First Aid Pharma Flashcards
-mixed w/ Sketchy Pharm for: antipsychotics and antidepressants
Sympathetic nervous system altering agents used in tx of glaucoma
- Alpha-agonists
- Epinephrine (alpha1) or brimonidine (alpha2) - Beta-blockers: Timolol, betaxolol, carteolol
Work to decrease aqueous humor synthesis
Diuretic used in the tx of glaucoma
Acetazolamide (works at PCT): carbonic anhydrase inhibitor to decrease aqueous humor production
Name two classes of drugs that increase outflow of aqueous humor in the tx of glaucoma
Increase aqueous humor outflow
- Cholinomimetics (pilocarpine, physostigmine): cause contraction of ciliary muscle and opening of trabecular muscle
- Prostaglandin F2alpha = Latanoprost
Mechanism of
(a) Loperamide
Mechanism of
(a) loperamide = immodium = opioid receptor agonist but specific to the gut
Mechanism of fentanyl
Fentanyl = opioid, works opioid receptors: opens K+ channels, closes Ca2+ channels => reduces synaptic transmission
2 Indications for opioids in addition to pain
- Diarrhea: loperamide = opioid w/o intestinal or CNS penetration, so just works to slow down gut w/o CNS effects
- maintenance for heroin addition (methadone, bupreorphine)
Mechanism of tramadol
Tramadol: “tram it all” so works on multiple nt
- agonist of mu-opioid receptor
- inhibits 5-HT and NE
- used for tx of chronic pain
First line drug for absence seizures
(a) Mechanism
Ethosuximide ‘sux to have silent seizures’
(a) Ethosuximide works by blocking thalamic T-type Ca2+ channels
First line anti-epileptic agent for
(a) Acute status epilepticus
(b) Ppx of status epilepticus
(c) Partial seizures
First line AED for
(a) Acute status = benzos!! Get that GABA action pumping
(b) Ppx for status = Phenytoin (inhibits Na+ channel)
(c) Partial seizures, both simple and complex, first line is carbamazepine (Na channel inhibitor)
AED used for both partial seizures and nerve pain
(a) Mechanism
Gabapendin: tx peripheral neuralgia and partial seizures (both simple and complex)
-not for generalized seizures
(a) Gabapending inhibits high-voltage-activated Ca2+ channels
AED that can also be used to tx bipolar d/o
(a) Mechanism
Valproate used to tx bipolar d/o and seizures: partial (both simple and complex) and GTC
(a) Valproate inhibits Na+ channels and increases GABA concentration by decreasing breakdown
AED that is first line in neonates
(a) Mechanism
Phenobarbital (barbiturate) is first line in neonates for partial (simple and complex) seizures and GTC
(a) Phenobarb increases GABA-A action (same as benzos)
Which AED must be titrated slowly 2/2 risk of Stevens-Johnsons?
Many AEDS carry risk of SJS (ethosuximibe, phenytoin, carbamazepine) but Lamotrigine has super high risk
Lamotrigine has to be titrated slowly
Differentiate mechanism of barbiturates and benzodiazepines
Both barbs and benzos bind to GABA-A receptor (at dif sites) but agonize receptor by increasing duration of Cl- channel opening vs. increasing frequency of opening
Barbs increase duration of Cl- channel opening
Tx of barbiturates vs. benzodiazepine OD
Benzo OD can be tx w/ Flumazenil which is a selective benzo receptor antagonist
-competitive inhibitor of benzo binding site on GABA-A receptor
Barbiturate OD tx is just supportive (assist respiration and maintain BP)
Explain the effect of blood and lipid solubility for anesthetics
The lower the blood solubility, the faster the induction and faster the recovery time
Higher lipid solubility = higher potency b/c more crosses the BBB
Main indication for thiopental
Thiopental = barbiturate IV anesthetic
-high potency and high lipid solubility (meaning it rapidly enters the brain), so used for induction of anesthesia and short surgical procedures
MC anesthetic used for endoscopy
Midazolam (benzo) = MC drug used for endoscopy
-can be used adjunctively w/ gaseous/inhaled anesthetics (isoflurane, N2O) and narcotics
Mechanism of ketamine
Ketamine = PCP analog that blocks NMDA receptors
-used as dissociative anesthetic
Mechanism of lidocaine as a local anesthetic
Lidocaine = amide that blocks Na+ channels (preferentially activated Na+ channels => most effective in rapidly firing neurons)
Depolarizing vs. nondepolarizing neuromuscular blocking agnets
Depolarizing (succinylcholine) are strong ACh receptor agonists that produce sustained depolarization to prevent muscle contraction
Nondepolarizing (vecuronium, rocuronium) competes w/ ACh for receptor (competitive antagonist for receptor)
Describe the tolerance developed by chronic opioid use
Tolerance meaning need higher dose of opioids for analgesia, BUT tolerance does NOT develop to mioisis and constipation!!!
