13. Regulation Of BP And Hypertensive Vascular Disease Flashcards

1
Q

Blood Pressure

A

Cardiac output- determined by myocardium contractibility, HR and blood volume

Peripheral resistance - humoral and neural factors

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2
Q

Atrial natriurtic peptide (ANP0

A

Released from heart in response to blood volume increase

Vasodilation and sodium excretion

Lower BP

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3
Q

Renin

A

Released from kidneys in settings of hypotension

Converts angiotenisgon - angiotengion I which is converted to angiotensin II in lungs

Angiotensin II - vasoconstrictor increase BP,
alderosterone production =increase renal sodium reabsorption (increase BP)

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4
Q

BP classifications

A

Normal less then 120 less then 80

Elevated 120-129. Less than 80

High blood pressure HT stage 1 - 130-139. 80-89

HT stage 2. 140 or above. 90 or above

Stage 3. Higher then 180. Higher then 120

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5
Q

Essential hypertension

A

Accounts for 90-95% of cases

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6
Q

Secondary hypertension

A

Renal - chronic renal disease (renin-angiotenisngin-aldosertone syndrom3e)

Endocrine - Cushing’s

Cardiovascular

Neurological - acute stress

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7
Q

Mechanisms of essential hypertension

A

90% idiopathic - unknown

Reduced renal sodium excretion = increase fluid volume, increase cardiac output, increase BP

Increase vascular resistance - vasoconstriction/ structural changes

Genetic factors

Environmental factors - salty diet, smoking, stress

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8
Q

Aneurysms

A

Abornomal vascular dilation

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9
Q

Types of anyerisms

A

True - bounded by all three vessel wall layers

False- extravascular hematoma that communicates intramuscular space, collection of blood and CT outside aortic wall, part of vessel wall has been lost

Dissection - blood enters atrial wall it’s self, tear in intima

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10
Q

Pathogenesis of anyerisms

A
  1. Inflammation
  2. Inadequate degredation of ECM
  3. Apoptosis of SMC due to ischemia
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11
Q

Aortic aneurysm

A

Most common cause is atherosclerosis

Weak spot in wall of aorta beings to bulge

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12
Q

Abdominal aortic aneurysms (AAA)

A

Etiology - true aneurysms, atherosclerosis

Pathogenesis is - inflammatory filtrate in atheroscletic lesion produce proteoletic enzymes-that degrade ECM

Clinical features: asymptomatic
Ruptures into peritoneal cavity with massive hemhorrahe
Occlusion of branch vessel
Athero-embolism

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13
Q

Thoracic aortic anyerisms

A

Compression of adjacent structures

Etiology - hypertension

Clinical features:

Respitory/ feeding difficulties 
Persistent cough
Pain
Cardiac abnormalities
Aortic dissection/rupture
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14
Q

Aortic dissection

A

Blood dissects the media and enters aortic wall forming blood filled channel

Major clinical consequence

Often leads to rupture causing sudden death through massive hemhorrage

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15
Q

Clinical targets prof aortic dissection

A

Hypertension

CT defects in that area of aorta

Atherosclerosis

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16
Q

Aortic dissection pathogenesis

A

In hypertensive patients aorta shows medial degeneration that is associated with loss of medial SMC and disorganized ECM

17
Q

Aortic dissection clinical features

A

Sudden onset of excruciating Chest pain ( can be confused with MI)

Death usually result of rupture into pericardium, thorax or abdominal cavity