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Pharm 2

Terms in this set (17)

Pt is being intubated and anesthesiologist notices m. fasciculations/ pain & hyperkalemia, eventually leading to paralysis. What are these AE for? MOA & Use of that drug?
succinylcholine

MOA: noncompetitive blockade of Na+ channels (binds to Nm causing depolarization, but then stays bound so ACh can't bind. Usually degraded by plasma esterases but some pts may be def resulting in prolonged paralysis.

Use: Intubation
*What NT do each of the following R respond to?

-Nm at NMJ
-Nn in SNS ganglia
-at SNS effector organ
-Nn in PNS ganglia
-M at PNS effector organ
*-M at SNS sweat gland
-Nm of somatic : Ach (@motor end plate of skeletal m. )

-Nn in SNS ganglia: Ach (paravertbrl gang & adrenal medulla)

-alpha1,2, beta1 of smooth m. SNS: NE
-D1 SNS renal/mesentrc vasc: DA

-Nn in PNS ganglia: responds Ach

-M at PNS effector organ: Ach

-M at SNS sweat gland : Ach
*You want to intubate a pt, or maintain them on ventilation. What drug will you use? How will you reverse these effects after?
roCURonium which is a nondepolarizing COMP Nm antag so Ach can't bind.

Reverse effects by increasing Ach at NMJ via AchE Inhib
You want to sedate a pt for surgery. What drug use? MOA? How are you going to reverse the affects after the surgery?
Succinylcholine which is a depolarizing NONcomp inhibitor of ACh.
MOA: AChE can't break down succinylcholine so it stays bound to Nm R causing Na+ channels to remain open :. na rush in K out

*AE: hyperkalemia, m. fasciculations before paralysis, malig hyperthermia
*Pt comes in with resting tremor, muscle rigidity, akathisia, akinesia, festination, aprosodia, dysarthria. What is the cause?
Disease: Parkinsons
Cause: DA neuron damage in substantia nigra :. dec DA in Nigrastriatal Path (mvmnt)

Pos sx:
-akathisia: involuntary mvmnts
-tremor at rest
-m. rigidity

Neg sx:
-festination: poor postural stability do move feet fast to keep them under you
-aprosodia: no emotion in voice
-dysarthria: inability to speak loudly
-akinesia: no facial expression/blink
-bradykinesia: slow gen of mvmnts
Pt comes in with constant feelings of depression along with diagnosed PTSD. You find that she has low levels of serotonin. What will you prescribe? And what are the AE you will notify the pt of?
SSRI (maybe Fluoxetine).
*AE: wt gain (5HT2C antag) & sexual dysfunc!!!!**

(these are most common reasons for non-compliance)
*Why prescribe benzo? MOA?
-allam, -pam
MOA: increase *FREQ* of Cl- channel opening (GABAa) in the pres of GABA (cause hyperpolarization of afferent & efferent)

Use: to reduce anxiety, seizures, as a m. relaxant, high doses are sedatives/anesth.

SE: ANTEROGRADE AMNESIA, sedation, risk of fall, resp depression (mostly just w/ depressant combos/ Iv admin), risk of tolerance/dep/withdrawal
**Anxiety signs & symptoms: (both acute & chronic)
[be able to differentiate]
Acute Anxiety sx: ie panic attack
- Tachy
-palpitations
-sweating
-chills
-trembling
-difficulty breathing
-dizzy
-tingling/numbness
-chest pain
-nausea
-stomach pain

Chronic Anxiety Sx: generalized anxiety
-Nervousness
-Restlessness
-Insomnia
-Plus acute Sx
Why prescribe Barbiturate? MOA?
MOA: keep Cl- channel open for longer dURation (GABAa)

Use: for sedation/anesthesia, tx status epilepticus, insomnia

AE: coma, resp depression

-don't need GABA pres
-unlike benzo, don't cause m. relax
-CYP450 enzyme inducer
*Pt comes in sedated/ obtunded after suicide attempt via OD on benzos. What med could use to tx?
Flumazenil is GABAa ANTAG :. blocks benzo effects
SE: can cause sz in pts dep on benzos
ALCOHOLIC