So constipation is a chronic side effect!! Doesn’t subside
Differentiate how dantrolene and baclofen prevent muscle contraction
Dantrolene prevents Ca2+ release from SR of skeletal muscle
-used in malignant hyperthermia and NMS
Baclofen inhibits GABA-B receptors at the level of the spinal cord => causes skeletal muscle relaxation
-for muscle spasms
Differentiate nt imbalance in
(a) Parkinsons
(b) Huntingtons
Neurotransmitter imbalance
(a) Parkinsons 2/2 loss of dopamine innervation in nigrostriatal pathway and excess ACh tone
(b) Huntingtons 2/2 increased DA, reduced GABA and reduced ACh
Mechanism of Ropinirole
(a) Indication in addition to Parkinsons
(b) Risk of Ropinorole
Ropinirole = non-ergot Dopamine2 receptor agonist
a) First line tx for restless leg syndrome
(b) Can worsen impulse control d/o (gambling, shopping, hypersexuality
What side effects does carbidopa help reduce when added to Levodopa
Carbidopa reduces side effects seen 2/2 increased peripheral DA (b/c inhibits peripheral DOPA decarboxylase)
Decreases GI symptoms (N,V), cardiac arrhythmias, and orthostatic hypotension
Doesn’t relieve the central neuropsychiatric side effects of anxiety, agitation
When to add selegiline to Parkinsons tx regimen
Selegiline = selective MAO-B inhibitor to decreased central degradation of DA, used in adjunct to L-dopa therapy (not alone!)
-helps w/ the wearing off and on-off phenomenon of L-dopa therapy
Name the positive and negative symptoms of schizophrenia
Schizophrenia
Positive symptoms: hallucinations, delusions, disorganized thoughts and behaviors
Negative symptoms: apathy, flat affect, lack of energy
Differentiate high potency vs. low potency typical antipsychotics
High potency typicals = Haloperidol, Trifluoperazine, Fluphenazine
- high affinity for D2 receptor => greater risk of EPS
- but less anti alpha1, anti-H1, and anti-muscarinic effects
Low potency typicals = Chlorpromazine, Thioridazine
-lower affinity for D2 receptor (so lower risk of EPS), but more anti-alpha1 (ortho hypo), anti-H1 (sedation), and anti-muscarinic effects
Main distinction btwn first gen (typical) and second gen (atypical) antipsychotics
Typicals exert effect mainly on positive symptoms of schizophrenia by D2 receptor blockade- higher risk of EPS, hyperprolactinemia, ortho hypo, sedation
While atypicals weakly antagonize D2, but potently inhibit 5-HT2A => tx both the negative and positive symptoms of schizophrenia w/ smaller risk of the above side effects
Explain the three groups of side effects of low potency antipsychotics
Low potency antipsychotics (chlorpromazine and thioridazine) exert effect by D2 receptor blockade to tx positive symptoms of schizophrenia
- anti-alpha1 effects => orthostatic hypotension
- anti-H1 effects centrally => sedation
- anti-muscarinic effects => dry mouth, constipation, blurred vision, urinary retention
Name the 4 movement effects seen as a side effect of high potency typical antipsychotic use in the order in which they arise
High potency typical antipsychotics (haloperidol, trifluperazine, fluphenazine) carry greatest risk of EPS
1st get acute dystonia (sustained muscle contraction, ex: torticollis) w/in hours
W/in days get akathisia (subjective motor restlessness)
W/in days to weeks see symptoms of drug-induced Parkinsonism
W/in months to years see tardive dyskinesia- mainly oral-facial dyskinesias (tongue/lip smacking)
Explain how haloperidol can cause amenorrhea
Haloperidol = high potency typical antipsychotic w/ D2 receptor antagonism
D2 receptor blockade in the tuberoinfundibular pathway removes the tonic inhibition of dopamien on prolactin => hyperprolactinemia
-high prolactin suppresses GnRH levels => reduced LH/FSH => amenorrhea
Clinical picture of NMS
(a) How to distinguish from serotonin syndrome
Neuroleptic malignant syndrome: ‘lead pipe’ rigidity, hyperpyrexia (like super high fever), altered mental status, autonomic instability (tachycardia), rhabdo
(a) NMS is 2/2 too much DA blockade: see hyporeflexia and muscle rigidity
- while serotonin syndrome (2/2 excess 5-HT agonism) see similar presentation (hyperpyrexia, AMS, autonomic instability) except w/ hyperreflexia and clonus
EKG abnormality seen in typical vs. atypical antipsychotics
Both typical and atypicals can prolong QT => increased risk of Torsades and ventricular arrhythmias
Differentiate the ocular findings seen in chlorpromazine vs. thioridazine therapy
2 low potency typical antipsychotics
Chlorpromazine => corneal deposits
Thioridazien => retinal deposits