HTN

Question 1

what is an aneurysm

contrast true vs false aneurysms

Answer 1

localized abnormal dilation of a blood vessel

true= attenuated but intact vessel with a thinned ventricular wall

false= defect in the wall; leads to an extravascular hematoma that freely interacts with the extracellular space

Question 2

What is an AV fistula

Answer 2

the direct connection between arteries and veins that bypass the capillary bed

can occur due to inflammatory necrosis of an adjacent vessel

Question 3

problems with AV fistulas

Answer 3

if they rupture in the brain, could cause an intracranial hemorrhage

shunting of blood from arterial to venous circulation, increasing preload; leads to high output cardiac failure

Question 4

associations of AV fistulas

Answer 4

the most common cause of ICH stroke in children

Question 5

what is a berry aneurysm

Answer 5

weakened arterial elastic lamina and media, causing bulging at the arterial bifurcations

Question 6

problems with berry aneurysms

Answer 6

if they rupture, can cause stroke

Question 7

associations of Berry Aneurysms

Answer 7

HTN

connective tissue diseases

Question 8

what is fibromuscular dysplasia

Answer 8

focal, noninflammatory, nonatherosclerotic fibrotic luminal narrowing in medium and large muscular arteries

Question 9

Problems with fibromuscular dysplasia

Answer 9

fibrosis

focally thickened vessels and intimal hyperplasia that results in luminal stenosis, which leads to renovascular HTN

if rupture, can cause hemorrhage at the site of rupture

Question 10

Associations of fibromuscular dysplasia

Answer 10

increased incidence in 1st degree relatives and young women

Question 11

what stimulates the production of renin

Answer 11

• JG cells become activated by hypotension and hypovolemia
• Macula densa senses hyponatremia
• Activated Beta 1 receptors stimulate increased sympathetic tone

Question 12

Results of RAAS activation

Answer 12

1. Renin activates Angiotensin 1 to activate Angiotensin 2 via ACE
2. Angiotensin 2 activates aldosterone and

• increases sodium reabsorption and water retention
• increases ADH release, making you thirstier
• activated Angiotensin 2 receptor signals arteriolar constriction

increases the extracellular volume and blood pressure

3. aldosterone increases urinary secretion of potassium in the distal tubule and collecting ducts, lowering the serum potassium

Question 13

differentiate essential vs secondary HTN vs malignant HTN

Answer 13

Essential HTN has no single identifiable cause

Secondary HTN has an underlying renal or adrenal cause

Malignant HTN- systolic > 200 and diastolic > 120, renal failure, retinal hemorrhage/ exudation and possible papilledema

Question 14

contrast primary and secondary aldosteronism

Answer 14

Primary Aldosteronism (Conn syndrome) is an excess of aldosterone caused by autonomous overproduction, usually at the adrenal cortex. It is typically due to adrenal hyperplasia or adrenal adenoma.

Secondary Aldosteronism is a condition caused by increased renin secretion

Question 15

compare and contrast the morphologic changes in benign HTN, hyperplastic arteriosclerosis and malignant HTN

Answer 15

Hyaline arteriolosclerosis: Arterioles show homogeneous, pink hyaline thickening with associated luminal narrowing

Hyperplastic arteriolosclerosis: vessels exhibit concentric, laminated (“onion-skin”) thickening of the walls with luminal narrowing, consisting of s_mooth muscle cells with thickened, reduplicated basement membrane_

Hyperplastic Arteriolosclerosis with necrotizing arteriolitis: same as above accompanied by fibrinoid deposits and vessel wall necrosis

Question 16

Compare and contrast atherosclerosis and Monckeberg medial sclerosis

Answer 16

Atherosclerosis is arterial wall thickening and loss of elasticity that occurs in small arteries and arterioles ; can cause downstream ischemic injury

Monckeberg Medial Sclerosis is the calcification of muscular arteries involving the internal elastic membrane, do not encroach on the vessel lumen and are usually not clinically significant

Question 17

greatest risk factor vs most common etiology of aneurysms

Answer 17

Greatest risk factor: atherosclerosis

Most common etiology: HTN

Question 18

Morphologic features of cystic medial degeneration

Answer 18

• smooth muscle cell loss—or change in synthetic phenotype—leads to scarring (and loss of elastic fibers)
• inadequate extracellular matrix synthesis
• production of increasing amounts of amorphous ground substance (glycosaminoglycan

Question 19

compare and contrast abdominal aortic aneurysms and thoracic aortic aneurysms with respect to:

• location, etiology and clinical features

Answer 19

Location

• AAA: below the renal arteries, but above the bifurcation into the iliac arteries
• TAA: Ascending Aorta

Etiology

• AAA: smoking, atherosclerosis, hypercholesterolemia and arterial HTN
• TAA: arterial HTN, bicuspid aortic valve, tertiary syphilis, connective tissue diseases, trauma and smoking

Clinical Features

• AAA: pulsatile abd mass, bruit on auscultation, lower back pain
• TAA: persistent cough, chest pressure thoracic back pain, difficulty swallowing and valve insufficiency

Question 20

clinical features of syphilitic aneurysms

Question 21

How do vessel dissections occur

Answer 21

blood separates the laminar plans of the media to form a blood-filled channel within the aortic wall

Question 22

risk factors of aortic dissection

Answer 22

men 40-60y/o with h/o HTN

connective tissue abnormalities

syphillis

trauma

Question 23

pathogenesis of an aortic dissection

Answer 23

1. transverse tear of the aortic intima
2. blood enters the media of the aorta and forms a false lumen within the intima-media space
3. hematoma forms and propagates longitudinally downward

Question 24

Clinical presentation of an aortic dissection

Answer 24

Sudden and severe tearing/ripping pain

Location: Anterior chest (ascending) or back (descending)

Interscapular or retrosternal pain

↑ BP

Asymmetrical blood pressure and pulse readings between limbs

Syncope, diaphoresis, confusion

Question 25

describe the radiologic findings of an aortic dissection

Answer 25

widened mediastinum on CXR

double-lumen observed on CT

Question 26

what vessels are involved in atherosclerosis

Answer 26

1. Lower aorta
2. coronary arteries
3. popliteal arteries
4. internal carotid arteries
5. circle of willis vessels

Question 27

what are the gross and microscopic morphologic changes of fatty streaks

Answer 27

Fatty streaks are composed of lipid-filled foamy macrophages. Beginning as multiple minute flat yellow spots, they eventually coalesce into elongated streaks 1 cm long or longer.

• not all are destined to become advanced lesions

Question 28

what are the gross and microscopic morphologic changes of atherosclerotic plaques

Answer 28

Gorssly, Atheromatous plaques are white-yellow and encroach on the lumen of the artery; superimposed thrombus over ulcerated plaques is red-brown. They are patchy, usually involving only a portion of an arterial wall and are rarely circumferential; on cross-section, the lesions, therefore, appear “eccentric”

• Plaques vary in size but can coalesce to form larger masses

Microscopically, they are composed of smooth muscle cells, macrophages, T cells, collagen, elastic fibers, proteoglycans and intracellular/ extracellular lipids

Question 29

classic radiologic presentation of fibromuscular dysplasia

Answer 29

beading on conventional angiography with dilated arterial segments > the original size of the vessel