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Pharm III > Flood 25 > Flashcards

Flood 25 Flashcards

1
Q

The ANS also influences bronchomotor tone via what system ?

A

The NANC ( non adrenergic noncholonergic ) system

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2
Q

Inhibitory of the NANC System is ?

A

NO and VIP ( vasoactive Intestinal Peptide )

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3
Q

The excitatory Transmitters of the NENC system?

A

Substance P and NKA, Cause neurogenic inflammation including bronchoconstriction

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4
Q

The mainstay of therapy for bronchospasm, wheezing, and airflow obstruction is?

A

Beta agonist

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5
Q

Where does extensive production and metabolism of arachidonic acid derivatives occur ?

A

In the lungs.

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6
Q

Icosatetraenoic acid is commonly known as

A

Arachidonic acid

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7
Q

What is the meaning of the term eicosanoids ?

A

It refers to the 20 carbon carboxylic acids derived from the metabolism of the lipid membrane component icosatetraenoic acid/arachidonic acid.

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8
Q

What does phospolipase A2 convert , and does its action lead to ?

A

The actions of phospholipase A2 convert the esterified form, as found in the membrane , and releases arachidonic acid from structural glycerol

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9
Q

Phospholipase A2 is responsible for the release of arachidonic acid from …

A

Structural glycerol

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10
Q

How many pathways may one free arachidonic acid follow ?

A

3 pathways .
Lipoxygenase pathway
Cyclooxygenase (COX) pathway
And cytochrome P 450 monoygenase system

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11
Q

What does lipooxygenase pathway produce ?

A

Leukotrienes
Lipoxins
Some HETEs( Hydroxyeicosatetraenoic acids )

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12
Q

What does the cyclooxygenade pathway produce ?

A

Prostaglandins
Thromboxane
Prostacyclin

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13
Q

What does the cytochrome P450 mooxygenase system produce ?

A

Cis -epoxyeicosatrienoic acids and HETEs that are different from the HETEs produced by the lipoxygenase pathway

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14
Q

What are the effects of leukotrienes in the lungs?

A

Promote INFLAMMATORY responses in the lung
BRONCHOCONSTRICTION and pulmonary vascular permeability
Chemotactic and chemokinetic for neutrophils
Facilitate eosinophil degranulation

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15
Q

In the lung, Leukotrienes are produce by ? (2)

A

Activated inflammatory cells within within the lung
+
Those arriving in response to inflammation

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16
Q

What substance has been identified as critical factor in the resolution of inflammation throughout the body ?

A

Lipoxins .

They inhibit eosinophil and neutrophil chemotaxis and adhesion .
They inhibit natural killer cell activation

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17
Q

What substances are endothelium dependent vasodilators of both pulmonary and systemic,microvasculature ?

A

Lipoxins

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18
Q

COX enzyme catalyzes the cyclization and oxygenation of ______, producing ______wich is converted to ______.

A 
Cyclization and oxygenation of 
1) arachidonic acid 
Producing 
2) Prostaglandin PGG2 
Which is converted to 
3) PGH2
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19
Q

What has tempered the use of COX2 inhibitors ?

A

The emergence of a small but real increase in cardiovascular risk

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20
Q

What disadvantage do new COX-2 specific inhibitor have compared to the nonspecific COX inhibitors that already widely used ?

A

Non specific COX inhitors : Acetaminophen, salicylates , NSAIDS like ibuprofen and naproxen show only slightly less COX -2 avidity than some of the newer COX 2 specific inhibitors . The new ones are not that much better . Plus COX2 inhibition = cardiac risk

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21
Q

Prostaglandin E2(PGE2) and PGI2 effect in the lung ?

A

They are Bronchodilators

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22
Q

PGF2a , PGD2, TXA2(thromboxane A2) cause what in the lung

A

Bronchoconstriction

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23
Q

Which of the prostaglandins are vasoconstrictor ( not talking bronchodilation here)

A

PGD2, PGE2, PGF2a, and TXA2 are potent vasoconstrictors

24
Q

Which prostaglandins are vasodilators?

A

PGE1 and PGF2 ( !not E2 and not F2a )

25
Q

What predominately produces 5 hydroxytryptamine or 5HT ?

A

GIT’s Chromaffin cells

26
Q

How does 5 Hydroxytryptamine become serotonin?

A

Ingested tryptophan undergoes 2 steps
1) tryptophan -5- hydroxylase
Then
2) L-amino acid decarboxylase

Then become serotonin

27
Q

Is the lung capable of producing serotonin ?

A

Yes,
Mast cells and neuroendocrine cells in the lung are capable of producing serotonin but uptake of tryptophan along the same enzymatic pathway

28
Q

What is the first pass uptake of Thiopental ?

What the pulmonary metabolism of Thiopental ?

A

Nearly 15% first pass

Little to no metabolism in lung

29
Q

The pulmonary uptake of Ketamine is ?

What is the pulmonary metabolism of Ketamine ?

A

Slightly less than 10 %

No subsequent metabolism in lung

30
Q

What is the pulmonary first pass uptake of propofol ? What is its pulmonary metabolism ?

A

30 % first pass uptake

Neglible metabolism by the lungs .

