Previous Notes Flashcards
How to differentiate between ASA 1-6
ASA 1: normal, healthy, non smoker
ASA 2: controlled systemic disease, no functional limitation (ie controlled HTN/DM, pregnant, smoker)
ASA 3: severe systemic disease w/ functional limitation (morbid obesity, ESRD on HD)
ASA 4: severe disease that is constant threat to life (ESRD but not on routine HD, recent <3mo TIA/MI, HFrEF, valve dysfunction)
ASA 5: moribund, not expected to survive without OR (ie massive trauma, ICH w mass effect, ruptured AAA)
ASA 6: brain dead, organ retrieval
Do we continue or stop these meds prior to surgery:
- ACEi/ARB
- Diuretic
- alpha 2 agonist
- ACEi/ARB: STOP - due to risk of refractory hypotension, need vasopressin or norepi
- Diuretic: STOP - due to risk of hypokalemia from loop diuretics and hypovolemia
- Alpha 2 agonist: CONTINUE - risk of rebound HTN
Do we continue or stop these meds prior to surgery:
- Metformin
- MAOi (selegiline)
- TCA (nortriptyline)
- Betablockers
- Metformin: CONTINUE in healthy patients
STOP in renal disease or surgeries affecting renal fx due to risk of metformin induced metabolic acidosis - MAOi (selegiline): CONTINUE - risk of pre-op HTN, but be wary and avoid meperidine (5HT reuptake inhibit) due to risk of Serotonin Syndrome and avoid sympathomimetics ie ephedrine and phenylephrine risk of hypertensive crisis
- TCA (nortriptyline): CONTINUE - check ECG in pre-op for prolonged QT and wide QRS due to sodium channel blockade
- Beta blockers: CONTINUE - risk of rebound HTN
Perioperative risks of morbid obesity and #1 cause of mortality in obese patients
risk of airway obstruction (hypercarbia), reduced wound healing/infection, hyperglycemia
DVT > PE is #1 cause of mortality in obese patients
What anatomy pertains to nausea?
Medication effects on areas?
Area postema: medulla, controls vomiting and opioids act in this area to trigger nausea
Nucleus tractus solitarii: dexamethasone acts on this
chemoreceptor trigger zone: near base of 4th ventricle which involve receptors of 5-HT, dopamine, and opioid (IE ondasetron)
What are MOA of ondasetron and aprepitant? side effects?
ondansetron: 5HT antagonist at chemoreceptor trigger zone
SFX: prolonged QT > headache > transaminitis > dystonia > cardiac event
aprepitant: NK1 receptor antagonist
SFX: malaise, rash, nausea
What are MOA of scopalamine and droperidol? side effects?
Scopalamine: antimuscarinic
SFX: dry mouth, tachycardia, blurry vision, urinary retention, constipation
(Tx anticholinergic crisis with physostigmine)
Droperidol: CNS antidopaminergic
SFX: extrapyramidal symptoms, dystonic rxn, prolonged QT
Mechanism of metoclopramide, uses?
Central: antidopaminergic
Peripheral: cholinergic agonist
- Increases lower esoph sphicter tone
- Use for enhanced GI motility
- PONV dose must be 25-50mg, otherwise ineffective at PONV for primary or secondary agent
Aspiration ppx regimen, who is at higher risk?
- Metoclopramide (antidopamine)
- Ranitidine (H2 antagonist, longer acting and less sfx than cimetidine)
- Na bicarbonate in pregnancy
High risk: pregnancy, delirium, severe DM (delayed gastric empty), hiatal hernia, morbid obesity, scleroderma, emergent surgery
What decreases lower esophageal sphincter tone? What increases it?
