develop and results in a tendency of bleeding, dilation of pre-existing capillaries and veins, widely distributed (severe epistaxis)
Kaposi Sarcoma
Neoplasm of border line or low-grade malignancy
Caused by HHV8 in combo with altered T-cell immunity
“Epidemic form” seen with AIDS
Angiosarcoma
Sarcoma of malignant endothelial cells, Most often in skin (can occur in soft tissue, breast & liver and bone) Poor outlook - agressive neoplasm older person if skin primary 5 year survival about 30% Different from Kaposi sarcoma
