Pathophysiology of Hypertension

Question 1

What 5 organ systems are involved in the pathophysiology of HT?

Answer 1

1. ) Heart
2. ) Brain and CNS
3. ) Endocrine
4. ) Blood Vessels
5. ) Renal system

Question 2

Use the equations:
MAP = CO X TRP
CO = HR X SV
to name 4 ways BP is increased

Answer 2

1. ) Increased Heart rate = increased CO
2. ) Increased myocardial contraction = Increase SV
3. ) Increased arterial constriction = Increased TPR
4. ) Increased blood volume = increased CO

Question 3

What is the primary cause of HT?

Answer 3

Increased resistance in arterioles = TPR

Question 4

Do the majority of people with HT have an increased CO?

Answer 4

No, it is slightly reduced especially as the pathology develops and compensatory mechanisms kick in.

Question 5

What initiates elevated TPR in HT?

Answer 5

1. ) Genetics - esp african americans and souther asians, salt sensitive families.
2. ) Liddle’s syndrome = mutation in a single gene leads to an increase in activity of the sodium channels in the epethilium of the renal sytem. More Na+ is reabsorbed (K+ is lost) and water follows = increased blodd volume and increased cardiac output.
3. ) Environmental influences e.g. salt intake, low K+ levels, obesity, stress alcohol consumption
4. ) Vasculature remodelling = increase in extracellular matrix and myocyte hypertrophy
5. ) Vasoactive substances : Endothelial-1 (ET-1) = vasoconstricor, noradrenaline (sympathetic tone), NO (NEEDED FOR VASULATURE TONE), Angiotensin2

Question 6

Where is angiotensinogen produced?

Answer 6

In the liver

Question 7

What converts angiotensinogen to angiotensin 1?

Answer 7

Renin from the kidney

Question 8

What converts angiotensin 1 to 2?

Answer 8

ACE (angiotensin converting enzyme) from the lungs

Question 9

What 5 actions does angiotensin 2 have?

Answer 9

1. ) Increases sympathetic activity = increase HR, SV, vascular tone, and resistance vessel tone
2. ) Increases Na and Cl reabsorption in the kdney = more K is lost but more water retentio = increase CO
3. )increases aldosterone secretion from the adrenal cortex (on kidney) = water retention
4. ) Directly acts on the vasculature to cause vasoconstricion
5. ) Acts on the posterior pituitary gland to release more ADH - more water adsorption in the collecting duct

Question 10

What is the neuroadrenergic hypothesis related to stress?

Answer 10

The noradrenaline that is released in response to stress (via SNS) acts directly on alpha 1 receptors of the small vessles and causes repeated arteriole constriction = hypertrophy of arterioles = permanent structural changes = maintained TPR and HT

Question 11

Explain the salt imbalance renal hypothesis.

Answer 11

If your NaCl intake is greater than NaCl renal excretion then BV will increase as will CO and BP. Normally, this is a transient effect as an increase in BV will lead to a decrease in aldosterone and AngII secretion which leads to a decrease in plasma volume. but 15-20% of Hypertensives are “salt sensitive” and they increase levels of aldosterone and AngII.

Question 12

What are the two groups of sensitives?

Answer 12

High renin activity (RAA) (renal salt retnetion = high renin, aldosterone and angiotensin levels = water retention)
Low renin hypertensives (have higher perfusion of the juxta glomerular cells of the kidneys which leads to decreased renin)

Question 13

What group of people normally suffer from High RAA?

Answer 13

white and under 55

Question 14

HT is a major risk factor for CVD including hypertensive heart disease. What is hypertensive heart disease?

Answer 14

The constant demand of BP on ventricle leads to left ventricular hypertrophy. This means that the LV increases in size = dilates and this can lead to cardiac failure

Question 15

What is the main goal of anti-hypertensive therapy?

Answer 15

Reduce CVD risk and end organ damage