Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology: Exam 2 > Lecture 3: Direct Acting Vasodilators > Flashcards

Lecture 3: Direct Acting Vasodilators Flashcards

1
Q

What is preload?

A
  • The passive stretching of muscle fibers in the ventricles.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes the stretching in Preload?

A
  • The stretching results from blood volume in the ventricles at the end of diastole
  • The more the heart muscles stretch during diastole, the more forcefully they contract during systole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is contractility

A
  • Refers to the inherent ability of the myocardium to contract normally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What influences contractility?

A

Preload, the greater the stretch the more forceful the contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is afterload?

A

(Resistance) Refers to the pressure that the ventricular muscles must generate to overcome the higher pressure in the aorta to get the blood out of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the narrow range that Arterial blood pressure is regulated?

A

120/80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is arterial BP regulated within a narrow range?

A

to provide adequate perfusion of the tissues without causing damage to the vascular system, particularly the arterial intima

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Arterial BP is directly proportional to _ _ and _ _ _

A

cardiac output and peripheral vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What two overlapping mechanisms control cardiac output and peripheral resistance? ⭐️

A
  1. Baroreflexes (symp nervous system)
  2. Renin-angiotensin-aldosterone system (RAAS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the effect of most antihypertensive drugs?

Antihypertensive: decreasing BP

A

Reducing cardiac output and/or decreasing peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the speed of the BP response mediated by baroreflexes (SNS)?

A

FAST= rapid, moment to moment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the speed of BP response mediated by the renin-angiotensin-aldosterone system (RAAS)?

A

SLOW= Long-term

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the locations and nerves used for baroreceptors?

A
  • Aortic arch receptors via the vagus nerve (CN X)
  • Carotid sinus receptors via carotid sinus nerve to nerve IX (glossopharyngeal)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Fill in the blanks for the factors that affect cardiac output

A
  • Heart rate
  • Contractility
  • Filling pressure (blood volume & venous tone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain the pathway of the baroreflexes (mediated by SNS) response to a decrease in BP (SHORT TERM)

A

Decrease in BP→ ↑ Sympathetic activity via baroreceptors → Activates ⍺1 on the heart (↑ venous return and ↑ resistance) & β1 on smooth muscle (↑ CO, contractility, releases renin)→Increases BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain the pathway of the Renin-angiotension-aldosterone systen (RAAS) response to a decrease in BP (LONG-TERM)

A

Decrease in BP→↓ in renal blood flow→Release renin (&↓ glomerular filtration)→↑ Angiotensin 2→↑ Aldosterone→ ↑ water/Na+ retention→ ↑ blood volume→ ↑CO→Increases BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the two ways in which renin is released?

A
  • Activation of β1 receptors (short-term)
  • Low renal blood flow (long-term)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain the renin-angiotensin-aldosterone system

A

Angiotensinogen w/ release of RENIN→Angiotensin I w/ ACE →Angiotensin II →( increases SNS activity, tubular reabsorption (Na+,Cl-,H2O), aldosterone, vasconstriction and ADH)→ALL leads to increase in BP

ACE= Angiotensin Converting Enzyme
ADH=Antidiuretic hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the negative feedback in the renin-angiotensin-aldosterone sytem

A

Kidney decreases the release of RENIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

From the RAAS pathway, what organ secretes Angiotensinogen?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

From the RAAS pathway, what organ secretes renin?

A

Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

From the RAAS pathway, what organs secretes Angiotensin Converting Enzyme (ACE)?

A

Lungs and kidneys (surface of pulmonary and renal endothelium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

From the RAAS pathway, what organ secretes Aldosterone?

A

Adrenal gland cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

From the RAAS pathway, what organ secretes ADH?

A

Pituitary gland (posterior lobe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Explain the pathway for cardiac myocyte contraction & relaxation

A

Symph. activation→releases NE→binds to β1 receptors→Gs increases cAMP→Increase Pk-a→Increases extracellular Ca2+ release→Intracellular Ca2+ release from SR→Binds to Troponin→Actin binds to Myosin→Contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What type of contractions does vascular smooth muscle undergo?