Lowers: pregnancy, obesity, inhaled anesthetics, opioid, propofol
Increases: succinylcholine, metoclopramide
Where will aspirated material usually end up in Supine patient
Posterior segment of right lower lobe
Anterior vs posterior ischemic optic neuropathy risk factors and presentation
Painless loss of vision, sluggish pupils
Anterior- risk after cardiac surgery
Posterior- risk after spine surgery
Vascular rf - prone, cad, dm, smoking, spine fusion, htn
Phase 1 vs phase 2 hypothermia
Phase 1: 1st hr anesthesia, heat loss from drug induced redistribution usually 1-2 degrees
Phase 2: heat loss due to radiation»_space; conduction, convection, evaporation
Describe neonates thermogenesis
Nonshivering thermogenesis from brown fat and skeletal muscle triggered by norepi, corticosteroids, and thyroxine
Drugs eliminated by RBC esterases
Remifentanil
Esmolol
Clevidipine
Drugs eliminated by pseudocholinesterase (aka plasma cholinesterase)
- Succinylcholine
- Ester-type LA (1× i), procaine, benzocaine, tetracaine
- Mivacurium
(Amide-type LA is two i’s, Lidocaine, bupivicaine, ropivicaine)
CYP and opioid pharmacology of codeine, hydrocodone, and oxycodone
CYP 2D6 activates codeine into morphine and also activates tramadol (peds have higher sensitivity to codeine due to higher CYP2D6 activity than neonates)
CYP2D6 metabolizes oxycodone into oxymorhone and noroxycodone which are weaker, and also hydrocodone into hydromorphone (strong active metabolite ie dilaudid)
SSRI and st John wort effects on CYP
St John wort induces CYPs
Most SSRI inhibit 3A4 and 2D6 like fluoextine, paroxetine, and sertraline
(2D6 is for opioid metabolism)
(3A4 for propofol, midazolam, Lidocaine metabolism)
How does Beta 2 agrenergic agonism cause bronchodilation
GPCR causes increase of cAMP and decrease of intracellular Ca
symptoms of propofol infusion syndrome
metabolic lactic acidosis
rhabdomyolysis
hyperkalemia
renal failure
HLD (high triglycerides)
pancreatitis
cardiac failure
NMDA receptors are activated by what and how do they function
activated by glutamate
increase intracellular Ca from depolarized voltage gated Ca channels
Ketamine MOA
NMDAr antagonist by blocking glutamate
indirect GABA/mu agonism
direct negative inotrope activity but causes CNS stimulation that increases sympathetic outflow
dissociates thalamus from the RAS
Etomidate MOA
GabaA agonist
can cause adrenal suppression by inhibiting 11Bhydroxylase
medications used to treat muscle spasms
baclofen
dantrolene
tizanidine
diazepam
anesthesia drugs metabolized by CYP3A4
propofol, alfentanil, midazolam, lidocaine
what are IgE-related symptoms of with adverse reaction to medications
urticaria
angioedema
dyspnea
dysphagia
bronchospasm
anaphylaxis
what effect does intrapulmonary or intracardiac shunts have on gas vs IV inductions?
intrapulmonary shunt will slow gas induction but no effect on IV induction with higher effect on less soluble gas
intracardiac right>left shunt will slow gas induction and increase IV induction
intracardiac left>right shunt has no effect on gas or IV induction speed
what is the physiology of muscle action potential
presynaptic nerve depolarizes from Ca channels which releases ACh
Postsynaptic nerve has ACh receptors which activate Na channels that lead to action potential
motor end plate, nicotinic AChr require two ACh or one succinylcholine molecule (which is 2x ACh attached by acetate methyl), these bind at the alpha subunits
what is prochlorperazine moa and use? what are risks and subsequent treatment?
antidopaminergic, can be used for nausea
risk of dystonia (facial/neck spasms)/extrapyramidal symptoms, treatment is diphenhydramine or benztropine
what is the pathway of pain signaling
1st order = transduction to dorsal horn
2nd order = dorsal horn decussate to contralateral spinothalamic tract and ascends to thalamus
3rd order = thalamus to postcentral gyrus