Pharm Ii Exam 1 - Autocoids 1&2

Front 1

1. Where is the H1 receptors concentrated?

Back 1

a. Hypothalmus

Front 2

1. Function of the H1 receptor

Back 2

a. Increase wakefullness
b. Inhibit appetite
c. Involved in regulation of:
-----drinking,
-----body temp,
-----secretion on ADH,
-----control of BP,
-----Control of nocioception

Front 3

1. Function of the H3 receptor

Back 3

a. reduce release of
-----histamine,
-----NE,
-----DA,
-----5-HT
------and in some areas, ACh

Front 4

1. Cardiovascular effects of H1 and H2

Back 4

a. H1 - Generalized dilation of arteries (smaller vessels)
-----The biggest cardio effect of histamine is here
b. H2 - Increased SA rate, force of contraction and AV automaticity in the heart
-----At normal levels these effects are not noticed
c. H1 & H2 - Combine to increase peripheral blood flow and decrease vascular resistance (redness).
d. H1 & H2 - Majority of “redness” is blocked by H-1 ANTAGONISTS
e. Edema
-----Loss of microvascular integrity
-----Leaking of fluid and molecules as large as proteins lead to the formation of hives.

Front 5

1. RESPIRATORY EFFECTS of H1 and H2 receptors

Back 5

a. H-1 Receptor (predominate effector)
-----Bronchoconstriction
-----Increase fluid secretion
-----Vagal-mediated bronchospasm & cough
-----Leukotrienes are the primary mediator in humans
----------------Asthmatics are sensitive to both histamine AND leukotrienes
b. H-2 Receptor
-----Bronchodilation

Front 6

1. GI effects of H1 and H2 receptors

Back 6

a. H1 receptors (minor effect)
-----Contraction of smooth muscle
b. H2 receptors (MAJOR effect)
-----Increased acid secretion from parietal cells
-----Relaxation of smooth muscle

Front 7

1. Cutaneous nerve endings effects from H1 and H2 receptors

Back 7

a. Pain/Itching - H-1 & H-2 receptor

Front 8

1. Adrenal Medulla effects from H1 and H2 receptors

Back 8

a. Increased Epinephrine release - H-1 receptor
b. No effect from H2 receptor

Front 9

1. Clinical Uses of Antihistamines

Back 9

a. Allergic Reactions
b. Motion Sickness & Vestibular disturbances
c. Nausea and Vomiting
d. Local anesthetic
e. Adjunct Rx in Parkinson’s and reverse EPS caused by phenothiazines

Front 10

1. 1st Generation antihistimines

Back 10

a. Diphenhydramine
b. Dimenhydrinate
c. Chlorpheniramine
d. Pyrilamine
e. Clemastine
f. Hydroxyzine
g. Bromphemoramine
h. Promethazine
i. Meclizine

Front 11

1. 2nd Generation antihistimines

Back 11

a. Fexofenadine
b. Loratadine
c. Desloratidine
d. Cetirizine

Front 12

1. Intranasal Antihistamine

Back 12

a. Azelastine

Front 13

1. Terfenadine & Astemizole were 2 second generation antihistamines removed from the market because they caused ______________

Back 13

a. PVC

Front 14

1. MOA of antihistimines

Back 14

a. Blockade of systemic H1 receptors (Competitive Antagonists)
-----prevents the actions of histamine already released from mast cells
b. Difference in First and Second generation
-----Ability to cross blood-brain barrier
-----Extent of antimuscarinic action
--------------This is what causes sedation
--------------Diphenhydramine (BENADRYL) is strongly sedating whereas fexofenadine (ALLEGRA) is not

Front 15

1. How long does it take for the onset of action of antihistimines

Back 15

a. 30 – 60 min

Front 16

1. Half lives of antihistimines

Back 16

a. Mopderate and variable
b. 4-20 hours

Front 17

1. .DOA for most antihistimines

Back 17

a. 3-6 hours

Front 18

1. Where are antihistimines metabolized?

Back 18

a. liver (CYP3A4 isozyme)

Front 19

1. which antihistimines are metabolized to active compounds?

