GI Drugs, Anticoagulation Flashcards
Drugs that decreased lower esophageal sphincter tone
Atropine Glycopyrrolate Dopamine Nipride Thiopental TCAs Beta adrenergic stimulants Inhaled anesthetics Opioids Propofol
Drugs that increase lower esophageal sphincter tone
Reglan Edrophonium Neostigmine Histamine Succinylcholine Pancuronium Metoprolol Alpha adrenergic stimulants Antacids
Metoclopramide mechanism of action, indication, contraindications, and dose
Mild dopamine receptor blocking effect
Cholinergic stimulation of GI tract, accelerates gastric emptying/decreases gastric volume, increases LES tone
Anti-emetic (antagonizes dopamine receptors in CTZ)
Contraindication: Parkinson’s disease, SBO, extrapyramidal symptoms
Dose: 10-20mg
Bicitra mechanism of action, side effects
Mechanism of action: Increases pH of gastric contents (but also increases gastric volume)
Side effects: Increased gastric volume, caution in patients with renal failure
H2 antagonists (“-idine” ex: Pepcid, zantac) mechanism of action
Competitively blocks H2 receptors on parietal cells (decrease acid secretion)
-Doesn’t affect gastric fluid currently present, moreso given for emergence prophylaxis
H1 vs H2 receptor affects
H1: Decrease HR, Bronchoconstriction
H2: Increase HR, bronchodilation, secretion of gastric acid, CNS stimulation
Droperidol mechanism of action, contraindication, dose
Dopamine antagonist (inhibit CTZ), anti-psychotic, alpha antagonist (vasodilation) *Black box warning for prolonging QT (need 12 lead before giving) -Contraindications: Parkinsons, pts with prolonged QT Dose: .625 mg
5-HT3 receptor antagonists (Zofran), dose
Blocks serotonin receptor centrally and peripherally
-Central receptors: Present at vomiting and CTZ centers
-Peripherally: Initiate vomiting reflex
Dose: 4-8 mg
H1 antagonist (Benadryl, Dramamine)
Block H1 and muscarinic cholinergic receptors in vestibular system (best for motion sickness)
Corticosteroids for PONV, contraindication, dose
Decadron, uncertain mechanism of action -Inhibit prostaglandin synthesis? Less inflammation -Increase release of endorphins Side effect: Increased blood sugar Dose: 4-8 mg
Chemotactic trigger zone (CTZ)
Area in postrema of brain stem
- Has dopamine, serotonin, histamine, muscarinic acetylcholine, and opiate receptors
- Gives messages to vomiting center
Vomiting center
Receives input from the chemotactic trigger zone and vagus nerve
-Can be stimulated by opioids (dose dependent, lower initial doses) and then inhibited by high dose opioids
Risk factors for PONV
History of PONV Female <50 years old High doses of intraop or postop opioids Surgery >1 hour Laparoscopic procedures
Overall coagulation steps (3) and which class of medications works during the different steps
1: Primary hemostasis: adhesion, activation, aggregation -> platelet plug formation
- Meds: Anti-platelet
2: Secondary hemostasis: Actions of coagulation factors -> stable clot formation
- Meds: Anti-coagulant
3: Regulation of coagulation: Fibrinolysis/clot breakdown by plasmin
- Meds: Thrombolytic/fibrinolytic medications
Average life span of platelet
7-10 days
Antiplatelet medications (overall MOA, 4 types)
Overall: Prevent platelet activation and aggregation
- COX inhibitors
- Phosphodiasterase inhibitors
- ADP receptor antagonists
- Glycoprotein IIb/IIIa receptor antagonists
COX inhibitors
COX=enzyme for prostaglandin synthesis -Inhibit production of thromboxane A2 (essential in plt activation/aggregation) ASA-irreversible inhibition NSAIDS-reversible inhibition Selective COX 2: Celebrex
Phosphodiasterase inhibitor
Dipyridamole
Inhibit phosphodiesterase->increased cAMP
-Blockade in uptake of adenosine
-Prostacyclin release from endothelium (vasodilate)
-Decreased response to ADP (essential for platelet activation/aggregation)
ADP receptor antagonist
Indirect (Plavix)
-Given in inactive form (prodrug), require liver metabolism into active metabolite
-Irreversible inhibition of ADP mediated platelet activation
-Stop 7-10 days preop
Direct (Ticagrelor, cangrelor)
-Administered in active form
-Reversible inhibition when discontinued
BP IIb/IIIa receptor antagonists
Direct inhibition of platelet aggregation
Ex: Abciximab
Contraindicated if surgery within 4-6 weeks
Anticoagulant medications
Inhibit coagulation factors (in circulation and being produced)
- Vitamin K antagonist
- Glycosaminoglycans
- Pentasaccharides
- Direct thrombin inhibitors
- Activated protein C
Vitamin K antagonist (ex, MOA, monitoring)
Warfarin
Vitamin K vital for production of factors II, VII, IX, X
-Doesn’t inhibit factors already in circulation (why onset time is so long)
Monitoring: PT/INR
Unfractionated heparin (Ex, MOA, complication, monitoring)
Glycosaminoglycan (anti-coagulant)
Inhibits factors II, IX, X, XI, XII
IIa and Xa are inactivated in a 1:1 ratio
Heparin induced thrombocytopenia: Immune mediated, heparin forms complex with platelet factor 4, generates IgG antibodies -> plt activation, thrombus formation, platelet consumption
Monitoring: PTT
Low-molecular weight heparin (Ex, MOA, benefits, monitoring)
Exogenous heparinoid
Lovenox
Inactivates factors II and X in a 1:4 ratio
Less protein binding->more consistent pharmacokinetics, greater bioavailability, longer elimination half-life, daily dosing
Decreased risk of HIT
No monitoring
Thrombolytic medications
TPA
Plasminogen activators convert plasminogen to plasmin -> dissolves fibrin and other plasma proteins/coagulation factors
-Better at dissolving newly formed clots than older ones
Protamine
Emergent reversal for heparin and LMWH
Dose: 1mg heparin : 100 units heparin in circulation
Side effects: Histamine release -> hypotension, pulmonary vasoconstriction -> RV failure, reaction if allergic to fish
TXA
Anti-fibrinolytic Binds to plasminogen, prevents conversion of plasminogen to plasmin Most effective early post op Half-life: 2-3 hours Serum levels therapeutic 3 hours after Route: IV or topical soak
