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Pharm Exam 5 -- Smooth Muscle, GI and OTC > Smooth Muscle (pt 3/4) Serotonin & Prostaglandins > Flashcards

Smooth Muscle (pt 3/4) Serotonin & Prostaglandins Flashcards

1
Q

What is Serotonin?

A

-Neurotransmitter
-Local hormone in the gut
-Component of the platelet clotting process – serotonin is found in platelets in the blood
-Found in plant & animal tissues, venoms & stings
-After synthesis, it is either stored or inactivated (by MAO)
-In the pineal gland – serotonin is a precursor to Melatonin

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2
Q

What functions are Serotonin involved in?

A

Mood
Sleep
Appetite
Temp regulation
Pain perception
Regulation of BP
Vomiting

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3
Q

Serotonin plays a role in what clinical conditions?

A

Depression
Anxiety
Migraines

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4
Q

Where is Serotonin predominantly located?

A

90% of the serotonin of the body is found in the enterochromaffin cells of the GI tract.
-Synthesize Serotonin
-Store it with ATP (granules)
-Released in response to mechanical or neuronal stimuli
-Paracrine action (local)

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5
Q

Where is the remaining 10% of Serotonin located?

A

Serotonergic neurons are located in the Raphe Nuclei of the brain stem.
-Also around blood vessels
-synthesize, store, and release serotonin as a neurotransmitter

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6
Q

What do you need to know about the different Serotonin receptor subtypes?

A

5-HT receptor Subgroups – 7 different subgroups
-5-HT3 = ligand gated ion channel
-5-HT3 = excitatory, ionotropic, Zofran
-All others are GPCR (metabotropic)

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7
Q

What are the Nervous System Effects of Serotonin (5-HT3)?

A

-GI tract & Medulla: Vomiting reflex due to chemical triggers
-Potent stimulator of pain and itching: Insect & plant stings
-Coronary Vascular Beds: Bezold-Jarisch Reflex (bradycardia and hypotension)

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8
Q

What are the Respiratory Effects of Serotonin?

A

-Small direct stimulant effect on bronchial smooth muscle
-Facilitates Ach release from bronchial vagal nerve endings
-May cause hyperventilation due to chemoreceptor reflex OR stimulation of bronchial sensory nerve endings

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9
Q

What are the CV Effects of Serotonin?

A

-Constriction of vascular smooth muscle: Powerful vasoconstrictor (reflex bradycardia). Pulmonary & renal vessels very sensitive

EXCEPT: Skeletal muscle & heart
-Dilates blood vessels
-If the endothelium is damaged, the coronary vessels will constrict

⬆Platelet aggregation

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10
Q

What are the GI Effects of Serotonin?

A

-Strong stimulant of GI Smooth Muscle
-Increases tone
-Facilitates peristalsis: Prokinetic
-No effect on secretions: ? Inhibitory effect; Non-conclusive research

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11
Q

What causes Serotonin Syndrome? (3 drugs)

A

Excess of serotonergic activity in the CNS.
-SSRIs
-2nd Gen Anti-Depressants
-MAOIs

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12
Q

What are the symptoms of Serotonin Syndrome?

A

-HTN
-Hyperreflexia, tremor, clonus
-Hyperthermia
-Hyperactive bowel sounds, diarrhea
-Mydriasis
-Agitation
-Coma

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13
Q

What is the treatment for Serotonin Syndrome?

A

-5-HT2 Antagonist
-Benzos (sedation)
-Muscle relaxants
-Intubation
-Ventilator

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14
Q

What drugs are the Serotonin Receptor Agonists?

A

-Buspirone (5-HT1A): Non-benzo anxiolytic
-Dexfenfluramine: Appetite suppressant (withdrawn cardiotoxicity)
-Sumatriptan (5HT1D/1B): Migraine HAs
-Cisapride: Treatment of reflux & motility disorders. Highly toxic – for compassionate use only
-Tegaserod: Irritable bowel syndrome
-Fluoxetine: SSRI for depression

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15
Q

What is a Carcinoid Tumor?

A

-Slow growing neuroendocrine tumor (emits NT like substances)
-Most commonly located in the intestine
-Usually begin in the digestive tract or the lung
-10% secrete excess levels of hormone especially Serotonin
-Potential for malignancy

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16
Q

What are the Serotonin Antagonists that are too toxic for general use?

