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Flashcards in Vascular Deck (20):

Systemic Hypertension

pressure above 140/90


Primary Hypertension

Unknown Etiology but accounts for 95% of cases
Risk factors include:
Race (higher in Africans Americans and lower in asians)
Lack of physical activity
High Salt diet


Secondary Hypertension: Cause and exam findings

Caused by Renal Artery stenosis (atheroslcerosis in men and fibromuscular dysplasia in females)
See increased plasma renin and unilateral atrophy of of the affected kidney


Mechanism of Secondary Hypertension

1) stenosis leads to ecreased blood flow to glomerulus
2) Juxtaglomerular Apparatus (JGA) responds by secreting renin
3) Renin converts angiotensinogen to Angiotensin I
4) ACE converts ATI to ATII
5) ATII raises BP by contracting arteriolar smooth muscle and promotes aldosterone release from adrenal glands
6) Aldosterone increases resorption of sodium in distal convoluted tubule


Fibromuscular Dysplasia

Developmental defect in blood vessel wall resulting in irregular thickening of large and medium sized arteries, especially the renal artery that leads to secondary hypertension


Benign vs Malignant Hypertension

Benign is mild elevated BP and is often clinically silent but slowly damages organs and vessels over time

Malignant is BP of 200/120 or higher and is medical emergency as it causes acute end-organ damage (renal failure, headache, and papilledema) and is a medical emergency)



Benign tumor comprised of blood vessels
Commony present at birth but regresses during childhood
Usually involves skin or liver
Raised lesions BLANCH when you press on them



Malignant proliferation of endothelial cells and is highly aggressive
Seen in skin, breast, and liver
Liver angiosarcoma is assosicated with exposure to polyvinyl chloride, arsenic, and Thorostat


Kaposi Sarcoma

Low grade malignant proliferation of endothelial cells associated with HHV8
Presents as purples patches, plaques, and nodules on skin that DO NOT BLANCH. May also involve visceral organs
See in Older eastern European Males and Immunocompromised
For eastern M. treat with surgery, AIDS give antiretrovirals, and transplant recipients you decrease immunosupression


Atherosclerosis- deffinition and common sites

Intimal plaque that obstructs blood flow in large and medium sized vessels. Consists of a necrotic lipid core (motly cholesterol) with a fibromuscular cap. Often undergoes dystrophic calciifcation
Commonly affects abdominal aorta, coronary artery, popliteal artery, and internal carotid artery.


Modifiable Risk Factors for Atherosclerosis

Hypertension, Hypercholesterolemia, smoking and diabetes


Nonmodifiable risk factors for atherosclerosis

Gender (male and post menopasual women as estrogen is protective)


Pathogenesis of Atherosclerosis

Damage to to endothelium allows lipid to leak into the intima
Lipids are oxidized and then consumed by macrophages forming foam cells
Inflammation and healing leads to deposition of extracellular matrix and proliferation of smooth muscle


Complications of Atherosclerosis

Usually no symptoms until it is at least 70% occluded
1) Stenosis leads to ischemia =Peripheral vascular disease (lower extremities like popliteal), Angina (narrowing of coronary arteries), Ischemic bowel disease (messenteric arteries)
2) Plaque rupture exposes damaged endothelium and get coagulation cascade and formation of a thrombus that completely occlude the whole vessel. Cause MI or stroke (MCA)
3) Plaque rupture with embolization downstream characterized by cholesterol crystals in embolus
4) Aneurysm (abdominal aorta) = plaque diminishes nutrients to I, M, A so the wall becomes weak and baloons out


Hyaline Arteriolosclerosis, 2 mechanisms, and end result

Caused by proteins leaking into the vessel wall, producing vascular thickening as seen as pink hyaline on microscopy.
1) Chronic hypertension = blood literally pushes the protein into the wall
2) Diabetes causes non enzymatic glycosylation of the basement membrane which makes it leaky to proteins
Leads to narrowing of the small arterioles with end organ ischemia. Classically produces glomerula scarring (arteriolonephrosclerosis) that slowly progresses to chronic renal failure. Seen as atrophied and scarred kidney


Hyperplastic Arteriolosclerosis

Thickening of the vessel wall by hyperplasia of smooth muscle ("onion skin appearance") as a result of malignant hypertension. Get narrow vessels that leads to end organ ischemia. May lead to fibrinoid necrosis of the vessel wall with hemorrhage. Classically causes renal failure with "flea bitten" appearance


Monckeberg Medial Calcific Sclerosis

Calcification of the media of muscular medium sized arteries. Is nonobstuctive and therefore clinically silent and usually only found incidentally.


Aortic Dissection
(definition, mechanism, classic presentation, complications)

Intimal tear with dissection of bllod through media of the aortic wall. Occurs in the proximal 10cem of the aorta (high pressure) with preexisting weakness of the media.
Presents as sharp, tearing chest pain that radiates to the back.
Most commonly caused by hypertension (get hylaine arteriolosclerosis of vasa vasorum, decreased nutrients to media and therefore weakness) or genetic defects in connective tissue such as Marfan syndrome (-fibrillin) or Ehlers-Danlos syndrome (-collagen)
Complications include pericardial tamponade, rupture with fatal hemorrhage, and obstruction of branching arteries (coronary or renal)


Thoracic Aneurysm deffinition, mechanism, and complications

Balloon like dilation of thoracic aorta.
Due to weakness in aortic wall and classically seen in tertiary syphilis (get endarteritis/inflammation of vasa vasorum and decreased nutrients to vessel wall therefore weakness) and a tree bark appearance.
Complications include dilation of the aortic valve root that results in aortic insufficiency, mopression of mediastinal structures (esophagus or airways) and formation of thrombosis/embolism


Abdominal Aortic Aneurysm

Balloon like dilation of abdominal aorta (below renal and above bifurcation)
Primarily due to atherosclerosis (male smokers, older than 60 with hypertension classically)
Major complications is rupture which presents with pulsatile mass, hypotension, and flank pain.
Can also get compression or local structures like the ureters or formation of thrombosis/embolism