GI Pharm Flashcards
1
Q
Occurence rate for PONV? Risk factors? Associated with?
A
- Estimated to occur in 30-40% of all GA
- Risk factors- occurs 70-80% of all GA
- patient: women, age <50, non smokers, history of PONV/Motion skiness
- surgical
- length of sx
- laparotomies
- lap procedures
- ENT
- Breast
- OBGYN
- plastic
- orthopedic sx
- anesthetic
- use of inhalational agents
- N2O
- Neostigmine
- opioids
- asociated with increased morbidity, dehydration, electolye imbalances, wound dehiscence, bleeding, esophageal rupture, airway compromise and low patient satisfaction
2
Q
Pathophys behind PONV?
A
- Chemoreceptor trigger zone (CRTZ)
- medulla oblongata
- detect noxious chemicals in blood stream (ie ethanol)
- signals via neural networks sent to vomiting center
- vomiting center
- medulla oblongata slightly caudal to CRTZ
- Neurotransmitters
- dopamine, serotonin, substane P, ACh, GABA
- Afferent signals to PSNS and SNS fibers and skeletal muscle alpha motor neurons
- Other anatomic sites that can stimulate vomiting on their own
- vestibular apparatus
- thalamus
- cerebral cortex- can consciously make yourself vomit
- GI tract chemoreceptors
3
Q
What is the approach to treatment of PONV?
A
- Multimodal approach best
- modulate actiivty in vomiting center and CRTZ
- Treatment options not discussed in detail this lecture:
- midazolam (benzo)- discussed in IV induction agents, in terms for PONV, may work to decrease synthesis and release of dopamine in the CRTZ. Can be given as antiemetic towards end of procedure (not ideal since causes drowsiness)
-
Dexamethasone (corticosteroid)- discussed in steroids lecture; unclear mechanism behind PONV mgmt; typically given post induction for antiemetic effect 4 vs 8mg?
- takes time to work
- may have psychosis
4
Q
What is scopalamine?
A
- Anticholingergic at muscarinic receptor
- competitively and reversibly binds to muscarinic receptors to inhibit binding of Ach
- tertiary amine= crosses BBB (sedation, CNS effects)
- Most often used transdermal
- 5mcg/hour for 72 horus
- best when placed at least 4 hours prior to noxious stimuli for prophylaxis versus management
- good for trip going home, won’t really help immediately for sx
- S/E
- Pupillary dilation, increased IOP–> avoid in glaucoma
- bronchodilation
- antisialogogue
- anticholinergic syndrome (restlessness, hallucinations, somnolence, and unconcisousness)
- treatment: pysostigmine
- sedation
- dry mouth
- moderate increase HR/CO
5
Q
What is reglan?MOA? Kinetics?
A
- Benzamide; prokinetic
- dopamine 2 receptor antagonist- acting centrally on CRTZ (crossess BBB) and peripherally to increase mobility of esophagus, stomach and intestine
-
increases ACh to increase GI tract mobility (agonist)
- contraction of LES and gastric fundus, increased gastric and small intestine motility, decreased muscle activiyt in pylorus and duodenum
- 5HT-4 agonist to increase cAMP to increase peristaltic activity
- kinetic only NO change in gastric pH
- Kinetics
- onset 1-3 min
- DOA 1-2 hours
- E1/2T- 2-4 HOURS
- PB= 30%
- Renal excretion 40% unchanged
6
Q
Side effects for reglan?
A
Side effects:
- extrapyramidal effects (contraindicated in parkinson’s, caution in RLS or other movement d/o
- restlessness
- cramping–> give slwoly over 3-5 min
- increase lactation
- increase HR/Decrease BP
- especially with zofran
- AV nodal block
- Akathesia
- dysrhythmias if used in conjunction with zofran
- CONTRAINDICATED IN BOWEL OBSTRUCTION
Dose:
- 10-20 mg IV slowly 15 -30 min prior to induction
- 0.15 mg/kg to children post T&A to reduce PONV in PACU
- cautious about admin in any pediatrics, espcially zofran
- peds not really at high risk PONV
7
Q
Droperidol? class, kinetics, dose?
A
- Butyrophenone; dopamine receptor antagonists at the CRTZ (antiemetic properties)
- Kinetics
- peak 30 min
- DOA= 12 hours
- Highly PB
- Dose= antiemetic 0.625 mg-1.25 mgIV
- haloperiodl 0.5-2mg
8
Q
S/E of deoperidol?
