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Pharm Block 2 > Smooth Muscle, Ren/Ang, Calcium blockers > Flashcards

Smooth Muscle, Ren/Ang, Calcium blockers Flashcards

1
Q

Smooth muscle dilators; which are direct vasodilators?

A

Hydralazine

Minoxidil

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2
Q

Smooth muscle dilators; which are membrane channel dilators?

A

Diazoxide

Calcium channel blockers

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3
Q

Smooth muscle dilators; which are organic nitrates?

A

Nitroglycerin

Nitroprusside

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4
Q

Which smooth muscle dilators act on venous/both/arterial?

A 
Nitroglycerin - VENOUS
Nitroprusside - ARTERIAL + VENOUS
Hydralazine - ARTERIAL
Minoxidil - ARTERIAL
Calcium Channel Blockers - ARTERIAL
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5
Q

Explain how Minoxidil works and what it is used for. Special considerations?

A
  • Opens K+-ATP channels, causing hyperpolarization favoring relaxation
  • Used to treat SEVERE HYPERTENSION
  • Causes fluid retention so use with a DIURETIC
  • Also used as Rogaine
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6
Q

Therapeutic uses for Hydralazine? How is it administered?

A
  • Used to treat SEVERE and EMERGENCY hypertension

- Pill w/ isosorbide dinitrate

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7
Q

Therapeutic use for Diazoxide? Mechanism?

A
  • Used to treat HYPERTENSIVE EMERGENCIES
  • Used to counter HYPOGLYCEMIA
  • K+ channel opener
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8
Q

Nitroglycerin is used to treat _____ and can cause ____ as a side effect

A

Heart failure, Hypotension

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9
Q

Nitroprusside is used to treat _____ and can cause ____ as a side effect

A

Hypertensive emergencies, Hypotension

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10
Q

Which drugs are used for hypertensive emergencies?

A

Nitroprusside
Diazoxide
Hydralazine

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11
Q

Difference between PDE3 and PDE5? What happens if you have an inhibitor of PDE3?

A

Theres more PDE3 in cardiac cells and it breaks down cAMP
Theres more PDE5 in smooth muscle cells and it breaks down cGMP
* think cardiac valves like TRIcuspid so it’s PD3
**inhibit PDE3? more cAMP -> relaxation of blood vessels, increase contraction of the heart

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12
Q

What are PDE3 inhibitors? What are they used for?

A

Milrinone
Inamrinone
Cilostazol
Treatment for heart failure

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13
Q

What are PDE5 inhibitors? What are they used for?

A

Sildenafil
Tadalafil
Treatment for erectile dysfunction

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14
Q

What is captopril?

A

An ACE inhibitor

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15
Q

What does Losartan do?

A

AT1 receptor antagonists

receptor for Ang2

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16
Q

What are the miscellaneous vasodilators?

A

Bradykinin
Fenoldopam
Prazosin

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17
Q

Bradykinin acts on __ receptors on ______ cells to release ______ which all lead to VASODILATION/VASOCONSTRICTION

A

B2
Endothelial cells
Activates PLA2 (releases AA, prostacyclin made), EDHF, NO
VASODILATION

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18
Q

All of the miscellaneous vasodilators act on both arterial and venous vessels. True or false?

A

TRUE

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19
Q

Fenoldopam acts on __ receptors in the _____ (organ) to increase ______. It is used to treat _____.

A

Dopamine 1 receptors
Kidney
Renal blood flow, Na excretion
Hypertensive crisis

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20
Q

Prazosin acts as a _______ by blocking the effects of ______

A

alpha-adrenergic blocker

Norepinephrine (since NE causes vasoconstriction)

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21
Q

What are the beta adrenergic agonist bronchodilators? What is their mechanism? Side effects?

A 
"FAST"
Formoterol
Albuterol
Salmeterol
Terbutaline
Acts via cAMP/PKA
Cardiotoxicity, tachycardia
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22
Q

What are the anticholinergic/muscarinic bronchodilators? What other effect do they have?

A

Ipratropium
Tiotroprium
Inhibits mucus secretions

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23
Q

What are the methylxanthine bronchodilators? Mechanism?

A

Theophylline
Aminophylline
Antagonist for adenosine receptors to block adenosine
Can also block PDE

24
Q

What are the widespread uses of CCB?

A

“HAT”
Hypertension
Angina Pectoris
Treatment of supraventricular arrythmias (including atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia)

25
Q

What kind of receptors do CCB bind? Where specifically (molecular)?

A

L-type Ca2+ Channels
Each receptor is a monomer with 4 transmembrane domains; each domain has 6 transmembrane spanning regions. CCB bind between the 5th and 6th region NEAR THE PORE.

26
Q

Can you prescribe more than one type of CCB? Why or why not?

A

No; there is a COMPLEX ALLOSTERIC RELATIONSHIP among the three CCB receptor sites and influences the gating mechanism of L-type channels. You don’t want to prescribe more than one class to avoid unpredictable effects.

27
Q

Mechanism of CCB?

A
  1. Keep channels in the non-conducting state for a longer period of time
  2. Relaxes arterial supply in the peripheral vascular smooth muscle; less effect on veins
  3. Reduce afterload (NOT preload because less effect on veins)
28
Q

Would CCBs work on neurons?

A

NO - CCB block L-type Ca2+ channels

There are N-type and P-type Ca2+ channels mediate neurotransmitter release in neurons

29
Q

Do CCBs work on skeletal muscle?

A

Not really;
They have a different isoform of L-type channels and doesn’t affect it’s ability to release their intracellular SR store of calcium to allow for contraction.

Skeletal L-type channels don’t allow for Ca2+ entry through membrane!

