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Cardiology > Vasoactive peptides and inhibitors, Antihypertensive Vasodilator Drugs 1 and 2 > Flashcards

Vasoactive peptides and inhibitors, Antihypertensive Vasodilator Drugs 1 and 2 Flashcards

1
Q

Components of blood pressure

A

CO (SV,HR) * SVR (PVR,RVR)

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2
Q

What is hypertension?

A

high blood pressure mostly due to sympathetic activity leading to elevated vascular resistance

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3
Q

Site of action: carbonic anhydrase inhibitors

A

proximal convoluted tubule

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4
Q

Site of action: thiazides

A

distal convoluted tubule

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5
Q

MOA: diuretics

A

na loss –> fluid loss –> reduce blood volume –> reduce CO –> reduce bp

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6
Q

How does the body compensate for long-term use of diuretics?

A

reduce plasma volume –> increase renin/aldosterone –> increase K+ loss/Na+ retention –> distal fluid reabsorption

  • net effect = lower ECF volume –> lower BP even in the face of compensation
  • likely secondary MOA by reduce PVR via NO
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7
Q

In which population do we have to be careful when prescribing thiazide diuretics and why?

A

elderly –> long duration of action = dehydration in older people

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8
Q

Who is most responsive to thiazide diuretics?

A

african americans and elderly –> response depends on vigor of adaptation process, response reduced in chronic renal insufficiency

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9
Q

Thiazide risks

A

sulfa allergy, hypokalemia, promotes insulin resistance by increasing plasma glucose, increase Tg/LDL cholesterol

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10
Q

Which tissues are most affected by calcium channel antagonists, why?

A

cardiac and smooth muscle –> rely on influx of extracellular calcium for depolarization

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11
Q

What kind of channels are blocked by most calcium channel antagonists?

A

L-type

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12
Q

2 classes of CCAs?

A

non dhpr, dhpr

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13
Q

When do nondhpr CCAs bind the L channel?

A

when they are open –> if frequency of stimulation is increased, (e.g. rapid arrhythmia), increased blockade

*nondphr is better in myocytes than in VSMC

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14
Q

When do dhpr CCAs bind the L channel?

A

resting state –> better binding in VSMCs

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15
Q

Indication for verapamil

A

superventricular arrhythmia and hypertension, non dhpr

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16
Q

Indication for diltiazem

A

superventricular arrhythmia + some hypertension, non dphr

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17
Q

Indication for nifedipine

A

hypertension, dphr

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18
Q

Danger of using DHPR

A

increase in HR, SVR, and RAAS as a reflex to peripheral vasodilation –> increased work of heart in those being treated for …their heart

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19
Q

4 stimulators of renin

A
  1. hypovolemia
  2. hyponatremia
  3. hypotension
  4. adrenergic activation
20
Q

Rate limiting step in RAAS

A

renin conversion of angiotensinogen to angiotensin 1

21
Q

What is the negative feedback for the action of renin?

A

systemic levels of angiotensin ii and amount of angiotensin ii bound to its receptors

22
Q

The vasoconstrictive properties of Angiotensin II is mediated by what receptor?

A

AT1

23
Q

Where are AT1 and AT2 receptors found?

A

AT1: vsm, kidney, adrenal, cortex, pituitary
AT2: uterus, fetus but can be INDUCED

24
Q

Effect of binding of angiotensin ii to AT1

A

vasoconstriction –> aldosterone release, cell proliferation, hypertrophy, matrix deposition

25
Q

Effect of binding of angiotensin ii to AT2

A

vasodilation –> bradykinin, NO, cGMP, antiproliferation, apoptosis

26
Q

Response to angiotensin ii in brain

A
  1. increase in sympathetic discharge
  2. release of ADH/ACTH (endocrine response)
  3. thirst and sodium appetite
27
Q

Response to angiotensin ii in adrenal medulla

A

release of catecholamines

28
Q

Response to angiotensin ii in peripheral vasculature

A

increases release/decreases uptake of NE, enhances sensitivity of NE –> vasoconstriction

29
Q

Response to angiotensin ii in adrenal cortex

A

stimulates synthesis and release of aldosterone from ZG –> augmented by hyponatremia and hyperkalemia

30
Q

Response to angiotensin ii in kidney

A

antidiuresis/antinatriuresis, reduced gfr, inhibit renin

31
Q

CVD effects of angiotensin ii

A
  1. hypertension
  2. cell proliferation/apoptosis, hypertrophy
  3. proinflammatory: impairs endothelial function (e.g. leads to oxidation of LDLR to oxLDLR), induces oxidation
32
Q

As angiotensin ii levels rise, ____ is activated leading to the proliferation of inflammatory cytokines like ___, ____, and ___.

A

nfkb –> vcam1, mcp1, il6 (CRP)

33
Q

Limitations of ACE inhibitors

A

non-specificity of enzyme, alternate pathways for production, poor side effect profile

34
Q

What 3 enzymes catalyze the production of AngII directly from angiotensinogen?

A

tpa, cathepsin G, tonin

35
Q

What 3 enzymes catalyze the production of AngII from AngI w/o ACE?

A

CAGE, cathepsin G chymase

36
Q

What is ACE escape?

A

after inhibiting ACE, angiotensin II levels can recover and exceed beginning b/c of secondary pathways like cathepsin G, chymase, etc.

37
Q

Despite ACE escape, ACE inhibitors reduce blood pressure. Why?

A

ACE is non specific –> also breaks down bradykinin thereby preventing vasodilation –> ACE inhibitors block this process and promote vasodilation

38
Q

Most common side effects of ACE-I

A

cough, angioedema, renal dysfunction, hypotension

38
Q

What do ARBs do to the negative feedback loop to renin?

A

receptor binding is 1 of 2 factors (the other being serum angII) that reduce renin production –> ARBs prevent this so reduce negative feedback (more renin)–> more ang ii to bind to at2 receptors (vasodilatory effect)

39
Q

What do ARBs do to the negative feedback loop to renin?

A

receptor blockade is 1 of 2 factors (the other being serum angII) that reduce renin production

39
Q

What do ARBs do to the negative feedback loop to renin?

A

receptor binding is 1 of 2 factors (the other being serum angII) that reduce renin production –> ARBs prevent this so reduce negative feedback (more renin)–> more ang ii to bind to at2 receptors (vasodilatory effect)

40
Q

What is the impact of DRI on outcomes?

A

no difference between inhibiting renin and using traditional therapies (ACEI, ARB, diuretics)

41
Q

What happens to PRA, Ang I level, Ang II level with: diuretics

A

up up up

42
Q

What happens to PRA, Ang I level, Ang II level with: renin inhibitor

A

down down down

43
Q

What happens to PRA, Ang I level, Ang II level with: ARB

A

up up up

44
Q

What happens to PRA, Ang I level, Ang II level with: renin inhibitor

A

down down down

Cardiology (41 decks)

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