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What are the factors that influence blood pressure (BP) and how do they relate to this measurement?
Blood Pressure (BP) =
Stroke Volume (SV) x Heart Rate (HR) x Peripheral Vascular Resistance (PVR)
How is cardiac output (CO) calculated?
Cardiac Output (CO) =
Stroke Volume (SV) x Heart Rate (HR)
What are the major regulatory biological systems that control blood pressure?
Cardiovascular

Renal

Nervous
How does the cardiovascular system control blood pressure?
Direct control of blood pressure by integrating signals from the sympathetic nervous system and renal system
By what mechanisms does the renal system regulate blood pressure
Na+, H20 management influences:
- Venous return (preload):
- Affects stroke volume
- Renin-angiotensin system:
- Affects peripheral vascular resistance
By what mechanisms does the nervous system regulate blood pressure?
Controls heart rate and vascular tone
- Affects cardiac output

Controls renin-angiotensin system
What component of blood pressure do diuretics mediate and how?
Stroke volume: decrease
- Reduce preload
What component of blood pressure do ace inhibitors and angiotensin receptor-blockers mediate and how?
Control BP via renal system, vasculature, and central nervous system
What components of blood pressure do β-blockers affect?
Heart rate

Cardiac output

Some renal
What components of blood pressure do calcium channel blockers affect?
Peripheral vascular resistance

Heart rate
What are the stages of blood pressure that are above normal and what are their systolic and diastolic parameters?
Normal:
- Systolic: < 120 mm Hg
AND
- Diastolic: < 80 mm Hg

Pre-hypertension:
- Systolic: 120-139 mm Hg
OR
- Diastolic: 80-89 mm Hg

Stage 1 hypertension:
- Systolic: 140-159 mm Hg
OR
- Diastolic: 90-99 mm Hg

Stage 2 hypertension:
- Systolic: ≥ 160 mm Hg
OR
- Diastolic: ≥ 100 mm Hg
What is the required measurement methodology in order to diagnose the various stages of hypertension?
Average of at least 2 seated readings during each of at least 2 visits
What are the concrete numerical goals of anti-hypertensive treatment in terms of blood pressure?
Rx: < 140/90 mm Hg

Diabetes or renal disease:
- < 130/80 mm Hg
What are the most common consequences of untreated hypertension?
Ischemic heart disease

Stroke
How many hypertensive patients are not at their goal blood pressure?
66%
Why do the classes of diuretics differ in their mechanisms of action?
Act on different classes of sodium channels
- Different locations in nephron
How do diuretics gain access to the tubule lumen in the nephron? (Mechanism)
1. Enter cell via organic ion transporters:
- Organic anion transporters:
Why are thiazide diuretics less effective when given in chronic renal failure?
More organic ions competing for transport
What is the first line of drug therapy for the hypertensive, uncomplicated patient?
Thiazide diuretics
Which loop diuretics have low bioavailability?
Furosemide
What vascular condition are loop diuretics used to alleviate?
Edema
Why are loop diuretics so effective at treating hypertension?
Work in thick ascending limb
- Site of most Na+ reabsorption
- Big effect
What type of diuretic is transported via organic cation transporters rather than organic anion transporters?
Potassium-sparing diuretics
Why does eplerenone have less side effects than spirolactone?
Eplerenone has a higher specificity for the aldosterone receptor
- Less likely to cross-react with steroid and androgen receptors
What is the receptor that mediates most actions of angiotensin II?
AT1
What is responsible for the angiotensin II escape after the first few weeks of treatment with an ACE inhibitor?
Normalized angiotensin II levels because of increased renin
- Loss of negative feedback of angiotensin II on AT1 receptors of juxtaglomerular cells
What does an increase in the dose of an ACE inhibitor do to the effect of the drug?
Prolongs duration

Does not increase activity
How do ACE inhibitors cause angioedema?
Increased bradykinin
Why would functional renal insufficiency result from treatment with ACE inhibitors and what are these renal deficits?
Increased dilation of efferent arteriole in glomerulus

Renal deficits:
- Decreased GFR
- Increased CR
What determines the kinetics and dynamics of angiotensin receptor blockers?
Side chain on biphenyl-tetrazole molecule
What is the mechanism behind why calcium channel blockers relax arteriolar smooth muscle?
Overall, less Ca2+ in the cell
- No activation of myosin light chain
What does normal β-adrenergic signalling lead to in muscle?
Increased Ca2+ in cell
- Increased contractility
What are good clinical outcomes when using α1-adrenergic blockers?
Good metabolic profile:
- Increased HDL
- Decreased triglycerides
- Decreased LDL

Improves insulin sensitivity
What are bad clinical outcomes when using α1-adrenergic blockers?
Orthostatic hypotension

Increased risk of heart failure

Increased risk of stroke

Increased of cardiovascular disease endpoints