A

Slow, sustained, tonic contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List the 3 ways contractions in VSM (vascular smooth muscle) are initiated?

A
  1. Mechanical stimuli
  2. Electrical stimuli
  3. Chemical stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Explain the mechanical stimuli that cause contraction in vascular smooth muscle (VSM).

A
  • Passive stretching of VSM can cause contraction.
  • Termed a Myogenic response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Explain the electricial stimuli that causes contractions in the (VSM).

A

Electrical depolarization of the VSM by opening voltage dependent Ca2+ channels, causing an increase in the intracellular concentraction of calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Explain the chemical stimuli that causes contractions in vascular smooth muslce (VSM).

A

A number of chemical stimuli such as norepinephrine, angiotensin II, vasopressin, endothelin-1, and thromboxane A2 can cause contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Explain vascular smooth muscle (VSM) contraction

A

Contraction: An increase in free intracellular Ca2+ (through Ca2+ channels or by release from internal stores (SR))

  • The free Ca2+ binds to calmodulin (CM)
  • Calcium-calmodulin activates myosin light chain kinase (MLCK) an enzyme that phosphorylates myosin light chains (MLC) in the presence of ATP
  • MLC phosphorylation leads to cross-bridge formation b/w the myosin head and actin filaments→VSM contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Explain vascular smooth muscle (VSM) relaxation

A

Relaxation: Reduced phosphorylation of MLC. This can result from:

  1. Reduced relase of Ca2+ by the SR or reduced Ca2+ entry into the cell
  2. Inhibition of MLCK by increased intracellular conc. of cAMP (Gs-R pathway)
  3. MLC dephosphorylation (nitric oxide (NO)→cGMP pathway)

Gs-R: Gs-linked vascular receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What type of drugs target MLC dephosphorylation?

A

Nitrate drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the pharmacodynamics of direct acting vasodilators?

A

Affects venous side with preload (capacitance) and affects resistance with afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

List the different drug classes of direct-acting vasodilators.

A
  • Nitrates
  • Hydralazine
  • Phosphodiesterase V inhibitors
  • Calcium Channel Blockers (non-dihydropyridine)
  • Calcium Channel Blockers (dihydropyridine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What drugs are Nitrates (nitric oxide donors)? (3)

A
  • Isosorbide dinitrate
  • Nitroglycerine
  • Nitroprusside
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What drugs are Hydralazine? (1)

A

Hydralazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What drugs are Phosphodiesterase V inhibitors? (1)

A

Sildenafil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What drugs are non-DHP calcium channel blockers (CCBs)? (2)

A
  • Diltiazem
  • Verapamil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What drugs are DHP calcium channel blockers (CCBs)? (2)

A
  • Amlodipine
  • Nifedipine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the mechanism of action of nitrates (nitric oxide donors)?

Drugs: Isosorbide dinitrate, Nitroglycerine, Nitroprusside

A
  • Release NO when metabolized
  • Relax smooth muscle: Vascular, corpora cavernosa, short-lived in others (e.g. bronchial, GI)
  • Inhibit platelet aggregation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Explain the natural pathway of Nitric Oxide Donors in the smooth muscle cells

A
  • Nitric Oxide (NO) is synthesized in the endothelial cell by eNOS (endothelial nitric oxide sythase) which turns L-arginine into NO
  • NO enters the smooth muscle cell (SMC) and activates guanylyl cyclase which produces cGMP
  • cGMP activates MLCP (myosin light chain phosphatase) which dephosphorylates myosin→Relaxtion
43
Q

Explain the drug pathway of Nitric Oxide Donors (Nitrates)

Drugs: Isosorbide dinitrate, Nitroglycerine, Nitroprusside

A
  • Direct administration of NO into the SMC (skips the synthesis step in the endothelial cell)
  • Increase cGMP (via guanylyl cyclase) activating MLCP
  • MLCP dephosphorylates myosin→relaxation