Back 19

a. Terfenadine (Seldane) = Fexofenadine (Allegra)
------ Terfenadine was removed from the market but its active component has not
b. Hydroxyzine (Atarax) = Cetirizine (Zyrtec)
c. Astemizole (Hismanal) = variety of compounds
------ Astemizole was removed from the market

Front 20

1. The most sedating antihistimines are:

Back 20

a. Diphenhydramine
b. Hydroxyzine
c. Promethazine

Front 21

1. Antihistamines with a high antiemetic effect

Back 21

a. Meclizine
-----Less sedating than others so commonly used to prevent motion sickness
b. Diphenhydramine
c. Hydroxyzine
d. promethyzine

Front 22

1. Adverse effects and Toxicity of antihistimines

Back 22

1) Dry mouth,
2) Sedation,
3) urinary retention
4) CNS depression
5) dizziness,
6) lack of coordination,
7) blurred vision,
8) tremors,
9) euphoria and insomnia
10) Paradoxical excitation in children

***Topical use - allergic reactions
-----Topical > oral (topical increases chances for allergic reaction more than oral)
1) allergic dermatitis
2) drug fever
3) photosensitization

***2nd most frequent complaints - GI
1) loss of appetite,
2) nausea,
3) vomiting,
4) constipation or diarrhea

***Interactions with other transmitter systems (Primarily 1st Generation)
-----Serotonin
-----Dopamine D2
-----Alpha adrenergic

Front 23

1. Which antihistimines have longer DOA (1st or 2nd)

Back 23

a. 2nd generation antihistamine has longer duration of action than 1st generation

Front 24

1. 5-HT Storage and Release

Back 24

a. stored in active form in vesicles
b. primary anatomical sites:
-----enterochromaffin cells of GI tract (90%)
-----dorsal raphe nuclei in brain stem
-----platelets (active transport)
c. released in response to various stimuli:
-----vascular damage (platelets)
-----mechanical and neural stimulation of GI
-----as a neurotransmitter from 5-HT neurons
-----from carcinoid tumor (carcinoid crisis)

Front 25

1. Only 3 types of 5-HT1 agonist drugs are presently employed clinically

Back 25

i. buspirone (Buspar) 5-HT1A selective
ii. sumatriptan (Imitrex) 5-HT1B/D selective
-----and others like zolmitriptan (Zomig) & naratriptan (Amerge) & rizatriptan (Maxalt) frovatriptan (Frova)
iii. tegaserod (Zelnorm); 5-HT4 selective
------now only for a crisis & only with FDA approval;

Front 26

1. _________________and ______________are both useful 5HT antagonist in the care of patients with carcinoid tumor

Back 26

a. cyproheotadine
b. methysergide

Front 27

1. Effects of histimine on Vascular smooth muscle

Back 27

a. Vasodilation and Edema

Front 28

1. Effects of histimine on Non vascular smooth muscle

Back 28

a. Contraction, i.e. bronchoconstriction

Front 29

1. Summary of effects of histimine

Back 29

a. Vasodilation and Edema
b. Contraction, i.e. bronchoconstriction
c. Itching
d. Increase in Gastric acid secretion

Front 30

1. Stimuli that increase cGMP have what effect on histimine?

Back 30

a. increase histamine release

Front 31

1. Stimuli that increase cAMP have what effect on Histimine

Back 31

a. oppose histamine release

Front 32

1. Effects of 5HT on Vascular smooth muscle

Back 32

a. Vasoconstriction (most of the time)

Front 33

1. Effects of 5HT on non vascular smooth muscle

Back 33

a. Contraction of GI and other NVSM

Front 34

1. Summary of effects on 5HT

Back 34

a. Vasoconstriction
b. Contraction of GI and other NVSM
c. CNS neurotransmission
d. Stimulates platelet aggregation

Front 35

1. MOA of Scopolamine

Back 35

a. Muscarenic antagonist

Front 36

1. Clinical use of Scopolamine

Back 36

a. Used to tx motion sickness and vestibular disturbances

Front 37

1. MOA of Diphenhydramine

Back 37

a. 1st generation H1 receptor antagonist

Front 38

• Clinical use of Diphenhydramine

Back 38

o Local anesthetic (High sedative effect)
o Medium antiemetic
o High anticholinergic
**bronchodilator (asthmatics)