A
- Slow HR
- drowsiness (higher doses)
- hallucinations
- EPS (Avoid in parkinsons- blocking dopamine)
-
Malignant neuroleptic syndrome (tachycardia, alterations BP, fluctuating LOC, muscle rigidity, hyperthermia, rhabdomyolysis, autonomic instability= mirror MR)
- treatment= amantadine- dopamine agonist and with mild anticholinergic effect
- QT prolongation and torsades de pointe (black box warning)
- additive with CNS depressant
- DO NOT GIVE WITH REGLAN- too much doapmine blocking, cardiac manifestations
9
Q
What is zofran? Kinetics, dose?
A
- 5-HT3 receptor antagonist antiemetic
- primarily works at CRTZ centrally and vagal nerve terminals peripherally
- not effectiv ein motion sickness or PONV caused by vestibular stimulation
- Kinetics
- onset 30 min
- DOA 4-8 hours
- e/12t= 3-4 hours
- VD 2L/kg
- PB 70%
- liver metabolism
- cross BBB
- Dose
- 4-8 mg IV over 2 min
- Peds- 0.05-0.15 mg/kg caution of use of drugs in peds! QT prolongation
- debate over beginning of sx vs end of sx
10
Q
S/E zofran?
A
- HA with rapid administration
- constipation
- slight prolongation of QT
- Sedation
- AV block (with co admin with metoclopramide)
- caution in liver disease
additional 5-HT antagonist: Dolasetron, grainsetron, palonosetron, ramosetron, tropisetron<– typically don’t give these in OR
11
Q
What is aprepitant? class? kinetics, metabolism dose?
A
EMEND
-
Neurokinin-1 (NK1) antagonist
- serves to antagonize substance P
- little to no affinity for serotonin, dopamine, and corticosteroid receptors
- PONV and N/V related to cancer chemotherapy (typically in combo with other antiemetics)
- VD 70L
- PB >95%
- Primary metabolism by liver, CYP3A4
- 1/2 T 9-13 hours
- s/e tiredness, diarrhea, constipation, low blood cell count
- DOSE PONV 40 mg IV prior to induction
12
Q
What is promethazine, chlorpromazine and prochlorperazine?
A
- Phenothiazines
- exert antiemetic effect by interaction with dopaminergic receptors in CRTZ
- H1 antagonist
- Following IV admin, clinical effects in 5 min
- use- blood transfusion reaction, allergic reaction, sedation, PONV
- Duration 4-6 hours
- plasma half life 9-16 hours
- liver metabolism
- contraindicated under 2 yo (fatal R depression/comatose stateS)
- sedation common conern
- dose: promethazine 6.25-12 mg IV, up to 25 mg
13
Q
Stats around aspiration precaution/prevention?
A
- 1/3 of aspiration cases occur with laryngoscopy, 1/3 with extubation and 1/3 during the procedure
- volume and acidity of aspirated gastric contents are primary determinants of pulmonary complications
- drugs that decrease volume or increase pH of gastric contents, decrease the severity of aspiration sequelae
- commonly predscribed
- treatment of peptic and duodenal ulcers, GERD
- don’t forget about relgan when talking about aspiration prophylaxis
14
Q
What are antacids?
A
- Neutralize (remove hydrogen ions) from gastric contents or decrease the secretion of HCl into the stomach
- help reduce pH of gastric already in stoamch
- Aluminum, calcium and mg salts<– we don’t admin these, pt already on these
- hydrogen ions in the stomach acid react with the base, forming a stable compound-consuming the hydrogen ions and increase pH >5
- Relieve symptoms of gastritis, improved rate of gastric ulcer healing and duodenal ulcer pain relief, increases gastric motility (neutralized pH increases gastrin release and gastri motility)
- if pH too high, impaired food digestion
- electolyte abnormalities
- drug interactions: increase rate of abosrption for salicylates, indomethaicin and naproxen; decreased bioavailability of PO cimetidine
15
Q
Sodium bicarb?
A
- Prompt rapid neutalization of stomach pH, may result in acid rebound
- Pt with HTN, Heart diseases, may not tolerate sodium load
31
Q
What are proton pump inhibitors?
A
- Block K-H ATPase (proton pump)
- totla shutdown of acid release because they work late in acid production cycle
- agents available
- “prazoles”
- lansoprazole
- pantoprazole
- esomeprazole
- omeprazole
- rabeprazole
- take time to start working. generally need 48-72 hours before decrease in acid production
33
Q
What anticholinergics are used for GI? Adverse effects?
A
- Dicyclomine (used in irritable bowel syndrome)
- muscarinic ACh receptor antagonist
- decreases acid secretion
- less effective than H2 antagonists and PPIs
- adverse effects
- dry mouth
- constipation
- blurred vision
- cardiac arrhythmias
- urinary retention
