Blood Vessels julia

Question 1

Intima (Internal elastic lamina) –> media (elastic or smooth mm) –> adventitia (loose connective tss and nn)

Large vs Medium vs Small = Elastic vs Muscular vs Arterioles

Question 2

Arteriovenous malformation

Answer 2

abnormal communication between high pressure arteries and low pressure veins -> blood bypasses the capillary system
- can rupture: SAH

MC: congenital
- acquired: trauma or inflammation

Question 3

Arteriosclerosis (hardening of aa), 4 General Patterns

Answer 3

Arteriosclerosis : small aa

Monckeberg medial sclerosis - not clinically significant; calcification of the medial layer of muscular arterie

Fibromuscular intimal hyperplasia : affects muscular arteries larger than arterioles, driven by inflammation and causes stenosis

Atherosclerosis:
- accumulation of atheromas - fatty deposits and calcification

Question 4

Atherosclerosis

Answer 4

Endothelial injury → monocyte recruitment → LDL oxidation → foam cell formation (macrophages engulf ox LDL) + accumulated foam cells = fatty streak → smooth muscle move from media to intima from activated macrophages and endothelial cells - PDGF, FGR → lipid accumulation + smooth cells produce collagen → plaque maturation with necrotic core and fibrous cap→ calcification from necrotic core release of calc and inflammatory mediators -> risk of rupture

Atherosclerosis - chronic inflammatory response of the arterial wall initiated by endothelial dysfunction/injury (this MUST occur)

= Intimal thickening + lipid accumulation

Endothelial dysfunction leads to monocyte adherence

–> LDL is oxidated and taken up by macrophages (monocytes that have entered tissue from blood are called macrophages) - chronic inflammatory state

–> This forms foam cells which are macrophages filled with LDL

–> Additionally, smooth muscle proliferation occurs from media to intima –> eventually atheromatous plaque matures

–> lipid accumulation

==> calcification of ECM

Question 5

BP equation and BP categories

Answer 5

essential: high blood pressure that develops without an identifiable, direct cause. 95%
- risk: genetics, diet, obese, sedentary, stress, age
- mechanism: overactive SNS, RAAS, endothelial dysfunction, insulin resistance

secondary: underlying cause
- renal, endocrine, CVD, neurologic, surgery

Question 6

HTN histopathology: essential vs malignant

Answer 6

Benign Essential hypertension:
- HYALINE arteriosclerosis
deposition of pink, glassy material and luminal narrowing
- due to plasma leakage and matrix synthesis

Severe/Malignant hypertension: HYPERPLASTIC arteriosclerosis
- concentric, laminated thickening of the smooth muscle cells, which gives an “onion-skin” appearance
- thickening of the walls with luminal narrowing
- fibrinoid deposits and necrosis of the vessel wall/necrotizing arteriolitis especially in KIDNEY

Question 7

Aneurysms: true, false, dissection

Answer 7

true: all layers affected

false - defect in vascular wall that causes a collection of blood (extravascular hematoma); wall of blood vessel NOT INTACT

dissection: blood enters a tear in intima and creates a pathway between the layers of the vessel

Question 8

Pathogenesis of aneurysm

Answer 8

Defective connective tss
- Poor intrinsic quality of vascular wall connective tss
- Abnormal transforming growth factor-beta (TGF-beta) signaling –> decreased ECM content and integrity w/ dilation
- inflammation + proteases –> weird collagen synthesis/degradation cycle

Vascular wall weakened by…
- Loss of smooth mm cells
- Inappropriate synthesis of non-collagenous/nonelastic ECM

Question 9

thoracic and abdominal aneurysm

Answer 9

thoracic aneurysm: MCC = HTN
- most do not have sx till rupture but sx can be chest pain, MI, difficulty swallowing/hoarseness

abdominal aneurysm: MCC = atherosclerosis
- < 4 cm = 0% rupture; 25%/yr: > 6cm

Question 10

Aortic dissection

Answer 10

= blood separates laminar planes of media
- Major risk factor = HTN

Develop medial degenerative changes

Usually @ ascending aorta’s intimal tear –> blood flow P pushes into media –> hematoma –> spreads –> rupture thru adventitia ~~> hemorrhage

Question 11

Vasculitides

Answer 11

mostly arterial, mostly auto-immune, may be drug-related
definition: vessel wall inflammation -> vessel size specific

findings:
- immune complexes
- ANCA - granulomatosis with polyangiitis; Temporal arteritis
- anti-endothelial cell antibodies: Kawasaki ds

Question 12

Temporal arteritis/Giant Cell arteritis

Answer 12

– affects arteries of head and temporal region in adults, vessels may be palpable –> chronic granulomatous inflammation

may present with blindness

Granulomas are present in vessel wall

Labs - Sedimentation rate is elevated, usually positive ANCA (anti-neutrophil cytoplasmic antibodies)

Question 13

Takayasu

Answer 13

– granulomatous inflammation of aorta and its major branches
- giant cells and necrosis present in vessel wall.
- usually women less than 40 years old
= “Pulseless” disease (pulseless upper extremities)

Due to obstruction of the main branches of the aorta, including the left common carotid artery, the brachiocephalic artery, and the left subclavian artery, Takayasu’s arteritis can present as pulseless upper extremities (arms, hands, and wrists with weak or absent pulses on physical examination).

