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Drugs for HTN > HTN background info > Flashcards

HTN background info Flashcards

1
Q

CO x PR = ?

A
  • Arterial Pressure - CO determined by: HR, contractility, blood volume, venous return - Peripheral resistance determined by arteriolar constriction (remodeling)
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2
Q

Why is the Poiseuille formula important when considering blood pressure?

A
  • A decrease in the radius of the blood vessel can lead to a significant increase to resistance of the vessel (by a factor of 4) - Remodeling –> decreased radius - Also, w/ remodeling, we also get proliferation of parallel vessels (vs vessels in series) and see another significant increase in resistance * 1/total R = 1/R1 + 1/R2 + 1/R3…
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3
Q

What is the prevalence w/ HTN?

A
  • ↑ w/ agem but lower in women before menopause (estrogen is protective) - > for AA - ~1/3 are asymptomatic and unaware that they have HTN
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4
Q

Predominant HTN form in elderly?

A

Isolated systolic HTN; often untrx * ~1/2 are receiving trx and only ~1/2 of those are being treated adequately

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5
Q

Modifiable RFs in pts w/ HTN?

A

smoking, 2nd hand smoke, DM, dyslipidemia/hypercholesterolemia, overwt/obese, physical inactivity/low fitness, unhealthy diet

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6
Q

Relatively fixed RFs for HTN?

A

CKD, FHx, ↑ age, low socioeconomic/educational status, M > F, obstructive sleep apnea, psychosocial stress

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7
Q

Normal BP in adults?

A

SBP < 120 mmHG & DBP < 80 mmHG

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8
Q

Elevated BP in adults?

A

120-129 mmHg/ <80 mmHg

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9
Q

Define Stage I HTN

A

SBP: 130-139 mmHg or DBP 80-89 mmHg

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10
Q

Define Stage 2 HTN

A

SBP > or = 140 or DBP > or + 90

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11
Q

What is the ultimate regulator of BP and why?

A

Renal blood volume pressure control bc of its “infinite gain” - Noting that blood volume changes lead to changes in renal secretions/excretions

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12
Q

BP set point changes

A

In HTN, the BP set-point is reset to a higher level, but can be either salt-resistant or salt sensitive - All pts are told to limit sodium intake bc increases sodium-retaining hormones that we can block

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13
Q

What is Primary HTN?

A
  • Most common form (~92%)
  • Can be subdivided:
  • Low renin (~25% more common in AA & elderly)
  • Normal renin (~60%)
  • High renin
  • no identifiable cause
  • chronic progressive d/o
  • drugs ↓ BP but do not trx underlying cause
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14
Q

What is secondary HTN?

A
  • HTN w/ identified primary cause
  • some people can be cured by treating the underlying cause
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15
Q

Conditions suggestive of secondary HTN?

A
  • Renal Parenchymal Dz (UTI, obstruction, PCKD)
  • REnovascular dz
  • Primary aldosteronism
  • Obstructive sleep apnea
  • Drug or alcohol induced
  • Pheochromocytoma
  • Cushing’s syndrome, hypothyroidism, hyperthyroidism, aortic coarctation, etc.
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16
Q

Frequently used meds that ↑ BP

A

EtOH, immunosuppressants, amphetamines, OCs, antidepressants, NSAIDs, atypical antipsychotics, recreational drugs, caffeine, systemic corticosteroids, decongestants, angiogenesis inhibitors, herbal supplements, tyrosine kinase inhibitors

17
Q

Srug targets for lowering BP

A
18
Q

What is the sympathetic baroreceptor reflex?

A
  • A reflex circuit that keeps arterial pressure at preset level on a second by second basis
  • Stretch receptors located in carotid sinus and aortic arch
  • Opposes attempts to reduce arterial pressure with drugs
  • Sympathetic nerves innervate the heart and travel along the BVs, forming multiple synapses such that the nerves resemble a sting of beads
19
Q

What are the Baroreceptor effector mechanisms?

A
  • alpha-1 adrenergic receptors located on the BVs to cause vasoconstriction; helps maintain venous return w/ postural changes
  • alpah-2 adrenergic receptors act in brain and in periphery in a presynaptic feedback inhibitory manner to ↓ sympathetic tone
  • beta-1 adrenergic receptors ↑ HR and contractility, and stimulate renin secretion by the kidneys
  • Beta-2 receptors dilate sk m vasculature
20
Q

Response of BP, PR, CO, & HR w/ different receptor stimulation

A
21
Q

What is phentolamine?

A
  • alpha-receptor antagonist
  • Short 1/2 life of ~ 19 minutes, w/ 97% gone in ~95 min
  • Adverse effx: acute prolonged hypotensive episodes, orthostatic hypotension, tachycardia, and cardiac arrhythmias; weakness dizziness, flushing, nasal stuffiness, NVD
22
Q

What is Phenoxybenzamine?

A
  • alpah-R antagonist; non-competitive
  • Adverse effx similar to phentolamine, plus miosis and occasional severe allergic rxns (angioedema)
23
Q

What happens if a daily a2-agonist or beta-blocker is stopped abruptly?

A

REBOUND HTN

  • unmasked beta-Rs –> excessive cardiac stimulation in response to nml CNS tone –> tachy, HTN, angina pectoris, MI, arrhythmias
  • Stopping alpha2-agonists releases CNS brake on SNS tone –> excessive SNS tone
24
Q

Why the decreased use in beta-blockers?

A
  • Beta-blocker use does not prevent MI, HF, or death as well as other therapies
  • is assoc w/ significantly higher incidence of stroke
25
Q

Describe the RAS

A
  • Angiotensin I cleaved from Angiotensinogen by renin is cleaved by ACE –> angiotensin II
  • Acitve Ang II can ↑ aldosteron secretion –> ↑ Na-K echange in the nephron–> retention of sodium and water (K loss) –> ↑ Blood vol –> ↑ BP
  • Active Ang II can cause direct systemic vasonconstriction (arterioles and veins) –> ↑BP
  • Ang II –> renal vasoconstriction –> ↓ renal BF –> ↓ GFR –> rentention of H2O and Na+ –> ↑ BV –> ↑ BP
26
Q

What are the effx of Angiotensin II?

A
  • vasoconstriction –> ↑ TPR
  • ↑ EC fluid volume by stimulating thirst, stimulating aldosterone secretion (retains Na+), & stimualtes ADH secretion (retain H2O)
  • Contributes to CV remodeling & causes more permanent changes in the BVs so less vasoconstriction is required to maintain a small bore
27
Q

What classes of drugs effect angiotenisn II formation of axn?

A
  • Aliskirin: blocks the conversion of angiotensinogen to angiotensin I by renin
  • ARBS: block the AT1 receptor
  • ACEI: blocks ACE, which is needed to convert AT1 –> AT2
28
Q

Why is there in an increase in TPR seen in chronic HTN pts?

A
  • It seems to follow an initial ↑ in CO, suggesting that colume overload was at fault, and TPR ↑ to compensate
  • In some instances, ↑ TPR is the initiating event
29
Q

RAS Inhibition Effects in the Kidney

A
  • GFR falls d/t ACE inhibition –> ↑ serum creatinine in all pts
    • Preserves kidney function in hyperfiltrating diabetics
    • can also harm physicials…<30% ↑ likely ok if no hyperkalemia

Drugs for HTN (7 decks)

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