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PHARM/MHD - Exam #4 > Pharm - Lec#4 - Nitric Oxide > Flashcards

Pharm - Lec#4 - Nitric Oxide Flashcards

1
Q

Nitric Oxide (INOMAX)

  • MOA
  • route
A

Covalent modification of proteins

  • inhalation
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2
Q

Nitric Oxide (INOMAX)

  • indications
  • side effects
A
  • Pulmonary Hypertension

- Vasodilation

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3
Q

Nitroglycerine

  • MOA
  • route
A

NO donor

  • sublingual
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4
Q

Nitroglycerine

  • indications
  • side effects
A

ACUTE CORONARY SYNDROME

  • hypotension
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5
Q

Hydralazine

  • MOA
  • route
A

NO donor, vasodilator

  • ORAL route
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6
Q

Hydralazine

  • indications
  • side effects
A
  • hypertension

SE:

  • headache
  • nausea
  • vomiting
  • hypotension
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7
Q

Sildenafil (viagra)

  • MOA
  • route
A

MOA: phosphodiesterase inhibitor

Route - oral

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8
Q

Sildenafil (viagra)

  • indications
  • side effects
A

Indications: hypertension

SE:

  • hypotension
  • drug interactions (if given with NITRATE)
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9
Q

L- Arganine

  • MOA
  • Route
A

MOA: NO donor

Route: Oral

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10
Q

L- Arganine

  • Indications (2)
  • Side effects
A

Indications:
ACS
Vascular Disease

SE: hypotension

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11
Q

What causes the generation of NO in the macrophage?

What is it generated from?

A

exposure to bacterial LPS

  • oxidation of the guanidine group of arginine
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12
Q

Acetylcholine & Carbachol causes the endothelium to release _____

A

EDRF (NO)

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13
Q

State the following for Nos1, Nos2, and Nos3:

  1. other name
  2. Tissue expression
  3. Constitutive/inducible
A

NOS1:

  • neuronal NOS (nNOS)
  • NEURONAL epithelium
  • constitutive
NOS2****
- iNOS
-macrophage, smooth muscle cells
- INDUCIBLE
(bad! associated with pathologic conditions)

NOS3:

  • endothelial nos (eNOS)
  • endothelial cells
  • constitutive
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14
Q

What NOS is only activated in pathologic states?

What causes this activation?

A

iNOS

  • induced by LPS
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15
Q

What is L- Arginine converted to generate NOS

What does it require as cofactors

A

L- Arginine to L - CITRULLINE

  1. NADPH
  2. FAD
  3. THF
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16
Q

Some nitric oxide donors such as oxygenated nitroprusside, spontaneously generates NO,

whereas others such as the _____ and organic ____ and _____ such as nitroglycerin require the presence of a THIOL compound such as cysteine.

A

furoxan
nitrates
nitrites

17
Q

What nitric oxide derivative is conveniently measured in SEPSIS?

A

NITRATE
(NO3-)

  • MOST STABLE
  • CONVENIENTLY MEASURED IN PATIENTS WITH SEPSIS!!!!
  • iNOS –> due to lipopolysaccharide of bacteria
18
Q

Why are low levels of GLUTATHIONE related to increased vascular pathology in CV disease and diabetes?

A

low glutathione = HIGH NO

  • increased NO results in greater hypotensive effects and INFLAMMATION
  • contributes to vascular pathology
19
Q

What are the 4 inhibitors of NO?

A
  1. L-arginine Derivatives (L-NMMA, L-NAME)
  2. Inhibitors of nitric oxide synthase synthesis
  3. Inhibitor of binding of arginine to NOs
  4. Scavengers of NO
20
Q

Excess production of NO results in the generation of _____ which is toxic to cells

A

peroxynitrite

21
Q

State the 5 inhibitors of NO

A
  1. L- NMMA
  2. L- NAME
  3. 7 - Nitroindazole
  4. BBS-2
  5. Hemoglobin!!
22
Q

What is a scavenger of NO that inhibits it?

A

HEMOGLOBIN!!!

23
Q

What are the beneficial and pathologic effects of NO?

A

The beneficial effects include smooth muscle relaxation, vasodilation, immune regulation, anesthetic and anti-athlerosclerotic responses.

The pathologic responses include free radical formation, nitrosylation of protein and irritant effects.

24
Q

What is particularly dangerous of taking Nitrates w/ sildenifil (viagra)

A

many patients are taking NITRATES & phosphodiesterase inhibitors like VIAGRA (sildenifil)

can generate severe hypotension AND SHOCK!!!!

(nitrates already lower BP, sildenifil increases this effect)

25
Q

How does NO generate smooth muscle relaxation?

A

NO -> bind GC by heme moiety–> convert GTP to cGMP –> DEPHOSPHORYLATION OF MYOSIN LIGHT CHAIN
= relaxation!

26
Q

State the vascular effects of NP

A

NO is also a potent inhibitor of the white cells adhesion to the endothelial surface.

It decreases the release of adhesion molecules such as the E-selectin on the endothelial surface.

NO has been shown to protect against ischemic and reperfusion injury. (TEST)

27
Q

State pulmonoary effects of NO

How is it administered

A
  • bronchodilator
    (used in kids for ARDS)
  • used for PULMONARY HTN!!!

INHALATION

28
Q

What reduces the shock & hypotension caused by iNOS activated by bacterial LPS?

A

L-NMMA

  • High levels of NO and dysoxia result in severe ischemia and perfusion defects
29
Q

How does NO inhibit platelet function?1

A
  1. inhibit adhesion, activation, aggregation
    - regulates the release of serotonin, growth factors and thromboxane from platelets
  2. NO also indirectly enhances fibrinolysis by inhibiting the release of antiplasmin from the platelets.
30
Q

How does NO affect organ transplants?

A

Nitric oxide acts as a cytoprotective agent and prevents cellular and platelet adhesion

  • Dietary arginine supplements are helpful in the management of transplantation patients
31
Q

Which NOS (1,2,3) is responsible of the inflammatory affects experienced in diseases like IBD, arthritis, etc?

A

NOS 3

- mediates ACUTE inflammation

32
Q

What is the most long acting NO donor?

A

Transdermal nitroglycerine 8-10 hours

33
Q

What is the MOA of NO?

A

Primarily produce smooth muscle relaxation by releasing endogenous NO which produces the following effects.

A.Stimulates guanyl cyclase
B.Increased production of cGMP
C.Dephosphorylation of myosin

34
Q

What are the indications of NO?

A

Selective pulmonary vasodilation

Treatment of newborn with persistent pulmonary hypotension (improves oxygenation)

Beneficial effects in cardiopulmonary bypass in adults, congestive heart disease, primary pulmonary hypertension, pulmonary edema , lung transplantation and sickle cell crisis.

PHARM/MHD - Exam #4 (20 decks)

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