Question 14

PAN (polyarteritis nodosa)

Answer 14

autoimmune + affects small and medium arteries
- histology shows segmental, transmural, necrotizing fibrinoid inflammation

Sx: depends on organs involved + any combination of these symptoms may be present; clinical features due to ischemia and infarction of affected organ
- general: ill and fatigued, have fevers, or have loss of appetite and weight
- skin arteries: skin sores that may appear as hard tender nodules or ulcer
- mesenteric: abdominal pain or blood in the stools
- heart arteries: SOB, chest pain
- kidneys: High blood pressure is common in PAN -> kidneys control blood volume -> major cause of MORTALITY - untreated = fatal, immunosuppression can result in result in remission or cure 90%**
- nerves: abnormal sensations, numbness or loss of strength

Question 15

Kawasaki

Answer 15

– vasculitis of coronary arteries

• usually affects children under the age of 4 years
• Early stages include a rash and fever. Symptoms include high fever and peeling skin
• In late stages: inflammation of medium size blood vessels (vasculitis). It also affects lymph nodes, skin, and mucous membranes, as in the mouth.

Kawasaki disease is usually treatable. Initial treatments include aspirin and IVIG

(Note - CDC has reported cases of multisystem inflammatory syndrome in children (MIS-C) associated with COVID-19, which may present with Kawasaki disease-like features. Signs and symptoms are temporally associated with COVID-19 but usually develop 2–4 weeks after acute COVID-19; children with MIS-C have serologic evidence of infection with COVID-19.)

Question 16

Granulomatosis with polyangiitis

Answer 16

– acute necrotizing granulomas of upper and lower respiratory tract and necrotizing granulomatous vasculitis of small vessels

There is usually renal involvement causing glomerulonephritis

ANCA is positive

Question 17

Buerger’s disease – aka thromboangitis obliteras

Answer 17

associated with smoking, usually in men and affects extremities

Mechanism unknown - It has been suggested that the tobacco may trigger an immune response in susceptible persons or it may unmask a clotting defect, either of which could incite an inflammatory reaction of the vessel wall.

This eventually leads to vasculitis and ischemic changes in distal parts of limbs

Question 18

Varicose veins

Answer 18

increased venous pressure and venous valve dysfunction

affects females more than males

Superficial veins of lower extremities most commonly affected

Dilated, tortuous, elongated, scarred vessels sometimes with calcification

Question 19

Raynaud’s

Answer 19

Vasoconstriction usually triggered by cold, emotional stress. Usually self-limited

pallor (white), cyanosis (blue), hyperemia (red)

Primary Raynaud phenomenon : does not progress, symmetrical

Secondary Raynaud phenomenon : worsens, assymetric, Lupus/atherosclerosis/Buerger dx

Question 20

Thrombophlebitis

Answer 20

90% deep veins of legs

causes edema, cyanosis, heat, pain, tenderness – however, may be asymptomatic

Question 21

Vascular tumors: benign

Answer 21

Hemangioma – benign blood tumor
- capillary hemangioma - MC, subcutaneous tissues and mucous membranes
- cavernous hemangioma - very vascular, does NOT regress
- juvenile hemangioma (strawberry-type hemangioma) - self-limiting in a few years

Lymphangioma (lymph version of hemangioma - simple and cavernous; benign, mostly in head, neck, axilla

Glomus tumor – benign, painful, especially under fingernails

Question 22

Vascular tumors: benign, intermediate, malignant

Answer 22

benign: Do not metastasize + exhibit rare mitoses (cells are not actively dividing at a high rate)
- hemangioma
- lymphagioma

intermediate: rarely metastasize
kaposi sarcoma

malignant: angiosarcoma
- frequent and early mets - esp to LUNG
- many mitoses. severe atypia

Question 22

Kaposi’s sarcoma

Answer 22

Kaposi’s sarcoma – intermediate between benign and malignant
- non-HIV usually found in European males (classic)
- HIV associated Kaposi’s sarcoma associated with virus; AIDS-defining illness!!!! - MC HIV related malignancy
- Kaposi sarcoma–associated herpesvirus (KSHV), also known as human herpesvirus 8 (HHV8)

presentation: red-purple patches or nodules and are generally asymptomatic - but can be slow and indolent