PT COMES IN WITH
BP= 220/110

AND OTHER SX SUGGESTIVE OF HF

ADMITTED AND GIVEN LASIX WITH
NITROPRUSSIDE

BP LOWERS, SEEM TO BE GETTING BETTER

NEXT DAY, PT :
CONFUSED/AGITATED
+
HAS A SEIZURE
this pt is going thru EtoH withdrawal & we should tx with benzo: Lorazepam or Oxezapam since likely to have liver damage and these are not met in liver

**EtOH withdrawal sx: sz, agitation, confusion, HTN, hyperthermia, nervousness, hallucinations
**Pt is given anesthesia for his surgery. It has a low B:G. what does this mean and what would you expect the potency, MAC50, and recovery to be like?
low B:G means more of anes in gas form so quick onset and quick recovery, but low potency :. high MAC50.

Important to note that this quick onset likely displaces O2 so once pt weened of this, they would want to increase pt O2 %. Also note, rapid acting agents are often used to initiate anesth, and longer acting agents are used to maintain anesthesia.

an example of fast acting is is N2O (nitrous oxide), and long acting/ potent is Halothane.
*pt being sedated with a balanced anesth (concoction) and all of a sudden started being agitated, having m. rigidity, increased CO2 levels, more rapid breathing, sweating and becomes very warm to touch. What may be the cause of this? What should the anesthesiologist give the pt to tx this??
This is Malignant Hyperthermia which is a hereditary disorder causing a ryanidine R mutation and sx present when given inhaled anesthetics (N2O, halothane, des/sevfluranes) and/or succinylcholine (NONcomp AcH inhib).

Tx with dantrolene which is a ryanidine R antag
**Pt is given a local anesthetic but onset is taking longer than expected. What may be some reasons for this?
*-pH change in tissue potentially from ischemia, acidosis, abscess, tumor. this changes the amount of anesth needed, onset, how affective. Local anesth are weak bases :. accept protons at low pHs, then become protonated and can't cross memb to get to target tissue. or if injected into target tissue that is basic, the WB is not going to get protonated/activated.
LOW pH = SLOWER ONSET (can combine anesth w/ bicarb to get more rapid onset)

-local blood flow (inc BF = dec duration)

-epi slows dist (bc vascoconstricts vessels :. keeps anesth in area and reduces absorp)
-do not do this is area w/ lim BS ie fingers, toes
42 y/o visibly intoxicated male presents to ED w/ stab wound to thigh. A decision is made to suture under local anesthesia only, the procedure is estimated to take 2 hours. Which anesthetic do you choose? What if he has severe liver damage from chronic ethanol consumption?
A. Procaine
b. Lidocaine
C.Ropivacaine
D. Sevoflurane
A. use an ester (one eye) local anesthetic NOT an amide (2 eyed) bc amides are met in liver :.. will accum in liver, whereas esters undergo plasma hydrolysis.

esters: -caines (1 eye) ie benzocaine
amides: -caines (2 eyes) ie Prilocaine

If he didnt have liver damage, use lidocaine over ropivacaine bc cheaper

D. is a general anesthetic
**Obese pt with chronic seizures (epilepsy). What would you want to prescribe for seizure management? MOA?
Since pt obese, would want to give antiepileptic drug (AED) that do not cause weight gain:
-zonisamide
-ethosuximide
-topiramate
MOA:
block- Na, Ca, Kainate R, glutamate AMPA
inhib- carbonic anyhdrase
inc- GABA
USE: tx focal & gen sz, obesity
AE: wt loss, glaucoma, met acidosis, urolithiasis
**Pt comes into ER with continous sz for over 5 minutes at a time (status epilepticus). what may have caused this? what are you going to tx with?
Sz can occur if:
-noncompliant w/ anticonvulsant, Benzos, EtOH w/drawal
-electrolyte imbalance (Na, Ca, inc K, Mg)
-drug toxicity (buproprion, lithium, tyramine (from MAOi) etc)

Order to tx:
1) Benzo (-zepam, -zolam) to break the sz
MOA: bind GABAa R to inc freq the Cl- channel is open
-Lorazepam is good option if have liver damage ( bc not met in liver (OTL))
- make sure monitor for resp depressn
2)Phenytoin to prevent recurrence
-monitor to catch potential arrythmia w/ Na blocker
3) need to determine underlying cause
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