How Blood-Brain Barrier Works: Tight junctions between endothelial cells,
prevents large, polar or protein-bound drugs from entering the CNS. Only lipid-
soluble, small, non-ionized drugs cross easily. Trick= “The brain is picky-likes
that are fat (lipid-soluble) and small.”
Ethosuximide MOA and why its preferred for absent seizures: Blocks T-
type calcium channels in thalamic neurons which prevents abnormal rhythmic
firing. Preferred for absent seizures because it specifically targets the thalamic
oscillations that cause absence seizures, unlike other drugs that affect multiple
systems->fewer side effects.
Explain ethosuximide moa to patient, the car analogy: “your brain cells
are like cars on a road. With absent seizures, the cars get stuck in a traffic loop.
Ethosuximide closes the faulty traffic light (T-type calcium channel), so traffic
flows normally again.”
Ezogabine MOA: Opens KCNQ potassium channels->stabilizes resting
membrane potential->reduces excitability. Trick: Think “Ezo= Easy flow of K+
out-> calms the neuron.”
Know gabapentin very well, the safety profile and how it doesn't
interact with other meds, know how higher doses is less effective and
doesn't get absorbed more by the GI, know that process well like 3-5
questions on gabapentin: Binds to alpha 2 subunit of voltage-gated calcium
channels, decreasing excitatory neurotransmitter release. Not metabolized by
the liver so no major drug interactions. Renally excreted. Uses saturable L-
amino acid transporter in gut->higher doses are NOT absorbed proportionally.
Example: 900mg absorbed better than 3600mg. Trick: “Gabapentin is like a bus-
> only so many seats (transporters). After that, the extra passengers (drug) just
don’t get on.”
Lamotrigine black box warning, skin rash, SJS, know signs: Severe rash-
> Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (TEN). Watch for rash,
fever, mucosal involvement (mouth/eyes). Trick: “Lamo=Lame rash risk”
Lamotrigine MOA: Blocks voltage-gated sodium channels, decreases
glutamate release.
The MOA questions were simple straight up, like how does this med
work.
Phenytoin side effects, I think question I had talked about gingival
hyperplasia.: Gingival hyperplasia (classic), ataxia, nystagmus, sedation,
hirsutism, coarse facial features. Assessment: ask about gum changes, dental
hygiene, unsteady gait, vision changes. Trick: “Phenytoin= Puffy gums+ shaky
steps”
Question was something along the lines of how would you assess if
your patient is having side effects or reaction to that drug.
Question on Gene mutation for Asian population that makes them
prone to SJS and TEN: HLA-B*1502 allele in Asian populations=increased risk
of SJS/TEN with carbamazepine, phenytoin, lamotrigine. Trick: “B= Bad blister
risk.”
Know induction of hepatic enzymes and inhibition, one increases the
drug effect and one decreases. Know which is which and how they
interact with other drugs like OC's and warfarin,etc.: Induction= speeds
up metabolism-> decreases drug levels/effects (e.g. carbamazepine, phenytoin,
,rifampin). Inhibition= slows metabolism-> increases drug levels/toxicity (e.g.
valproate, fluoxetine). Ex.: oral contraceptive=reduced efficacy with inducers.
Warfarin= risk of clotting with inducer or bleeding with inhibitor.
Monitor bicarb for topiramate, it asked what to monitor or why you
monitor bicarb.: Monitor bicarbonate-can cause metabolic acidosis. Trick:
“Top= Topples bicarb.”
All the questions about buspirone were on there.: MOA: Partial agonist a
5-HT1A receptors. Use: Generalized anxiety disorder (NOT for acute attacks).
Key: Takes 2-4 weeks, no sedation, no abuse potential.
FGA related gynecomastia was on the test: Side effect: Increases
prolactin=gynecomastia, galactorrhea. Tardive dyskinesia=most troublesome
because it’s irreversible. Long-term goal of FGA therapy= prevent relapse,
manage symptoms with lowest effective dose.
All Buproprion questions were on the test: MOA: Norepinephrine &
dopamine reuptake inhibitor (NDRI). Key points: No sexual side effects,
contraindicated in seizures & eating disorders.
Black box warning for antispychotics for adults was on there( risk for
death, cva, cognitive decline): Increased risk of stroke, CV events, and
death.
Know why TD is most troublesome, Irreversible and life threatening.
Primary goal of Long term therapy with FGA's.
The med combinations for weight loss, 2-3 questions on each of those.
Phenteramine/ Topiramate and the other combo. Know how they work
and which one is safe for which patient population.:
Phentermine/Topiramate (Qsymia): Phentermine= stimulant (decreases
appetite). Topiramate= anticonvulsant (Increases satiety). Avoid in pregnancy
(teratogenic).