Targeting MLCP (wouldn’t want drugs that target the same thing, e.g. Vigara)

44
Q
  • What are the organic Nitrites & Nitrates (+ how many NO do they have)?
  • Where are they metabolized?
  • How long is their half-life?
  • What does it target?
A
  • Amyl Nitrate (1 NO)
  • Isosorbide dinitrate (2 NO)
  • Nitroglycerin (3 NO)
  • Metabolized ONLY in the vein (↓preload)
  • Short half-life
  • ONLY IN VEINs
45
Q

What is the inorganic NO donor?
Where is it metabolized?
What does it target?
What is a Side Effect?

A
  • Nitroprusside (1 NO)
  • Metabolized in blood cells
  • Targets BOTH veins and arteries
  • Cyanide toxicity (d/t cyanide in formula)

Cannot use a lot, only in emergency

46
Q

Explain the effects (on the heart) caused by Organic NO donors. (Pharmacodynamics)

Amyl NItrate (1 NO), Isosorbide dinitrate (2 NO), Nitroglycerin (3 NO)

A

Target is the vein

  • Increase capacitance venules to decrease preload
  • ↓ preload→the heart doesn’t have to work as hard
  • Increase oxygen demand, improved collateral flow
  • Increase blood flow to coronary arteries to supply the heart
  • Less blood in the heart to pump, more blood supplying the heart
47
Q

Explain the effects (on the heart) caused by Inorganic NO donors (pharmacodynamics)

Nitroprussside (1 NO)

A

Works on both arteries and veins

  • Increase capactiance of the vein to reduce preload
  • Decrease resistance of the arteries to reduce afterload
48
Q

What are the factors of

  • Oxygen supply?
  • Oxygen demand?
A

Oxygen Supply

  • AV Oxygen Difference (O2 in arteries vs O2 in vein)
  • Regional Myocardial Distribution
  • Coronary Blood Flow (How much blood supplies O2 to the heart)

Oxygen Demand

  • Contractility
  • Heart Rate
  • Preload
  • Afterload
49
Q

What is the ideal difference between oxygen supply and oxygen demand? And how is this equilibrium reached?

A
  • Ideal: O2 supply equal to or greater than O2 demand
  • Occurs by increasing O2 supply and decreasing O2 demand
50
Q

What happens when there is ischemia?

A
  • Heart isn’t getting enough blood which can cause angina (no O2 to the heart so pain)
  • O2 supply < O2 demand (more demand than supply)
  • If left too long will lead to MI
51
Q

What can we give to help ischemia?

A

Give organic NO donor (Isosorbide dinitrate (2 NO), Nitroglycerin (3 NO))

  • Can increase coronary blood flood and give the heart more O2
  • Reduce Preload=Less O2 demand
  • Increase O2 supply, decrease oxygen demand
52
Q

What are the classes of ANGINA? (3)

A
  1. Stable angina-Exertion
  • When you work hard and have heart pain
  1. Unstable angina - Plaque
  • severe atherosclerosis-> coronary is blocked by platelet
  1. Variant angina-Spasm
  • Contracts and blocks blood flow
53
Q

What angina can organic NO donors treat?

Isosorbide dinitrate (2 NO), Nitroglycerin (3 NO)

A

Stable angina

54
Q

What angina(s) can Organic NO donors NOT treat? and why?

Isosorbide dinitrate (2 NO), Nitroglycerin (3 NO)

A
  • Unstable angina
  • Variant angia
  • Reducing preload in these cases does not help
55
Q

What is the clinical use of Isosorbide dinitrate (mononitrate)?

Nitrites ( Organic NO donor)

A
  • STABLE angina
  • Heart failure
56
Q

What are the clinic use(s) of Nitroglycerin?