31
Q

Ketamine has no subsequent metabolism in lung. True or False ?

A

True

32
Q

Propofol has negligible metabolism by lungs. True or False ?

A

True

33
Q

Thiopental has little or no metabolism in lungs. True or false ?

A

True

34
Q

Why does the lung play a critical role in the renin-angiotensin system ?

A

Because of the pulmonary’ s endothelium’s high concentration of ACE

35
Q

Blood pressure, vascular volume and adrenergic stimulation causes the kidneys to respond by cleaving prorenin , the result then is ….

A

Renin catalyzes the formation of angiotensin I from angiotensin .

36
Q

What converts Angiotension 1 to the critically important vasocontictor Angiotensin 2 ?

A

ACE ( Angiotension Converting Enzyme )

37
Q

Where is ACE found ?

A

1) On vascular endothelium throughout the body as well as in
2) the plasma,
3) the pulmonary endothelium has an abundance of ACE as a surface or ectoenzyme on the vascular membrane

1) vascular endothelium
2) Plasma
3 Pulmonary endothelium

38
Q

What happens to newly formed Angiotensin II ?

A

It simply immediately returns to the blood.

It’s not taken up nor metabolized by endothelial cell.( thats why ACE I help with HTN )

39
Q

What is Bradykinin ?

A

A nine amino acid peptide produced in multiple sites throughout the body from kininogen thorough the action of plasma kallikrein .

40
Q

What is bradykinin in King’s English please ?

A

It is a peptide produced in multiple sites throughout the body .

From what you might ask ?
Plasma Kallikrein act on Kininogen and from that kininogen you get bradykinin .

41
Q

What does Bradykinin do exactly ?

A

It has wide ranges effects including :

1) antithrimbotic
2) profibrinolitic
3) modulation of NO and prostacyclin
4) specific to the lung , vasodilating effect on normal pulmonary vessels BUT vasoconstrictive when the pulmonary endothelium is destroyed ( in animals mind you)
5) it is a BRONCHOCONSTRICTOR

42
Q

What degrades Bradykinin ?

A

Degraded by ACE . And more than 90% eliminated on first pass through lungs .

43
Q

Since ACE is inhibited when you take and ACE I , bradykinin does not get degraded , and that has both beneficial and not so beneficial side effects which are :

A

Bad :
Angioedema and cough
Good :
Decreased MI , improved renal function .

44
Q

What is the mechanism of action of Magnesium ‘s vasodilating effects?

A

LIKELY through its effect on membrane channels involved in calcium flux
+
Through its action in the synthesis of cAMP

1)Calcium flux
+
2) synthesis of cAMP

45
Q

Magnesium does not appear to be an important cofactor for endothelial -dependent pulmonary vasodilation. True or False

A

False, it totally appears to be an important cofactor in that matter
It even successfully help wean NO in PHTN .
Also used to treat persistent PHTN if the newborn ( but that controversial )

46
Q

Pain can _____ PVR

A

Increase

47
Q

How does Periop TEA ( Thoracic epidural analgesia ) affect lungs

A

TEA may decrease PAP though
1) decreased in CO
Or
2) via attenuation of the pulmonary sympathetic outflow ( cause you blocked it with LA !!!)

48
Q

TEA could technically do what to RV function in acute PHTN patients ?

A

Depress RV function ( at least it did in pigs )

49
Q

What effect for unilateral paravertebral block have on heart ?

A

Decrease Myocardial contractility by 30%!!!! And SIGNIFICANTLY decrease systemic BP .
But a little epinephrine and stop all that drama .

50
Q

Is epidural anesthesia ok in PHTN patients ?

A

Yes , a few reports say yes

51
Q

The pulmonary vasculature’ s response to sympathetic activation will generally result in

A

An increase in PVR

52
Q

Ach administration induces what pulmonary response ?

A

Pulmonary relaxation

53
Q

Innervation and receptor content of the pulmonary vasculature is complex . Neurotransmitter receptors in this system include (8)

A

1) adrenergic
2) cholinergic
3) dopaminergic
4) histamine
5) serotonin
6) Adenosine
7) Purines
8) peptide

54
Q

In patients with chronic secondary PHTN undergoing cardiac surgery , both those 2 meds increase PAP and PRVI w/ minimal change in CI. What meds are we referring to ?

A

Epinephrine and phenylephrine

55
Q

Norepinephrine or phenylephrine which may be a better choice in anesthetized patients with chronic secondary PHTN undergoing cardiac surgery ?

A

Bc norepinephrine decreased the mean PAP to MAP ratio , but phenylephrine did not, Norepinephrine my be a better choice for these patients

56
Q

While norepinephrine may be better in patient with chronic secondary PHTN , what relevant observation was made about phenylephrine?

A

Phenylephrine restores perfusion tot he ischemia right ventricle and therefore increase CO .

This shows the importance of coronary artery perfusion in the setting of right ventricular strain and that MAINTENANCE of system pressure by whatever method may be most important principle in those patients .

57
Q

The ideal pulmonary vasodilator should have

A

A rapid onset, a short half life and produce regional pulmonary vasodilation

Pharm III (11 decks)

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