Naltrexone/Bupropion (Contrave): Naltrexone= opioid antagonist. Bupropion=
antidepressant. Avoid in seizure disorder, opioid users.
1-2 questions about fexofenadine and grapefruit juice: grapefruit juice
decreases the absorption of fexofenadine.
Multiple questions about diphenhydramine, how its safe for sleep and
non-habit forming: sedating antihistamine, safe short-term for sleep. Not
habit forming (unlike benzos).
Cromlyn MOA: Mast cell stabilizer-prevents histamine release. Used in asthma
prevention, NOT ACUTE ATTACKS.
Montelukast MOA: Leukotriene receptor antagonist (blocks LTD4). Used for
asthma prophylaxis, allergic rhinitis. NOT FOR ACUTE ATTACKS.
All the meds from week 5 pretty much asked straight forward question
about the MOA.
Also asked when you would use each one, like preventative or for acute
settings.
💊 Phenazopyridine
Class: Urinary tract analgesic (NOT an antibiotic).
, MOA: Exerts a local anesthetic effect on the mucosa of the urinary tract, relieving
dysuria, urgency, frequency, and burning sensation.
Indication:
o Short-term relief of urinary tract discomfort (usually with a UTI).
o Always used in combination with antibiotics, not alone.
Dosing: Typically prescribed for ≤ 2 days while antibiotics start working.
⚠️ Key Teaching Points
Urine discoloration: Turns urine (and sometimes tears) bright orange/red → stains
clothing and contact lenses.
Side effects: GI upset, headache, rare hemolytic anemia or kidney/liver toxicity (with
prolonged use).
Contraindications:
o Renal impairment
o Hepatic impairment
Not for long-term use: Symptomatic relief only.
🦠 COVID-19 Treatment
Outpatient (high-risk): Nirmatrelvir/ritonavir (Paxlovid).
Hospitalized, O₂ required: Remdesivir ± dexamethasone.
Severe (on high-flow O₂/vent): Dexamethasone + immunomodulator (e.g., tocilizumab).
Key point: Monoclonal antibodies are variant-dependent and less used now.
👶 Palivizumab
Monoclonal antibody against RSV F protein.
Use: Prevention (not treatment) of RSV in high-risk infants (premature, congenital
heart/lung disease).
Trick: “Pal” protects babies from RSV.
💊 Oseltamivir
Class: Neuraminidase inhibitor.
MOA: Prevents release of new influenza virions from infected cells.
Use: Influenza A & B. Works best if started within 48 hrs of symptoms.
prevents large, polar or protein-bound drugs from entering the CNS. Only lipid-
soluble, small, non-ionized drugs cross easily. Trick= “The brain is picky-likes
that are fat (lipid-soluble) and small.”
Ethosuximide MOA and why its preferred for absent seizures: Blocks T-
type calcium channels in thalamic neurons which prevents abnormal rhythmic
firing. Preferred for absent seizures because it specifically targets the thalamic
oscillations that cause absence seizures, unlike other drugs that affect multiple
systems->fewer side effects.
Explain ethosuximide moa to patient, the car analogy: “your brain cells
are like cars on a road. With absent seizures, the cars get stuck in a traffic loop.
Ethosuximide closes the faulty traffic light (T-type calcium channel), so traffic
flows normally again.”
Ezogabine MOA: Opens KCNQ potassium channels->stabilizes resting
membrane potential->reduces excitability. Trick: Think “Ezo= Easy flow of K+
out-> calms the neuron.”
Know gabapentin very well, the safety profile and how it doesn't
interact with other meds, know how higher doses is less effective and
doesn't get absorbed more by the GI, know that process well like 3-5
questions on gabapentin: Binds to alpha 2 subunit of voltage-gated calcium
channels, decreasing excitatory neurotransmitter release. Not metabolized by
the liver so no major drug interactions. Renally excreted. Uses saturable L-
amino acid transporter in gut->higher doses are NOT absorbed proportionally.
Example: 900mg absorbed better than 3600mg. Trick: “Gabapentin is like a bus-
> only so many seats (transporters). After that, the extra passengers (drug) just
don’t get on.”
Lamotrigine black box warning, skin rash, SJS, know signs: Severe rash-
> Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (TEN). Watch for rash,
fever, mucosal involvement (mouth/eyes). Trick: “Lamo=Lame rash risk”
Lamotrigine MOA: Blocks voltage-gated sodium channels, decreases
glutamate release.
The MOA questions were simple straight up, like how does this med
work.
Phenytoin side effects, I think question I had talked about gingival
hyperplasia.: Gingival hyperplasia (classic), ataxia, nystagmus, sedation,
hirsutism, coarse facial features. Assessment: ask about gum changes, dental
hygiene, unsteady gait, vision changes. Trick: “Phenytoin= Puffy gums+ shaky
steps”
Question was something along the lines of how would you assess if
your patient is having side effects or reaction to that drug.