Nitrates (Organic NO donor)

A
  • Acute decompensated heart failure
  • acute myocardial infarction
  • Stable angina
  • hypertensive emergency
  • hypotension induction
  • perioperative hypertension
  • acute pulmonary hypertension
57
Q

What is important about nitrates (nitroglycerin) and HTN?

A
  • It is only used for emergency: hypertensice emergency, hyptension induction, perioperative hypertension
  • NOT CHRONIC TXT OF HTN
58
Q

What is the clinical use of Nitroprusside?

Nitrite (Inorganic NO donor)

A

Hypertensive emergency

59
Q

What are the short acting NO donors and what are the long acting NO donors?

A
  • Short: nitroglycerin, nitroprusside
  • Long: nitroglycerin and isosorbide dinitrate
60
Q

What is the fate and excretion of nitroprusside

LOW yield

A

Metabolized by intraerythrocytic reaction with hemoglobin, further metabolism in liver, metabolites excreted in urine

61
Q

Explain the Organic nitrate/nitrite tolerance

A
  • Continous 24-hour plasma levels of organic nitrates result in insurmountable tolerance (tachyphylaxis)
  • Nitrate-free period of more than 10 hours is needed to prevent or attenuate tolerance
  • TOLERANCE IS NOT DEVELOPED TO NITROPRUSSIDE
62
Q

Which Nitrate has NO tolerance?

A

Nitroprusside

63
Q

What are the Adverse effects, contraindications, and interactions with Isosorbide dinitrate (mononitrate) and nitroglycerin?

A

Adverse Effect

  • Hypotension
  • Dizziness
  • Headache
  • Flushing
  • Syncope

Contraindications:

  • Tolerance
  • Increased intracranial pressure,
  • Pregnancy

interactions:

  • Sildenafil (e.g. Viagra will kill you)
64
Q

What are the Adverse Effects, and Contraindications of Nitroprusside?

A

Adverse Effects:

  • Hypotension
  • Dizziness
  • Headache
  • Flushing
  • Syncope
  • Cyanide toxicity

Contraindications:

  • Prolonged infusion
  • Pregnancy
65
Q

List the drugs that are phosphodiesterase V inhibitors

A
  • Slidenafil
  • Tadalafil
  • Vardenafil
66
Q

Explain the pharmacodynamics of phosphodiesterase V inhibitors (PDE5 Inhib.)

Sidenafil

A
  • PDGE5 inhibitors inhibit PDE5 which breaks down cGMP
  • cGMP is not broken down (↑ cGMP)
67
Q

What is the route of adminstration, onset of action and absorption, fate, excretion of sildenafil, tadalafil and vardenadil

A
68
Q

What are the clinical use(s) and side effects of Sildenafil?

PDE5 Inhibitor

A
  • Clinical use: Erectile Dysfunction, Pulmonary arterial hypertension
  • Side effects: Severe hypotension and death if combined with nitrates (priapism)
69
Q

The image below shows the mechanism of Sildenafil and other nitrates affect on SMCs. Explain how the major side effects occur

A

sildenafil and nitrates both increase cGMP so this would lead to severe dilation and hypotension so severe is can cause death

70
Q

What is the mechanism of action and pharmacology of Hydralazine?

A
  • MOA is unknown
  • Required NO from the endothelium so if endothelial is not working the drug will not work
  • Targets arteries and decrease resistance to decrease afterload
71
Q

What are the clinical use(s) and side effects/adverse reactions of Hydralazine?

A

Clinical use:

  • Hypertension
  • Hypertensive emergency in pregnancy
  • Heart failure

Side Effects:

  • Dizziness
  • Headache
  • Angina
  • Tachycardia
  • Peripheral edema
  • Lupus-like syndrome
72
Q

What do we NOT use for angina?

A

Hydralazine

73
Q

What is the effects of hydralzine on organic nitrate tolerance?
What is the drug name?

A
  • Can cause tolerance to disappear
  • NOT used for angina BUT can be adminstered w/ mitrate to ↓ tolerance
  • Drug Name: BiDil
74
Q

Explain why Hydralazine is not used for angina.