Front 39

1. DOA of Diphenhydramine

Back 39

a. 10 hours

Front 40

1. MOA of Dimenhydrinate

Back 40

a. 1st generation H1 receptor antagonist

Front 41

• DOA of Dimenhydrinate

Back 41

o 8 hours

Front 42

• Clinical use of Dimenhydrinate

Back 42

o High sedative effect
o Medium antiemetic effect
o High anticholinergic effect

Front 43

• MOA of Chlorpheniramine

Back 43

o 1st generation H1 receptor antagonist

Front 44

• DOA of Chlorpheniramine

Back 44

o 6 hours

Front 45

• Clinical use of Chlorpheniramine

Back 45

o Medium sedative effect
o No antiemetic effect
o Medium anticholinergic effect

Front 46

• MOA of Pyrilamine

Back 46

o 1st generation H1 receptor antagonist

Front 47

• MOA of Clemastine

Back 47

o 1st generation H1 receptor antagonist

Front 48

• MOA of Hydroxyzine

Back 48

o 1st generation H1 receptor antagonist

Front 49

• active metabolite from Hydroxizine

Back 49

o Cetirizine

Front 50

• DOA of Hydroxyzine

Back 50

o 6 hours

Front 51

• Clinical Use of Hydroxyzine

Back 51

o High sedative effect
o High antiemeic effect
o Medium anticholinergic effect

Front 52

• MOA of Bromphemoramine

Back 52

o 1st generation H1 receptor antagonist

Front 53

• MOA of Promethazine

Back 53

o 1st generation H1 receptor antagonist

Front 54

• DOA OF Promethazine

Back 54

o 12 hours

Front 55

• Clinical use of Promethazine

Back 55

o Useful to tx nausea/vomiting due to chemo/radiation therapy
-----High antiemetic effect
o Local anesthetic
-----High sedative effect
o High anticholinergic effect

Front 56

• MOA of Meclizine

Back 56

o 1st generation H1 receptor antagonist

Front 57

• DOA of Meclizine

Back 57

o 12 hours

Front 58

• Clinical use of Meclizine

Back 58

o Medium sedative effect
o High antiemetic effect
-----Less sedating than others with a high antiemtic effect so often used for motion sickness
o High anticholinergic effect

Front 59

• MOA of Fexofenadine

Back 59

o 2nd Generation H1 receptor antagonist

Front 60

• DOA of Fexofenadine

Back 60

o 12 hours
o Because it has a shorter duration of action it must be taken 2 times a day as compared to other 2nd generation drugs that have a DOA of 24 hours

Front 61

• MOA of Loratadine

Back 61

o 2nd Generation H1 receptor antagonist

Front 62

• DOA of Loratadine

Back 62

o = 24 hours

Front 63

• MOA of Desloratidine

Back 63

o 2nd Generation H1 receptor antagonist

Front 64

• MOA of Cetirizine

Back 64

o 2nd Generation H1 receptor antagonist

Front 65

• This is the active metabolite of hydroxyzine

Back 65

o Cetirizine

Front 66

• DOA of Cetirizine

Back 66

o = 24 hours

Front 67

• MOA of Azelastine

Back 67

o Intranasal Antihistamine

Front 68

• DOA of Azelastine

Back 68

o = 12 hours

Front 69

• Clinical use of Azelastine

Back 69

o Used in allergic rhinitis
-----Relieves the sneezing, itching, and watery discharge

Front 70

• Side effects of Azelastine

Back 70

o Drowsiness / sedation (has a low sedative effect)
o Dry mouth
o Weight gain

Front 71

• MOA of Buspirone

Back 71

o 5-HT1A partial agonist

Front 72

• Clinical use of Buspirone

Back 72

o Anti Anxiety / depression

Front 73

• MOA of Sumatriptan

Back 73

o 5-HTAB/D selective agonist

Front 74

• Clinical use of Sumatriptan

Back 74

o Antimigraine and cluster headaches
-----Only for ACUTE migraine attack and not for prophylaxis
----in an acute headache the vessels are dilated...since the triptans are 5HT agonist they will promote constriction