Instead, they sense voltage changes and tells L-type channels to change conformation and release Ca2+ (like an ON and OFF switch)

30
Q

Do all cardiac cells express L-type Ca2+ channels? How do artial/ventricle cells compare to SA/AV cells?

A

YES
Atrial/ventricular cells = fast response/contractile cells - use L-type channels for CONTRACTION
SA/AV cells = slow response cells - use L-type channels for upstroke of action potential

31
Q

Is smooth muscle dependent on calcium influx for contraction?

A

Yes!
They rely solely on L-types for excitability and contraction. They don’t generate action potentials but show GRADED membrane potential changes

32
Q

What does “use-dependent” and “voltage-dependent” refer to?

A

Refers to the type of binding
Use-depedent binding targets cardiac cells; CCB need to bind deeper into the pore when the channel is open more frequently. SA/AV nodes fire rapidly giving more access to the drugs inner binding sites
Voltage-dependent binding targets smooth muscle cells; CCB bind channels on the OUTSIDE found in a more depolarized state (-65 vs -80 in cardiac)

33
Q

Dihydropyridines are contraindicated in pts with _____ because it can cause _____

A

Tachycardia

Reflex increase in HR, increase in myocardial contraction, increase O2 demand

34
Q

Non-dihydropyridines are contraindicated in pts with _____ because ______

A

CHF

A CCB would just slow SA/AV firing and exacerbate the CHF, and reduced inotropsim

35
Q

Which CCB has the longest half life? Shortest?

A

Longest: Amlodipine (30-50 hours)
Shortest: Nifedipine (1.9-5.8 hours)

36
Q

Which CCB has the highest F? Lowest F?

A

Highest: Amlodipine
Lowest: Verapamil

37
Q

All CCBs are protein bound. True or false?

A

True; amlodipine is the most protein bound at 97-99%

*dihydropyridines are protein bound MORE than the phenylalkylamines and benzothiazemines

38
Q

What are the major side effects of dihydropyridines like amlodipine and nifedipine?

A

Headache, hypotension and peripheral edema

*due to potent vasodilatory effects

39
Q

Which CCB causes constipation as a side effect?

A

Verapamil; due to high affinity of this CCB to L-type calcium channels in the GI smooth muscle

40
Q

Worsening of CHF and AV block are adverse effects of what CCB?

A

Verapamil since it is cardioselective

Use caution with beta blockers

41
Q

Which CCB is the most well tolerated?

A

Diltiazem because it has similar but less potent cardiac effects. Also less dramatic peripheral vasodilation than nifedipine.

42
Q

Sinus bradycardia is contraindicated with dihydropyridines. True or false?

A

False; dihydropyridines are not cardioselective

43
Q

Hypotention is contraindicated in with all CCBs. True or false?

A

True, most with dihydropyridines because its a more potent peripheral vasodilator.

44
Q

A patient has AV conduction defects. Which class of CCB do you use and why?

A

Use dihydropyridines since verapamil and diltiazem are cardioselective and are contraindicated.

45
Q

What are all the ren/ang system drugs we have learned and what is their role?

A

Metoprolol - beta adrenergic receptor blocker
Propranolol - beta adrenergic receptor blocker
Aliskiren - inhibits renin
Captopril - ACE inhibitor
Enanopril - ACE inhibitor
Lisinopril- ACE inhibitor
Losartan - AT1 receptor blocker

46
Q

What is the half life of Ang2?

A

4 minutes

47
Q

What are the ways in which renin release in controlled?

A
  1. ) Intrarenal baroreceptors in the afferent arteriole - sense changes in wall tension (lower wall tension -> more renin release)
  2. ) Macula densa cells detect sodium load in distal tubule (less sodium -> more renin release)
  3. ) Sympathetics mediated by beta1 adrenergic receptors (more sympathetic activation -> more renin release)
  4. ) Inhibit Ang2 negative feedback system (add AT1 receptor blocker or ACE inhibitor -> more renin release)
48
Q

Mechanism difference between AT1 and AT2 receptors?

A

AT1 receptor is through Galpha-q -> PLC -> IP3 and DAG

AT2 receptor mechanism is unknown

49
Q

What are the AT1 receptor mediated effects caused by Ang2?

A 
"VVACI"
Vasoconstriction to increase BP
Vascular proliferation
Aldosterone secretion
Cardiac myocyte proliferation
Increased sympathetic tone
50
Q

What are the AT2 receptor mediated effects caused by Ang2?

A

“VAA”
Vasodilation
Antiproliferation
Apoptosis

51
Q

What drugs block aldosterone action?

A

Spironolactone

Eplerenone

52
Q

What CNS effect does Ang2 have?

A

Promotes thirst, ADH release, positive water balance

53
Q

What effect does Ang2 have on norepinephrine and epinephrine?

A

It promotes NE release and inhibits NE reuptake

It promotes E release

54
Q

What effects does aldosterone have?

A

Expression of Na and K epithelial transport genes (Na reabsorption and K secretion)
*Acts on principal and intercalated cells of collecting duct
Heart fibrosis and hypertrophy

55
Q

All the ren/ang system drugs are orally active. True or false

A

TRUE

56
Q

Ren/ang system inhibitors are contraindicated in _____ patients

A

Pregnany - can cause fetal wasting

57
Q

Can ACE inhibitors act as vasodilators? Why or why not?

A

Yes; they inhibit production of Ang2, which acts on AT1 receptors on smooth muscle to vasoconstrict. If you inhibit it, you promote vasodilation.

ACE also breaks down bradykinin so if you inhibit ACE, you increase bradykinin -> vasodilation

Pharm Block 2 (7 decks)

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