⭐️

A

Coronary steal phenomenon

  • Will vasodilate healthy vessels and less O2 will go through constricted vessels leading to angina
75
Q

What is the ROA, onset and absorption, fate and excretion of hydralazine

LY

A
76
Q

What are the effects on distinct vascular beds with Nitrates, Nitroprusside and Hydralazine?

A
  • Nitrates=Affect VEINS only (↓ Preload)
  • Nitroprusside=Affect BOTH veins and arteries (↓ Preload and Aferload)
  • Hydralazine= Affects ARTERIES onl (↓Afterload)
77
Q

What is the MOA and pharmacology of Calcium channel blockers (CCBs)?

non-DHP: Diltiazem, Verapamil
DHP: Amlodipine, Nifedipine

A
  • Block calcium channels
  • Decrease calcium influx into the cell- decrease ER/SR calcium loading (can NOT activate MLCK)
  • Effects depend on selectivity
78
Q

What are the cardiac and vascular effects of CCBs?

non-DHP: Diltiazem, Verapamil
DHP: Amlodipine, Nifedipine

A

Cardiac Effects (↓ Afterload)

  • Decrease contractility (negative inotropy)
  • Decrease HR (negative chronotropy)
  • Decrease conduction velocity (negative dromptropy)

Vascular Effects

  • Smooth muscle relaxation (vasodilation)
79
Q

Explain what happens when a CCB is bound to the calcium channels on the SMCs.

A

No extracellular Ca2+=No intracellular Ca2+= NO constriction

80
Q

How do CCBs effect distinct vascular beds?

A

Affects mainly the ARTERIES

81
Q

What is the difference between DHPs and NON-DHP CCBs?

non-DHP: Diltiazem, Verapamil
DHP: Amlodipine, Nifedipine

A
  • DHPs: Just target Vasculature (arteries)
  • NON-DHPs: Target the Heart (HR and contractility) and Vasculature (arteries)
82
Q

What are the relative vascular and cardiac effects of CCBs (NON-DHPs & DHPs)?

A
  • Non-DHP (D.V.): causes Vasodilation and decrease HR/Contractility
  • DHP(-dipine): just affect vasculature

non-DHP: Diltiazem, Verapamil
DHP: Amlodipine, Nifedipine

83
Q

Explain the pharmacokinetics of DHP CCBs (amlodipine and nifediphine) with onset of action and plasma half life

A
  • Amlopine takes longer to work but last longer
  • Nifedipine has a quick onset but doesn’t last long
84
Q

What is the first line of treatment of adults with systolic/diastolic hypertension without other compelling indications?

Target: <130/80 mmHg

A
  1. Thiazide/thiazide-like
  2. ACEI
  3. ARB
  4. CCB
85
Q

What do we do if 20 mmHg above target?

A

duel therapy, triple or quadruple therapy

86
Q

What are CCBs particularly useful for treating? And in what population?

A

Treating hypertension in low renin producers such as African-Americans and elderly patients

87
Q

What has less effect on exercise performance than β-blocker and will not affect electrolytes like diuretics?

A

Dihydropyridine CCBs (DHP CCBs)

  • Amlodipine
  • Nifedipine
88
Q

Long duration of action (CCBs) provides what?

A

superior long term outcomes

89
Q

Explain the ACCOMPLISH Trial

A
  • Patients were given two different drug combinations
  • Combination 1: ACEI/HCTZ (hydrocholorothiazide)=Red line
  • Combination 2: ACEI/CCB (amlodipine)=Blue line
  • Over 42 months, combination 2 decreased risk by 20%, this is due to the long duration of action of the CCB
90
Q

List out all the preferred antihypertensive combinations? (3)

A
  • ACEI or ARB + Thiazide
  • ACEI or ARB + CCB
  • CCB + Thiazide (black population)
91
Q

List out the Acceptable antihypertensice combinations? (4)

A
  • CCB + Thiazide (non-black population)
  • β-blocker + DHP CCB or thiazide
  • Thiazide + K sparing diuretic
  • Aliskiren + Thiazide or CCB
92
Q

List out the NOT Preferred antihypertensice combinations? (4)

A
  • ACEI + ARB (Contraindications)
  • β-blocker + ACEI or ARB (perferred only post-MI of HF)
  • β-blocker + Non-DHP CCB (will decrease HR too much)
  • β-blocker + central acting (i.e. clonidine, etc, changing nerve impulses in the brain)
93
Q

What is the first line of treatment for isolated systolic hypertension?