A

p-Chlorophenylalanine & p-Chloroamphetamine

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17
Q

What is Reserpine?

A

A Serotonin Antagonist.
-Blocks aminergic transmitter vesicles from uptake and storage of serotonin, norepinephrine & dopamine (Blocks storage)
-Treatment of HTN
-Adverse Effects: sedation, fatigue, nightmares, depression, EPS, diarrhea, GI cramps

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18
Q

What are other misc Serotonin Receptor Antagonist Drugs?

A

-Phenoxybenzamine (5-HT2): Irreversible α-blocker (tx of Pheo)
-Ergot Alkaloids (can be agonist or antagonist depending on type of Ergot)
-Cryoheptadine (5-HT2 & H1)
-Ondansetron

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19
Q

Describe Cryoheptadine (5-HT2 & H1)

A

-Prevents smooth muscle actions of both receptors
-No effect on gastric secretion
-Antimuscarinic effects & sedation
-Tx: Carcinoid Tumor & Cold Induced Urticaria

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20
Q

What is Ondansetron used for?

A

-Prototypical 5-HT3
-Prevention of N/V due to surgery or Chemo Tx
-Can be used during Pregnancy

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21
Q

What are Prostaglandins?

A

-Chemical mediators found in most body tissues (systemic actions)
-Regulate cell functions
-Promote the inflammatory response

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22
Q

Where are PGD2 located?

A

Airways, brain, mast cells

23
Q

What are the effects of PGD2?

A

Bronchoconstriction

24
Q

Where are PGE2 located?