Front 75

• MOA of Tegaserod

Back 75

o 5-HT4 selective agonist

Front 76

• Clinical use of Tegaserod

Back 76

o Only for a crisis and only with the FDA approval
o Used for IBS (constipation)

Front 77

• MOA of Methysergide

Back 77

o 5-HT2 selective antagonist

Front 78

• Clinical use of Methysergide

Back 78

o Migraine prophylaxis
o Diarrhea in carcinoid tumors (carcinoid syndrome)

Front 79

• MOA of Cyproheptadine

Back 79

o 5HT2 selective antagonist
o Anti- H1

Front 80

• ROA of Cyproheptadine

Back 80

o Liquid
o Tablet

Front 81

• Clinical use of Cyproheptadine

Back 81

o Antiperistalic in carcinoid crisis (carcinoid syndrome)
o DOC for urticaria (hives)
o Purities
o Also used to counteract sexual dysfunction of 5-HT reuptake inhibitors (i.e. fluoxetine)

Front 82

• MOA of Clozapine

Back 82

o 5HT2 selective antagonist
o Non selective antagonist at dopamine receptors

Front 83

• Clinical use of Clozapine

Back 83

o Negative symptoms of schizophrenia

Front 84

• Adverse effect of Clozapine

Back 84

o May cause agranulocytosis
----Clozipine is selective for 5HT2, and non selective for dopamine receptors
--it is used to treat negative symptoms of schizophrenia

Front 85

• MOA of Ondansetron

Back 85

o 5HT3 selective antagonist

Front 86

• Clinical use of Ondansetron

Back 86

o GI disorders
o Chemotherapy – induced nausea / vomiting

Front 87

• MOA of Granisetron

Back 87

o 5HT3 selective antagonist

Front 88

• Clinical use of Granisetron

Back 88

o GI disorders
o Chemotherapy – induced nausea / vomiting

Front 89

• MOA of Dolasetron

Back 89

o 5HT3 selective antagonist

Front 90

• Clinical use of Dolasetron

Back 90

o GI disorders
o Chemotherapy – induced nausea / vomiting

Front 91

• MOA of Sibutramine

Back 91

o Serotonin reuptake inhibito
o Removed from market b/c adverse cardio effects
o Inhibits 5-HT, nor epi, DA reuptake

Front 92

• Clinical use of Sibutramine

Back 92

o Anorectic
o Appetite supression
o ***** Removed from market b/c adverse cardio effects

Front 93

1) Synthesis / release of eicosanoids

Back 93

a) not stored;
b) made and released from free intracellular arachidonic acid
-----AA released from membrane phospholipids by phospholipase A2; activated by physical, chemical, and drug interaction
-----amount intracellular AA controlled by re-incorporation of AA back into membranes
c) prostaglandins (PG) and leukotrienes (LT) two main groups of AA-derived products with activity

Front 94

1) cyclooxygenase is used to make which eicosanoids?

Back 94

(1) PGE1,
(2) PGE2,
(3) PGF2a,
(4) PGI2,
(5) TXA2

Front 95

1) COX exists in two isozymes: (which one is inducible, which one is constituitive???TQ)

Back 95

(1) COX-1 (constitutive) and COX-2 (inducible)

Front 96

1) Inhibitors of eicosanoids

Back 96

i) corticosteroids
ii) NSAIDS (aspirin, ibuprofen)
iii) LT synthesis inhibitors (zileuton; chap 27)
iv) LT antagonists

Front 97

1) corticosteroids effects on eicosanoids

Back 97

(1) block all pathways of eicosanoid synthesis by stimulating synthesis of inhibiting proteins called annexins and lipocortins:
(2) block phospholipase A2 action

Front 98

1) NSAIDS (aspirin, ibuprofen) effects on eicosanoids

Back 98

(1) block only cyclooxygenase pathways (PG and TX) but not 5-lipoxygenase (LT)
(2) aspirin and most NSAIDS not selective for COX1 or COX2

Front 99

1) LT synthesis inhibitors (zileuton; chap 27) effects on eicosanoids

Back 99

a) block 5-lipoxygenase, but not COX, and production of LTs

Front 100

1) LT antagonists (zafirlukast, montelukast ) effects on eicosanoids

Back 100

a) block LT action at LT1 receptors

Front 101

1) General MOA of prostoglandins
***what kind of signal do they induce

Back 101

(a) bind to prostanoid receptors (PG Rs -7 types)
(b) all PG Rs are linked to g-proteins with cAMP (+/-) and phospholipase C signaling pathways

