Vascular

Question 1

Systemic Hypertension

Answer 1

pressure above 140/90

Question 2

Primary Hypertension

Answer 2

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

Question 3

Secondary Hypertension: Cause and exam findings

Answer 3

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

Question 4

Mechanism of Secondary Hypertension

Answer 4

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

Question 5

Fibromuscular Dysplasia

Answer 5

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

Question 6

Benign vs Malignant Hypertension

Answer 6

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)

Question 7

Hemangioma

Answer 7

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

Question 8

Angiosarcoma

Answer 8

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

Question 9

Kaposi Sarcoma

Answer 9

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

Question 10

Atherosclerosis- deffinition and common sites

Answer 10

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.

Question 11

Modifiable Risk Factors for Atherosclerosis

Answer 11

Hypertension, Hypercholesterolemia, smoking and diabetes

Question 12

Nonmodifiable risk factors for atherosclerosis

Answer 12

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

Question 13

Pathogenesis of Atherosclerosis

Answer 13

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

Question 14

Complications of Atherosclerosis

Answer 14

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

Question 15

Hyaline Arteriolosclerosis, 2 mechanisms, and end result

Answer 15

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

Question 16

Hyperplastic Arteriolosclerosis

Answer 16

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

Question 17

Monckeberg Medial Calcific Sclerosis

Answer 17

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

Question 18

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

Answer 18

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)

Question 19

Thoracic Aneurysm deffinition, mechanism, and complications

Answer 19

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

Question 20

Abdominal Aortic Aneurysm

Answer 20

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