A

NO ACE if just systolic HTN

  1. Thaizide/thiazide like
  2. ARBs
  3. CCB
94
Q

How does DHPs and Non-DHP work on oxygen supply and oxygen demand factors?

A
  • DHPs: Coronary Blood flow & Afterload
  • Non-DHPs: Contractility, Heart rate, Afterload and Coronary blood flow
95
Q

What CCBs are used for stable angina, unstable angina and variant angina?

A
  • Stable Angina : ALL CCBs + (organic nitrates)
  • Unstable Angina: Non-DHP CCBs ( blocked vessel. Non-DNP dec HR/contaction so will decrease O2 demand)
    Variant Angina: All CCBs
96
Q

What are the Adverse effects, contraindications and interactions with Non-DHP CCBs?

Non-DHP (Diltiazem, Verapamil)

A

Adverse Effects

  • Headache
  • Dizziness
  • Constipation
  • Edema
  • AV block
  • Bradycardia
  • Hypotension

Contraindications

  • Sick sinus syndrome
  • Heart failure
  • 2nd/3rd heart block
  • Hypotension

Interactions

  • Beta-blockers
  • Grapefruit (Inhibits metabolism, can increase concentration)
97
Q

What are the Adverse effects, contraindications and interactions with DHP CCBs?

DHP (Amlodipine, Nifedipine)

A

Adverse Effects

  • Headaches (7.5%)
  • Edema
  • Hypotension
  • Palpitations
  • Nocturia/polyurea

Contraindications

  • Hypotension (Amlodipine & Nifedipine)
  • Heart failure (Nifedipine)

Interactions

  • Beta-blocker withdrawal
    Grapefruit
98
Q

What are the clinical uses of Non-DHP CCBs?

Non-DHP (Diltiazem, Verapamil)

A
  • Effort, variant and unstable angina
  • Hypertension
  • Atrial fibrillation and atrial flutter (injection)
  • Paroxysmal supraventricular tachycardia (PSVT)
99
Q

What are the clinical uses of DHP CCBs?

DHP (Amlodipine, Nifedipine)

A
  • Hypertension
  • Effort and variant angina
  • Subarachnoid hemorrhage (Nimodipine)
100
Q
  1. A patient goes to the ER after experiencing chest pain. He states that he just finished an intense workout prior to the pain. Which of the following medications could be prescribed to the patient to treat his angina?
    a. Nitroprusside
    b. Isosorbide dinitrate
    c. Sildenafil
    d. Hydralazine
A

b. Isosorbide dinitrate

101
Q
  1. Which of the following is a NOT PREFERRED antihypertensive medication?
    a. Metoprolol and Diltiazem
    b. Thiazide and Verapamil
    c. Diltiazem and Aliskiren
    d. Atenolol and Amlodipine
A

a. Metoprolol and Diltiazem

102
Q
  1. Nitroglycerin can be given during a hypertensive crisis due to its drastic effects on blood pressure. What is the mechanism of action to allow this?
    a. Blocks Ca channels
    b. Decreases cGMP.
    c. Produces NO within smooth cells.
    d. Increases cGMP
A

d. Increases cGMP

103
Q
  1. Which of the following drugs does not have an affect with an injured endothelium?
    a. Nitroprusside
    b. Nitroglycerin
    c. Hydralazine
    d. Amlodipine
A

c. Hydralazine

Pharmacology: Exam 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions