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DT3- EXAM 1 > Vasodilator Drugs- Melissa (3)* > Flashcards

Vasodilator Drugs- Melissa (3)* Flashcards

1
Q

What is the overall mechanism of vasodilators?

A

BP= TPR x CO

  1. Aterial dilation–> LOWER TPR
  2. Venous Dilation–> LOWER Venous Return
    - -> LOWER CO
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2
Q

Amlodipine:

Drug class?

A

Ca++ Channel blocker: Dihydropyridines*

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3
Q

Verapamil, Diltiazem:

Drug Class?

A

Ca++ Channel blocker: Non-dihydropyridines

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4
Q

Describe the direct effects (MOA) of Ca++ Inhibitors on vasculature (1) and the heart (3):

A

Vasculature:
1. INHIB L-Type Ca++ Channels–> vasodilation (more arteries)–> LOWER TPR (DHPs > non-DHPs)

Heart:

  1. INHIB L-Type Ca++ Channels (Verapamil>Diltiazem»>DHPs)
  2. INHIB Phase 2 (plateau) of AP in atrial/vent muscle (slow cntrxn)
  3. INHIB Phase 0 Depolarization (slow HR/AV block)
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5
Q

3 therapeutic uses for ca++ channel blockers:

A
  1. Angina
    (coronary dilation, vasodilation–> ^O2 supply + lower O2 demand)
  2. Supraventricular tachy (A-fib, PSVT)–>Verapamil
  3. HTN
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6
Q
  • 2 contraindications for all ca++ channel blockers:

- 3 Contraindications for Verapamil/Diltiazem:

A

ALL:

  1. Hypotension
  2. Severe Hepatic Disease

Verapamil / Diltiazem:

  1. CHF
  2. AV block/ LV dysfunction
  3. Sick Sinus Syndrome
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7
Q

Verapamil Cardio Effects:

  1. vasodilation
  2. HR
  3. Cardiac contractility
  4. AV nodal conduction
\+ = Increase
- = DECREASE
0 = NONE
A
  1. ++
  2. -
  3. -
  4. –
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8
Q

Diltiazem Cardio Effects:

  1. vasodilation
  2. HR
  3. Cardiac contractility
  4. AV nodal conduction
A
  1. ++
  2. 0/ -
  3. 0/ -
  4. -
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9
Q

Amlodipine (DHPs) Cardio Effects:

  1. vasodilation
  2. HR
  3. Cardiac contractility
  4. AV nodal conduction
A
  1. +++
  2. 0/ +
  3. 0/ +
  4. 0
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10
Q

Rank severity of HypoTN caused by ca++ blockers:

Verapamil/ Diltiazam/ Amlodipine

A

Verapamil: ++
Diltiazam: +
Amlodipine (DHPs): +++ (responsible for decreasing TPR!)

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11
Q

Rank severity of CHF caused by ca++ blockers:

Verapamil/ Diltiazam/ Amlodipine

A

Verapamil: ++
Diltiazam: +
Amlodipine (DHPs): 0/+

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12
Q

Rank severity of AV block caused by ca++ blockers:

Verapamil/ Diltiazam/ Amlodipine

A

Verapamil: ++
Diltiazam: +
Amlodipine (DHPs): 0

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13
Q

Why do DHPs have more balanced vascular and cardiac effects?

A

Trigger baroreceptor reflex

Meaning—-increased HR/ fluid retention (edema possible)

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14
Q

Which two ca++ channel blockers DECREASE HR/ contractility / O2 demand?

A

Verapamil + Diltiazem

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15
Q

4 drug-drug interactions with ca++ channel blockers:

A
  • CYP3A4 inhibitors/ inducers
  • B blockers (V, D)
  • Digoxin (V) -Antiarrythmics
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16
Q

Minoxidil:
Drug class
Effects (2)

A

K+ Channel ACTIVATOR–> hyperpolarization of vascular SM

  1. Potent arterial dilator–> LOWER TRP
  2. ^ compensatory: HR, CO, fluid retention
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17
Q

Minoxidil: 3 clinical applications

A
  1. Refractory HTN (combo tx)
  2. Malignant HTN
  3. ROGAINE for baldness!

(probably causes too much fluid retention to use for acute CHF)

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18
Q

4 ADRs of Minoxidil + drugs to coadmin in order to avoid them:

A
  1. ^ Fluid Retention (COADMIN diuretic)
  2. Tachy*** (COADMIN B-blocker)
  3. Cardiac tamponade (due to fluid retention)
  4. Hypertrichosis (bad unless you’re bald)
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19
Q

MOA Guanylyl Cyclase Activators:

A

^ Gualylyl Cyclase–> ^ cGAMP–> ^ Vasodilation

20
Q

Sodium Nitroprusside:
Drug Class
Effects (1)
ROA

A

Guanylyl Cyclase Activators:

Arteriodilation = venodilation

  1. DECREASE TPR, BP, CO
  2. ^ HR

*IV infusion only, very short t1/2

21
Q

3 Therapeutic uses for Sodium Nitroprusside:

A

HTN Crises, Acute CHF, MI

22
Q

Adverse rxns to Sodium Nitorprusside:

Acute (1), Chronic (1)

A

Acute: Severe HypoTN
Chronic: Thiocyanate/ CN toxicity

23
Q

Sx. Thiocyanate toxicity:

A
  1. N / weakness

2. Disorientation / Delirium

24
Q

Sx. CN- toxicity:

A
  1. CN-cytochrome oxidase–> cytotoxic anoxia
  2. Hypoxia/Resp. Arrest
  3. Convulsions
25
Q

Describe the mechanism by which Nitroprusside becomes toxic CN / thiocyanate:

Where does this mechanism occur?
By what enzyme is it catalyzed

A

Nitroprusside + SN–> CN

CN + Thiosulfate–> Thiocyanate
Rhodenase in the liver

26
Q

Organic nitrates:

Drug class + 2 Drugs in this group

A

Guanylyl Cyclase Activators:

  1. Nitrolglyceride
  2. Isosorbide Dinitrate (ISDN)– long acting, most used
27
Q

Describe the effects of organic nitrates on CV system in low and high doses:

A

Venodilation»Arteriodilation

LOW Dose:
VENOUS DILATION– Practice step question!!!!
Do not be tricked, doesn’t dilate coronary ARTERIES.
1. ^ venous dilation –> DECREASE CO
2. ^ HR, TPR, ~BP (MONDAY DISEASE)

HIGH Dose:

  1. Arterial AND venous dilation –> DECREASE CO, TPR, BP
  2. ^ HR (reflex)
28
Q

How are organic nitrates metabolized?
What are the long acting nitrates metabolized into?
What is their ROA?

A 
Hepatic metabolism (glutathione-organic nitrate reductase)
long acting nitrates denitrated to active metabolites
(ISDN, ISMN)

IV/ subling/ transderm (avoid hepatic portal sx)

29
Q

3 Therapeutic applications for organic nitrates:

A
  1. Angina
  2. CHF
  3. acute MI
30
Q

2 ADRs of organic nitrates:

A
  1. Excessive HypoTN/ Angina

2. Tolerance (do patch on/ patch off long term)

31
Q 
Nitric Oxide: 
Drug Class
ROA? 
t1/2? 
Excretion?
A

Gualylyl Cyclase Activator

Inhalation; t1/2= seconds; renal excretion

32
Q

Therapeutic indication for NO?

What are 2 ADRS?

A

Hypoxic Resp Failure w/ pulm HTN in near term neonates

ADRS:

  1. pulm edema (from NO2 formation)
  2. hypoxemia (from sudden w/drawal)
33
Q

Hydralazine:
Drug class?
Effects?
2 Therapeutic uses?

A

Gualylyl Cyclase Activator
* Potent ARTERIAL (only!) vasodilator
TX: CHF, HTN

34
Q

What is the most important ADR associated with Hydralazine?
Which patients are most susceptible?
Is it reversible?

A

+ANA–> LUPUS LIKE SYNDROME*** (spares the kidneys)
- Generally reversible

Higher risk: Slow acetylators taking than 200mg/ day

35
Q 
Fenoldopam: 
Drug Class? 
ROA? 
Therapeutic Use? 
ADR?
A

FenolDOPAM

  • *D1-R AGONIST (peripheral vasodilation)
  • Admin IV for HTN Emergency

*Can cause hypersensitivity rxn (via sodium metabisulfate)

36
Q

Sildenafil, Tadalafil, Vardenafil:
Drug Class + MOA?
Therapeutic use (2)?

A

INHIB PDE Type 5–> ^NO-induced cGAMP (stop breakdown) –> sm muscle relaxation

  1. Erectile dysfunction
  2. BPH (induces micturition)

“SildenaFIL, TadalaFIL, VardenaFIL keep the penis FILLED”

37
Q

3 DD interactions with PDE inhibitors?

A
  1. Organic nitrates
  2. A- blockers
  3. CYP3A4 interactions
38
Q

Lisinopril, Enalapril, Captopril:
Drug Class?
MOA + 6 Effects?

A 
ACE Inhibitor! 
ACEi--> DECREASE ANG II--> DECREASE: 
1.  Aldo 
2. ANG II vasocnstrxn 
3. ANG II adrenergic vasocnstrxn
4. ANG II cardiac remodeling (via decrease NE/catechol.)
5. Bradykinin metabolism
6. ^ PGs

NOTE: Look for ending in pril = ACEi

39
Q

Therapeutic indications for ACEi (4) ?

A
  1. HTN
  2. CHF
  3. Post-MI
  4. Prevent Diabetic Nephropathy
40
Q

4 important ADRs associated with ACEi?

A
  1. Fetopathic nephrotoxicity- in DIT warm up ?s
  2. Hypersensitivity: rash/ pruritus / angioedema
  3. COUGH! (^ Bradykinin + ^ PGs)
  4. Renal vascular stenosis (renal excretion)
41
Q

2 contraindications for ACEi?

A
  1. preggos
  2. K+ supplements
    BECAUSE: ACEi decreases Aldo, therefore increases K+
42
Q 
Losartan, Valsartan: 
Drug class? 
MOA (2)+ Effects? 
Therapeutic use? 
ADRs? 
Contras?
A

ANG-R Blockers
MOA:
1. Block ANG II-R
2. Competative inhib ANG I-R

Effects, therapeutic use, ADRs, Contras are SAME AS ACEi w/ less cough

43
Q 
Aliskiren: 
Drug Class? 
Effects?
Therapeutic uses?
Contras?
A

Renin Inhibitor–> DECREASE AG I
Effects, ADR, Contras same as ACEi w/ less cough
Tx: HTN

“AlisKIREN = KIlls RENin”

44
Q

Which drugs do we admin to prevent diabetic nephropathy?

A

ACEi’s

45
Q

Which vasodilators are influenced by CYP3A4 inhib/inducers?

A
  1. Ca++ channel blockers

2. PDE-5 inhibitors

46
Q

Which vasodilator is used to treat baldness?

A

Minoxidil

47
Q

To which vasodilator do patients develop tolerance with long term use?

A

Organic nitrates (patch on patch off)

This concept will be presented on boards as “Monday’s Disease”–patient works in explosives factory/somewhere where they are exposed to NG, develops tolerance to vasodilation effects during work week and becomes DESENSITIZED over the weekend. This results in patient feeling the rebound effects–tacky, dizzy, HA, maybe heart palpitations every Monday when he/she returns to work. Don’t miss this!

DT3- EXAM 1 (26 decks)

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