Blood vessels

1. tunica intima

2. tunica media

3. tunica externa

=> in all vessels EXEPT capillaries

elastic and muscular arteries

small mudcular arteries and arterioles

postcapillary venules

Cardiac output x perioheral vascular resistance

RAAS system x Natriuretic peptides

• multiple small changes in renal sodium

homeostasis and/or vessel wall tone or structure

• genetic factors (single gene polymorphisms)

• enviromental factors

• vasoconstictive influences

• reduced renal sodium excretion

Renovascular hypertension -RAAS

Neurologic disorders

Cardiovascular disorders

Endocrine abnormalities

older patients, chronic hypertension diabetes

pink hyaline wall thikening -> luminal wall narrowing

Laminated “onion-skin” thickening -> luminal narrowing fibrinoid deposites, necrotizing arteriolitis

small arteries and arterioles

downstream ischemic injury

muscular arteries (internal elastic memebrane)

over 50

lower and upper limbs, visceral arteries

lession are not clinically significant

Multifactorial, slowly progressive disease

underlies the pathogenesis of coronary, cerebral and peripheral vascular disease

large and medium elastic and muscular arteries

mechanical obstruction of blood flow

rupture -> obstructive vascualar trhrombosis

=> ischemic injury & weakening of vessel wall (aneurism)

intimal lesion

Genetic abnormalities

Family history

Increasing age

Male gender

Hyperlipidemia (hypercholesterolemia)

Hypertension (60% risk of IHD)

Cigarette smoking

Diabetes mellitus

LDL – complex that delivers cholesterol to peripheral tissues

saturated fats trans-unsaturated fats

obesity smoking

HDL - Complex that mobilized cholesterol from the Periphery (vesel wall)

omega-3-fatty acids exercise moderate consumption of ethanol

Inflammation (CRP-acute phase reactant, synthesized by the liver)

hyperhomocystinemia

Metabolic syndrome (central obesity, insulin resistance, dyslipidemia, hypertension, hypercoagulability and proinflamatory state)

Lipoprotein A (altered form of LDL)

Factors affecting hemostasis

Lack of exercise, stressful life style, obesity...

1. foam cells

2. fatty streak

3. intermediate lesion

4. atheroma

5. fibrous plaque

6. plaque rupture/fissure and thrombosis

calcification

hemorrage

fissuring

ulceration

Atherosclerotic stenosis

Acute plaque change

Thrombosis

Focal vasoconstriction

Vessel wall weakening

- lower abdominal aorta

- coronary arteries

- popliteal arteries

- internal carotid arteries

- vessels of the circle of Wilis

localizeed abnormal vascular dilations

Poor intrinsic quality of the vessel matrix (elastic tisue loss)

Marfan sy (inadequate fibrillin synthesis, aberant TGF-β activation)

Ehlers Danlos sy (defective collagen III synthesis)

Vitamin C deficiency (defective collagen cross linking)

Imbalance of matrix (collagen) degradation and synthesis (inflammation, increased MMP expression)

Loss of smooth muscle cells or ECM synthesis

(atherosclerotic thickening, medial ischemia)

Artherosclerosis -> abdominal aorta

Hypertension -> ascending thoracic aorta

trauma

vasculitis

congenital defects

infections -> mycotic aneurysms

Major cause -> severe complicated atherosclerosis

variants -> Inflammatory AAA, IgG4 related disease, mycotic AAA

Complications -> rupture, obstruction of the vessel branching off aorta, embolism, compression

causes -> hypertension , terialy syphilis

Predilection for small vessels (vasa vasorum)– obliterative endarteritis Ischemic injury of the aortic media: mesoaortitis luetica

-> can compress sternum -> cause osteomalacia

Aortic valve dilatation with valvular insufficiency or narrowing of the coronary ostia

samptoms -> Persistent cough Respiratory difficulties Difficulty in swallowing Pain Cardiac disease

blood filled channel in the aortic wall

classification pre or post of brachiiocephalic artery

Men, 40-60 yrs

hypertension

Marfan sy

Iatrogenic

Pregnancy

Underlying substrate: medial hypertrophy of vasa vasorum associated with degenerative changes - cystic medial degeneration

Immune mediated inflammation

↳ complement, T-lymph.

Direct vascular invasion by infectious pathogenes

Noninfectious VAsculitis

Infectious Vasculitis

Depend on the specific vascular bed that is affected (downstream ischemia)

Symptoms of systemic inflammation

Clinical and pathologic overlap among entities

~ 20 primary forms of vasculitis

• immune complex deposition

• anti-neutrophil cytoplasmic antibodies

  • ANCAs

    -> anti-proteinase-3 (PR3-ANCA)

    -> anti-myeloperoxidase (MPO-ANCA)

    -> ANCA activated neutrophils - EC injury

• Anti-endothelial cell antibodies

• autoreactive T cells

Chronic inflammatory disorder

Elderly population man over 80

Granulomatous inflammation (T-ly)

Biopsy (patchy !)

Nodular intimal thickening

Temporal a.

Ophthalmic a.

Vertebral a.

Aorta

Granlomatous vasculitis of medium and large sized arteries under 50

affects aorta and arch vessels

Mononuclear infiltrates Giant cells

patchy medial necrosis

irregular hickening of vessel wall i

ntimal hyperplasia

adventitial fibrosis

small and medium muscular arteries

renal and visceral

chrinic hb infection

in young adults

pul. circulation

episodic with long symptom-free intervals

- nonspecific systemic findings

- hypertension, abdominal pain and bloody stools, peripheral neuritis, muscular pains

Th: immunosuppression

Childhood

capillaritis

skin, kidney, Gi tract, jointgs

Trigger -> microorganisms, drugs

Heavy tabacco smokers

< 35 yrs

Segmental, trombosing inflammation of medium and small size arteries (tibial, radial a.)

deep leg veins

periprostatic, pelvic venous plexus, dural sinusues

complication -> pulmonary embolism

risc factors -> imobilization, congestive hf, alignancy, pregnancy, obesity

mirgatory thrombophlebitis -> malignancy associated hypercoagulability

tumors of blood filled vessels

infancy and childhood

lezions of head and neck

extensive internal lesion of liver

thin walled capillaries scant stroma

Large, dilated spaces filled with blood More infiltrative, localy destructive Involve deep structures, liver, CNS Part of von Hippel-Lindau disease

newborn skin

growth rapidly complete regrssion by 7 y

skin, oral mucosa, often following trauma

blled easily, ulcerate