Hypertensive Vascular Disease Flashcards

1
Q

What is essential/primary HTN?

A

HTN occuring without an identifiable cause

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2
Q

What are the three mechanisms by which RAAS elevates BP?

A
  1. Increased sympathetic output
  2. Increased mineralocorticoid secretion
  3. Direct vasoconstriction
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3
Q

What role does Atrial Naturietic Factor play in regulating BP?

A

ANF increases when BP is high and causes an increased secretion of Na

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4
Q

In the case of HTN, what is the end result of autoregulation?

A

Always increased peripheral resistance

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5
Q

What is the prothrombotic paradox associated with HTN?

A

Patients with HTN often experience thrombotic events such as stroke/MI and show Virchow’s triad:

  1. BF abnormalities
  2. Endothelial Damage
  3. Hypercoagulable state
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6
Q

WHat is GLucocorticoid-remediable Aldosteronism and how does it contribute to HTN?

A

Autosomal DOMINANT trait that causes excess aldosterone production, increased Na retention, and increased BP

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7
Q

What is the Syndrome of Apparent Mineralocortoid?

A

Autsomal RECESSIVE form of early-onset HTN in which cortisol is allowed to accumulate and stimulate mineralocorticoid receptors

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8
Q

What is Liddle Syndrome?

A

Autsomal dominant gain of function mutation in chromosome 16 that codes for amiloride-sensitive epithelial sodium channels. Channels are constitutively active in the renal tubules despite low levels of mineralocorticoid

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9
Q

By what mechanism do all mutations that cause hereditary HTN work?

A

By increasing renal Na reabsorption

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10
Q

What vessels typically contribute most to the amount of blood flow thru capillary beds of the kidney?

A

Resistance vessels (arterioles)

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11
Q

A patient has benign arteriosclerois. A cross section of a renal intralobular artery shows irregular thickening of the intima. What is this indicative of?

A

Mild chronic HTN

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12
Q

What is benign arteriolosclerosis typically associated with?

A

Benign Nephrosclerosis

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13
Q

What is malignant HTN?

A

Elevated BP that causes rapidly progressive vascular compromise with the onset of Syx disease of the brain, heart, or kidney

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14
Q

What examination allows for the visualization of malignant HTN on vasculature? What type of changes are seen?

A

Opthalmoscopic exam; Ischemic necrosis (“cotton wool spots”)

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15
Q

Describe the pathogenesis of vascular damage in malignant HTN

A

Segmental dilation due to necrosis of smooth muscle cells. Endothelial integrity is lost resulting in leakage of plasma proteins into the vessel wall (fibrinoid necrosis)

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16
Q

What is the vascular response to acute injury?

A

“Onion-skin” appearance - proliferation of smooth muscle cell proliferation