A

Brain, Kidneys, Platelets
Vascular Sm. Muscle

25
What are the effects of PGE2?
-Bronchodilation -Gastroprotection -↑Activity of GI Sm. Muscle -↑Sensitivity to pain -↑Body temperature -Vasodilation
26
Where are PGF2 located?
Airways, Eyes, Uterus Vascular Sm Muscle
27
What are the effects of PGF2?
-↑Activity of GI Sm. Muscle -Bronchoconstriction -↑Uterine contraction
28
Where are I2 located? (Prostacyclin)
Brain, Endothelium, Kidneys, Platelets
29
What are the effects of I2? (Prostacyclin)
-↓Platelet aggregation -Gastroprotection -Vasodilation
30
Where is Thromboxane A2 located?
Kidneys, Macrophages, Platelets, Vascular Sm. Muscle
31
What are the effects of Thromboxane A2?
-↑Platelet aggregation -Vasoconstriction
32
The constrictive effects on smooth muscle are mediated by______, and the dilation is mediated by______.
Constriction: mediated by the release of Ca (effected by CCBs) Dilation: mediated by increased cAMP
33
Arachidonic Acid can become Prostaglandins via ____ or ____.
COX-1 or COX-2
34
Describe COX-1?
-Synthesized continuously -Physiologic PGs -Present in all tissues/cells (platelets, endothelial cells, GI tract, kidneys) -Essential in synthesis of TXA2 (plt aggregation). Inhibition of COX1 inhibits Thromboxane A2, inhibiting plt aggregation for the lifetime of the platelet (8-10 days)
35
Describe COX-2.
Pathologic PGs. -Present in several tissues (not all): brain, bone, kidneys, GI tract, female reproductive system -Inactive until stimulated by pain & inflammation -Inducible pain and inflammatory.
36
Traditional NSAIDs block _____, while Celecoxib is safer because it only takes out_____.
NSAIDs block COX-1 and COX-2 enzymes Celecoxib blocks just COX-2.
37
What are the clinical uses of Prostaglandins?
-Female Reproductive Sys: Induction of labor and Dysmenorrhea -Male Reproductive Sys: Erectile dysfunction -Pulmonary HTN: I2 ↓peripheral, pulmonary & coronary vascular resistance -Patent ductus arteriosus (↓E2 = closure) -Organ transplant rejection -Osteoarthritis -Rheumatoid Arthritis -Glaucoma -MI/Stroke prevention
38
What is the MOA of NSAIDs (Aspirin, Ibuprofen)?
Inhibit COX-1 & COX-2. -Analgesic: Inhibiting prostaglandins that promote pain -Antipyretic: Inhibiting pyrogenic (fever inducing) prostaglandins -Anti-inflammatory Effects: Inhibiting prostaglandins that promote edema
39
T/F: NSAIDs treat symptoms, but do not cure the underlying disorder.
True. Just symptom mgmt.
40
What are the anti-platelet effects of Aspirin?
-ASA binds irreversibly to platelet COX-1 -Prevents the synthesis of Thromboxane A2 -Inhibits platelet aggregation -Irreversible: Effect lasts for the lifetime of the platelet (7-10 days) -Use has declined due to the adverse effects of the GI tract and the advent of newer drugs -Low-dose ASA still in use for MI and stroke (anti-platelet effect – decreased clot formation)
41
Aspirin and ALL NSAIDS except for Acetaminophen and COX-2 Specific do what?
-Inhibit platelet aggregation -Interfere with blood coagulation -Increase the risk of bleeding
42
What are the antiplatelet effects of NSAIDs (non-Aspirin)?
-NSAIDS bind reversibly with platelet COX-1 -Anti-platelet effects lasts only while the drug is present in the blood -Platelet function returns after 4 half-lives of the drug
43
What are the normal Kidney effects of Prostaglandins?
-Increase bloodflow via vasodilation at times of decreased bloodflow -Counters the vasoconstrictive effects of Angiotensin II, Norepinephrine & other constricting substances
44
What is aspirin effective in treating?
-Prototype -Effective in mild to moderate pain Skin, muscles, joints and other connective tissue -Ex. Arthritis -PO: plain, enteric coated (can irritate lining of GI tract if uncoated), chewable tablets -Unstable in liquid -PR: suppositories -Nephrotoxic at high doses
45
How can aspirin therapy become nephrotoxic?
-Aspirin therapy inhibits prostaglandins that dilate the renal blood vessels -Constriction of renal arteries and arterioles -Decreases the bloodflow to the kidneys -Decreases GFR -Increases the retention of salt and water
46
How does Ibuprofen compare to Aspirin?
-Ibuprofen is a Propionic acid derivative -Better tolerated than aspirin, but more money. -Both cause all the same adverse effects/ -Has decreased GI irritation/GI upset compared to aspirin.
47
What do you have to be careful of with the administration of ibuprofen?
-Beware of accidental OD: combined use of prescription and non-prescription forms of NSAIDS -Monitor BUN/Creatinine due to potential for renal damage -Use lower doses in patients with liver or renal impairment
48
What are the benefits of Celecoxib (Celebrex)?
-Selective COX-2 Inhibitor -Less gastric irritation -No antiplatelet effects -Potentiate pre-existing HTN -Highly protein bound -Half-life 11 hours -Often given PO pre-op
49
Describe Acetaminophen (Tylenol).
-Commonly used Aspirin supplement -Does not cause N/V, GI bleeding or disrupt coagulation -Equal to Aspirin in analgesia & antipyrexia -Lacks anti-inflammatory effects -OD = fatal liver damage -Tablet, liquid, rectal suppository, & IV -Marketed OTC in many analgesics & cold remedies -Prescribed with codeine, hydrocodone, or oxycodone -Enhance analgesic effects
50
What are contraindications to the use of NSAIDs?
-Peptic ulcer disease -GI or other bleeding disorders (Drinkers, eso varices) -Hypersensitivity reaction -Cross-sensitivity between ASA & NSAIDS -Impaired renal function -ASA is C/I in children with influenza/chickenpox (Reye’s syndrome) -Alcoholics (NO TYLENOL) -Asthma ASA irritates GI lining (bleeding) ASA and NSAIDs can induce bronchospasm; use caution in asthmatics.
51
What is Reye's Syndrome?
Confusion, swelling of brain, and liver damage. Occurs in children recovering from some viral infection or with a metabolic disorder who are given ASA.
52
What are the considerations for NSAID use in pediatrics?
-Acetaminophen for fever and/or pain -Ibuprofen for fever -No Aspirin (Reye’s Syndrome: Rapidly progressive encephalopathy after acute viral illness)
53
What are the considerations for NSAID use in geriatrics?
-Acetaminophen: safe in recommended doses. Caution in liver damage and alcohol use/abuse -Aspirin: safe in small doses for prevention of MI & Stroke (81 mg) -ASA/NSAIDS: safe in PRN dosing for pain or pyrexia. Monitor GI effects, Take with food, Monitor renal function

Pharm Exam 5 -- Smooth Muscle, GI and OTC (10 decks)

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