Question on Gene mutation for Asian population that makes them
prone to SJS and TEN: HLA-B*1502 allele in Asian populations=increased risk
of SJS/TEN with carbamazepine, phenytoin, lamotrigine. Trick: “B= Bad blister
risk.”
Know induction of hepatic enzymes and inhibition, one increases the
drug effect and one decreases. Know which is which and how they
interact with other drugs like OC's and warfarin,etc.: Induction= speeds
up metabolism-> decreases drug levels/effects (e.g. carbamazepine, phenytoin,
,rifampin). Inhibition= slows metabolism-> increases drug levels/toxicity (e.g.
valproate, fluoxetine). Ex.: oral contraceptive=reduced efficacy with inducers.
Warfarin= risk of clotting with inducer or bleeding with inhibitor.
Monitor bicarb for topiramate, it asked what to monitor or why you
monitor bicarb.: Monitor bicarbonate-can cause metabolic acidosis. Trick:
“Top= Topples bicarb.”
All the questions about buspirone were on there.: MOA: Partial agonist a
5-HT1A receptors. Use: Generalized anxiety disorder (NOT for acute attacks).
Key: Takes 2-4 weeks, no sedation, no abuse potential.
FGA related gynecomastia was on the test: Side effect: Increases
prolactin=gynecomastia, galactorrhea. Tardive dyskinesia=most troublesome
because it’s irreversible. Long-term goal of FGA therapy= prevent relapse,
manage symptoms with lowest effective dose.
All Buproprion questions were on the test: MOA: Norepinephrine &
dopamine reuptake inhibitor (NDRI). Key points: No sexual side effects,
contraindicated in seizures & eating disorders.
Black box warning for antispychotics for adults was on there( risk for
death, cva, cognitive decline): Increased risk of stroke, CV events, and
death.
Know why TD is most troublesome, Irreversible and life threatening.
Primary goal of Long term therapy with FGA's.
The med combinations for weight loss, 2-3 questions on each of those.
Phenteramine/ Topiramate and the other combo. Know how they work
and which one is safe for which patient population.:
Phentermine/Topiramate (Qsymia): Phentermine= stimulant (decreases
appetite). Topiramate= anticonvulsant (Increases satiety). Avoid in pregnancy
(teratogenic).
Naltrexone/Bupropion (Contrave): Naltrexone= opioid antagonist. Bupropion=
antidepressant. Avoid in seizure disorder, opioid users.
1-2 questions about fexofenadine and grapefruit juice: grapefruit juice
decreases the absorption of fexofenadine.
Multiple questions about diphenhydramine, how its safe for sleep and
non-habit forming: sedating antihistamine, safe short-term for sleep. Not
habit forming (unlike benzos).
Cromlyn MOA: Mast cell stabilizer-prevents histamine release. Used in asthma
prevention, NOT ACUTE ATTACKS.
Montelukast MOA: Leukotriene receptor antagonist (blocks LTD4). Used for
asthma prophylaxis, allergic rhinitis. NOT FOR ACUTE ATTACKS.
All the meds from week 5 pretty much asked straight forward question
about the MOA.
Also asked when you would use each one, like preventative or for acute
settings.
💊 Phenazopyridine
Class: Urinary tract analgesic (NOT an antibiotic).
, MOA: Exerts a local anesthetic effect on the mucosa of the urinary tract, relieving
dysuria, urgency, frequency, and burning sensation.
Indication:
o Short-term relief of urinary tract discomfort (usually with a UTI).
o Always used in combination with antibiotics, not alone.
Dosing: Typically prescribed for ≤ 2 days while antibiotics start working.
⚠️ Key Teaching Points
Urine discoloration: Turns urine (and sometimes tears) bright orange/red → stains
clothing and contact lenses.
Side effects: GI upset, headache, rare hemolytic anemia or kidney/liver toxicity (with
prolonged use).
Contraindications:
o Renal impairment
o Hepatic impairment
Not for long-term use: Symptomatic relief only.
🦠 COVID-19 Treatment
Outpatient (high-risk): Nirmatrelvir/ritonavir (Paxlovid).
Hospitalized, O₂ required: Remdesivir ± dexamethasone.
Severe (on high-flow O₂/vent): Dexamethasone + immunomodulator (e.g., tocilizumab).
Key point: Monoclonal antibodies are variant-dependent and less used now.
👶 Palivizumab
Monoclonal antibody against RSV F protein.
Use: Prevention (not treatment) of RSV in high-risk infants (premature, congenital
heart/lung disease).
Trick: “Pal” protects babies from RSV.
💊 Oseltamivir
Class: Neuraminidase inhibitor.
MOA: Prevents release of new influenza virions from infected cells.
Use: Influenza A & B. Works best if started within 48 hrs of symptoms.
