13. Regulation Of BP And Hypertensive Vascular Disease Flashcards
Blood Pressure
Cardiac output- determined by myocardium contractibility, HR and blood volume
Peripheral resistance - humoral and neural factors
Atrial natriurtic peptide (ANP0
Released from heart in response to blood volume increase
Vasodilation and sodium excretion
Lower BP
Renin
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)
BP classifications
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
Essential hypertension
Accounts for 90-95% of cases
Secondary hypertension
Renal - chronic renal disease (renin-angiotenisngin-aldosertone syndrom3e)
Endocrine - Cushing’s
Cardiovascular
Neurological - acute stress
Mechanisms of essential hypertension
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
Aneurysms
Abornomal vascular dilation
Types of anyerisms
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
Pathogenesis of anyerisms
- Inflammation
- Inadequate degredation of ECM
- Apoptosis of SMC due to ischemia
Aortic aneurysm
Most common cause is atherosclerosis
Weak spot in wall of aorta beings to bulge
Abdominal aortic aneurysms (AAA)
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
Thoracic aortic anyerisms
Compression of adjacent structures
Etiology - hypertension
Clinical features:
Respitory/ feeding difficulties Persistent cough Pain Cardiac abnormalities Aortic dissection/rupture
Aortic dissection
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
Clinical targets prof aortic dissection
Hypertension
CT defects in that area of aorta
Atherosclerosis