Front 102

1) Basic MOA of Leukotrienes

Back 102

(a) work at LT receptors;
(b) use phospholipase C signaling pathway
(c) receptor antagonist drugs targeted for LT1 receptor

Front 103

1) Vascular effects of eicosanoids

Back 103

i) arterial smooth muscle relaxed by PGE2 and PGI2 results in vasodilatation;
ii) TXA2 and PGF2 a vasoconstrictors all immediate breakdown
-----so effects serve to regulate the microcirculation

Front 104

1) GI tract effects of eicosanoids

Back 104

i) effects of PG and TX on gut muscle vary;
ii) Adverse effects - administration of clinically-used PGs often leads to:
----- colicky cramps;
-----diarrhea,
-----N/V

Front 105

1) Airways effects of eicosanoids

Back 105

i) respiratory smooth muscle is relaxed by
-----PGE2 and
-----PGI2
ii) respiratory smooth muscle is contracted by
-----TXA2 and
-----PGF2 a

Front 106

1) Reproductive organs effects by eicosanoids

Back 106

a) female:
-----role of PGs in reproduction surmised since original discovery in human semen,
-----a major clinical use of PG to stimulate uterine contractions and cervical ripening
b) male:
-----role of PG unknown,
-----major source in semen is seminal vesicle not prostate
-----low PG in seminal fluid is associated with infertility

Front 107

1) Central and peripheral nervous system effects by eicosanoids

Back 107

a) Fever –
-----pyrogens cause release of PGE2 in brain which produces fever (pyresis);
-----PGE2 synthesis is blocked by NSAIDs
b) Sleep –
-----PGD2 produces sleep when infused into cerebral ventricles
c) Neurotransmission –
-----PGEs inhibit the release of norepinephrine from sympathetic nerve endings

Front 108

1) Eicosanoids used for Abortion (abortifacient)

Back 108

a) Misoprostol (PGE1) when used with RU486
b) Dinoprostone (PGE2)
c) Carboprost (PGF2a)

Front 109

1) Dosage of Dinoprostone

Back 109

i) dose:
------vaginal suppository; 20 mg high into vagina, additional 20 mg inserted at 3-5 h until abortion is complete
ii) max. dosage:
------240 mg or continuous use for 48 h

Front 110

1) eicosanoids used for for cervical ripening effects and preparation for labor induction:

Back 110

i) PGE2 used instead of oxytocin or ergonovine to stimulate uterine contractions
ii) i.e. dinoprostone (PGE2)
-----Cervidil,
-----Prepidil

Front 111

1) Eicosanoids used for for postpartum bleeding:

Back 111

(1) carboprost tromethamine
-----when resistant to ergonovine

Front 112

1) Dosage of Carboprost tromethamine

Back 112

(1) deep IM injection
(2) repeat at 15-90 min, no more than 2 mg

Front 113

1) Eicosanoid uses in the Cardio vascular system

Back 113

a) Thrombosis
-----aspirin inhibits TXA2 via platelet cyclooxygenase and may reduce effects of MI
b) patent ductus arteriosus
-----fetal ductus arteriosus kept open by local PGE and PGI release
-----Rx: alprostadil (PGE1, PROSTIN VR Pediatric)
c) erectile dysfunction
-----Rx: Alprostadil (PGE1, Caverject, Edex or Muse kits ) used for its vasodilator effect

Front 114

1) what is the main Eicosanoids used to tx Pulm HTN
--how does it do this?

Back 114

a) PGI2 dilates pulmonary vessels and increases pulmonary blood flow, can be used in primary pulmonary hypertension
b) Rx: epoprostenol (Flolan)

Front 115

1) Eicosanoids used for the GI system

Back 115

a) Misoprostol
i) gastric cytoprotection by PGE1 by preventing and promoting ulcer healing, esp. after long-term NSAID use

Front 116

1) Eicosanoids used for the eyes (Ocular)

Back 116

a) Newest PG drugs to hit market:
b) e.g.
-----Latanoprost (XALATAN), a PGF2a analog
-----Travoprost
----- Unoprostone
c) indicated for reduction of elevated intraocular pressure in open-angle glaucoma and ocular hypertension who are resistant to other treatments

Front 117

1) Function of Endothelins

Back 117

a) Inhibitors of Endothelin Synthesis & Action

Front 118

1) Potential Uses of endothelins

Back 118

(1) pulmonary arterial hypertension
(2) Likely a powerful teratogen. NOT for females unless on hormonal birth control.

Front 119

1) Effects of PGD2

Back 119

a) Weak inhibitor oif platelet aggregation
b) When infused into cerebral ventricles it produces sleep

Front 120

1) Effects of PGE1

Back 120

a) Effects on Vascular smooth muscle
-----Vasodilation
b) Effects on Non vascular smooth muscle
-----Relaxation of bronchial muscles
-----Contraction of uterine muscles
c) Other effects
-----Inhibition of gastric acid secretion
d) Biochemical and physiological actions
-----Bronchial vasodilation
-----Inhibitor of lipolysis
-----Inhibits plateet aggregation
-----Contraction of GI smooth muscle ***(major effect)

Front 121

1) Effects of PGE2

Back 121

a) vasodilation
b)Relaxation of bronchial muscles
c)***Contraction of uterine muscles
d) Stimulates hyperalgesic response (sensitize to pain)
e) Inhibits platelet aggregation
f) Cytoprotection: protects GI epithelial cells from acid degredation
-----Reduces gastric acid secretion
g) Promotes inflamation
h) PGE2 inhibits the release of NE from sympathic nerve endings

Front 122

1) Effects of Prostoglandin F2

Back 122

a) Vascoconstriction
b) Contraction of bronchial and uterine smooth muscles
c) Increase in aqueous humor outflow
d)Stimulates breakdown of corpus leuteum (leuteolysis): animals
e) Stimulate uterine smooth muscle contraction

Front 123

1) Effects of Prostoglandin I2

Back 123

a) vasodilation
b) relaxation of NVSM
c)Inhibition of platelet aggregation
d)Sensitize / amplify nerve pain response

***these are 4 of the same characteristics of PGE2

Front 124

1) Effects of Thromboxane A2

Back 124

a) vasoconstriction
b) contraction of NVSM
c) Stimulation of platelet aggregation
----- Vasoconstrictors TXA2 abd PGF2 break down immediately…so their effects are used to regulate the microcirculation
d) Decreases cAMP levels in platelets
e) Stimulates the release of ADP and 5-HT from platelets

Front 125

1) Effects of LTB4

Back 125

a) Biochemical and physiological actions
-----Increases leukocyte chemotaxis and aggregation

Front 126

1) Effects of LTC/D4

Back 126

a) Biochemical and physiological actions
-----Slow reacting substance of anaphylaxis
-----Potent and prolonged contraction of ileal smooth muscle (animals)
-----Contaction of lung parenchymal strips (animals)
-----Bronchoconstriction (humans)
-----Increased vascular permeability (animals)

Front 127

1) MOA of Alprostadil

Back 127

a) PGE1 analog

Front 128

• Clinical use of Alprostadil

Back 128

o to maintain ductus arteriosus
-----in neonates w/ congenital heart defect until surgery can be preformed
o Erectile dysfunction (vasodilator effect)

Front 129

• Adverse effects of Alprostadil

Back 129

o Apnea (10%)
-----Especially when under 2kg
o Penile pain (when used for ED)

Front 130

• Dose of Alprostadil

Back 130

a) IV infusion & maintain at lowest rate until surgery

Front 131

1) MOA of Misoprostol

Back 131

a) (PGE1 analog)

Front 132

• Clinical use of Misoprostol

Back 132

o gastric protection (cytoprotection)
-----by promoting ulcer healing, esp after long term NSAID use
o also as abortifacient when used with RU486 (mifepristone)

Front 133

• Adverse effect of Misoprostol

Back 133

o Diarrhea (titrating helps prevent)
o Uterine contractions
o Absolute contraindication in pregnant women

Front 134

• MOA of Dinoprostone

Back 134

o PGE2 analog

Front 135

• Clinical use of Dinoprostone

Back 135

o Used for abortions (12-20 weeks),
-----Non malignant trophoblastic disease (hydatiform mole)
-----Incomplete abortion with other means
o labor induction,
o cervical ripening

Front 136

• Adverse effect of Dinoprostone

Back 136

o Pyresis (50%)
o Diarrhea (40%)
o Headache (10%)
o Hypotension (10%)

Front 137

• MOA of Carboprost

Back 137

o PGF2a analog
o Causing Vasoconstriction

Front 138

• Clinical use of Carboprost

Back 138

o Used for 1st or 2nd trimester abortions
o post-partum bleeding,
-----when resistant to ergonovine

Front 139

• Adverse effects of Carboprost

Back 139

o Abnormal contractions (7%)
o N/V (6%)
o Fetal heart bradycardia and deceleration (17%)
o Diarrhea
-----From stimulation of the GI contractions

Front 140

• MOA of Epoprostenol

Back 140

o PGI2 analog

Front 141

• MOA of Epoprostenol

Back 141

o direct vasodilatation of pulmonary and systemic arterial vascular beds;
o inhibition of platelet aggregation

Front 142

• Clinical Use of Epoprostenol

Back 142

o primary pulmonary hypertension
-----long term IV tx

Front 143

• Adverse effects of Epoprostenol

Back 143

o Dizziness
o Headache
o N/V
o Diarrhea
o Myalgia
o Flushing
o Tachacardia

***remember it is uedd to tx pulmonary HTN via IV

Front 144

• MOA of Treprostinil

Back 144

o PGI2 analog

Front 145

• Clinical use of Treprostinil

Back 145

o primary pulmonary hypertension
-----Sub-q continuous infusion.

Front 146

• MOA of Travoprost

Back 146

o PGF2a analog
o Causes an Increase in Aqueous fluid outflow

Front 147

• Clinical use of Travoprost

Back 147

o Open angled Glaucoma
-----In those resistant to othetr tx
o Ocular HTN
-----In those resistant to othetr tx

Front 148

• Adverse effect of Travoprost

Back 148

o Increase brown color in iris by increasing melanin in melanocytes
-----May lead to permanent eye color change

Front 149

• MOA of Unoprostone

Back 149

o PGF2a analog
o Causes an Increase in Aqueous fluid outflow

Front 150

• Clinical use of Unoprostone

Back 150

o Open angled Glaucoma
-----In those resistant to othetr tx
o Ocular HTN
-----In those resistant to othetr tx

Front 151

• Adverse effect of Unoprostone

Back 151

o Increase brown color in iris by increasing melanin in melanocytes
-----May lead to permanent eye color change

Front 152

• MOA of Latanoprost

Back 152

o PGF2a analog
o Causes an Increase in Aqueous fluid outflow

Front 153

• Clinical use of Latanoprost

Back 153

o Open angled Glaucoma
-----In those resistant to othetr tx
o Ocular HTN
-----In those resistant to othetr tx

Front 154

• Adverse effect of Latanoprost

Back 154

o Increase brown color in iris by increasing melanin in melanocytes
-----May lead to permanent eye color change

Front 155

• MOA of Bosentan

Back 155

o Inhibitors of Endothelin Synthesis & Action
o Antagonists for ETA and ETB receptors
-----nonselective antagonist,

Front 156

• Clinical use of Bosentan

Back 156

o Pulmonary Artery HTN
-----blocks BOTH the transient lowering of BP and the prolonged increase

Front 157

• Adverse effects of Bosentan

Back 157

o Likely a powerful teratogen. NOT for females unless on hormonal birth control

Front 158

• MOA of Ambrisentan

Back 158

o Inhibitors of Endothelin Synthesis & Action
o Antagonists for ETA and ETB receptors
-----much higher affinity for ETA receptors
• blocks BOTH the transient lowering of BP and the prolonged increase

Front 159

• Clinical use OF Ambrisentan

Back 159

o Pulmonary Artery HTN
-----blocks BOTH the transient lowering of BP and the prolonged increase

Front 160

• Adverse effects OF Ambrisentan

Back 160

o Likely a powerful teratogen. NOT for females unless on hormonal birth control