Study Guide for Week 1:
Principles of Pharmacology & Labs in Psychiatry
Pharmacokinetics
• Study of drug absorption, distribution, metabolism, and excretion
o Absorption: enters bloodstream
 affected by formulation, route of administration, gastrointestinal health, etc.
o Distribution: spreads through body tissues and fluids
 influenced by protein binding, lipophilicity, and blood flow
o Metabolism: broken down, primarily in the liver by enzymes (cytochrome P450 system),
converting to active or inactive forms
o Excretion: removed from the body, primarily through the kidneys (urine) or liver (bile/feces)
➢ Ex:
▪ Bioavailability: fraction of a drug reaching systemic circulation
▪ Half-life: time for the drug concentration to decrease by half
▪ Clearance: rate at which a drug is eliminated from the body
▪ Other factors (age, genetics, and organ function altering drug metabolism)
Pharmacodynamics
• Study of how drugs produce effects on the body, mechanisms involved
o Receptor Binding: interaction with specific receptors to produce effects (agonists activate,
antagonists block)
o Dose-Response Relationship: relationship between drug dose and magnitude of response
(efficacy and potency)
o Therapeutic Index: ratio of toxic dose to therapeutic dose, indicates drug safety
o Adverse Effects: unwanted effects caused by drug action on unintended targets or
pathways
➢ Ex:
▪ Variability: differences in drug effects based on individual factors (genetics, age)
▪ Tolerance: reduced effect of a drug over time requiring higher doses
▪ Sensitivity: increased susceptibility to a drug's effects in specific populations
Tmax
Time to reach its maximum concentration (Cmax) in bloodstream after administration
Indicates rate of absorption and onset of action
➢ Ex:
▪ Short Tmax: desired for rapid-relief drugs (painkillers or sedatives)
▪ Affected by formulation: IR vs. ER
▪ RoA: Oral, intravenous, or transdermal
•
•
Cmax
•
•
➢
Maximum concentration achieved in the bloodstream after administration
Reflects extent of absorption, correlates with therapeutic and toxic effects
Ex:
▪ High Cmax: increases efficacy but raises the risk of side effects
▪ Useful in assessing peak-related toxicities like QT prolongation
Cmin
•
•
➢
Lowest concentration in the bloodstream, typically measured just before the next dose
Ensures therapeutic activity during dosing interval
Ex:
▪ Used to monitor drugs with narrow therapeutic windows like lithium or warfarin
▪ Prevents subtherapeutic levels or accumulation-related toxicity
AUC (Area Under the Curve)
• Represents total exposure over time, calculated from concentration-time graph
• Indicates extent of drug absorption and systemic availability
➢ Ex:
▪ Higher AUC: greater drug exposure, possibly indicating efficacy or toxicity
▪ Useful for comparing different formulations or administration routes
NNT (Number Needed to Treat)
• Average number of patients who need to be treated for one patient to benefit
➢ Ex:
▪ If NNT is 5, treating 5 patients results in 1 additional positive outcome
▪ Lower NNT indicates higher treatment efficacy
NNH (Number Needed to Harm)
• Measure to estimate number of patients (average) would need to be treated with an intervention or
medication for one patient to experience a harmful side effect
o Quantify the risk of an adverse outcome associated with a treatment
➢ Ex:
▪ If NNH is 50, one in 50 patients will experience harm
▪ Higher NNH indicates a safer treatment
Volume of Distribution (Vd)
• Theoretical volume required to contain a drug at the same concentration as in plasma
• Reflects how extensively a drug spreads into tissues versus remaining in plasma
➢ Ex:
▪ High Vd: Extensive tissue distribution (lipophilic drugs)
▪ Low Vd: Drug remains mostly in plasma
▪ Used to predict loading doses and drug concentrations
Active Metabolite
• Metabolized form of a drug that retains pharmacological activity
• Contributes to therapeutic or adverse effects of the parent drug
➢ Ex:
▪ Codeine metabolized to morphine, which provides analgesic effects
▪ Monitoring metabolites important for drugs with delayed or prolonged effects
Substrate
• Drug or compound metabolized by a specific enzyme system, such as cytochrome P450 enzymes
• Susceptible to drug-drug interactions if the enzyme is inhibited (slowing metabolism) or induced
(speeding metabolism)
➢
Ex:
▪
Warfarin metabolized by CYP2C9; inhibitors like fluconazole can increase bleeding risk
Effect Size
• Quantitative measure of the strength or magnitude of a drug’s therapeutic effect
• Commonly used in clinical trials to compare treatments
➢ Ex:
▪ Larger effect sizes indicate stronger treatment benefits
▪ Helps assess clinical relevance beyond statistical significance
1) Explain the concept of a drug’s half-life.
Time required for the concentration of a drug in the bloodstream to decrease by half, a pharmacokinetic parameter
that influences dosing and behavior in the body which varies from person to person, determined by how quickly
each person metabolizes and eliminates.
a) Why is this important to understand as a budding psychopharmacologist (think: dosing, withdrawal,
steady state, serum levels)?
▪ Dosing Schedule: predict frequency and minimize side effects
o helps determine the frequency of dosing to maintain therapeutic effects while
minimizing side effects, especially for drugs with narrow therapeutic windows
▪ Withdrawal Management: preventing withdrawal and switching medications
o helps to predict the likelihood and severity of withdrawal symptoms when stopping the
medication and guides appropriate tapering schedules
▪ Achieving Steady State: therapeutic and monitoring timing
o efficacy It takes ~ 5 half-lives to reach steady state, which is essential for consistent
therapeutic effects and for determining when to check serum drug levels for monitoring
▪ Serum Levels: avoiding toxicity and personalized medicine
o awareness of half-life informs expectations for peak and trough serum levels, helping to
prevent toxicity or subtherapeutic effects through proper dose adjustments
2) What is the relevance of lipid solubility in prescribing psychiatric medications? (Aiken Ch. 3)
• Crossing blood-brain barrier: Lipid-soluble drugs penetrate brain effectively by crossing bloodbrain barrier, essential for psychiatric effects
• Onset of action: High lipid solubility enables rapid absorption into brain, leading to faster
therapeutic effects in acute conditions
• Volume of distribution: Widely distributed in tissues, including fat, resulting in prolonged half-life
and infrequent dosing schedules
• Clearance and accumulation: Tendency to accumulate in fat stores, leading to slower clearance,
requiring cautious dosing and monitoring to avoid toxicity
• Drug interactions and side effects: Heavily metabolized by liver enzymes (CYP450 system),
increasing risk of interactions and side effects, especially with polypharmacy
3) What does the liver do to our medications (explain biotransformation/hepatic metabolism)?
Role of the liver:
Processes medications → transforms into water-soluble forms for excretion
• Detoxifies substances → reduces toxicity or converts to active/inactive metabolites
Phases of Hepatic Metabolism
Phase I Reactions (Functionalization)
o Oxidation, reduction, hydrolysis → modify drug molecules
o Involves cytochrome P450 enzymes (CYP450) → adds or exposes functional groups (e.g.,
hydroxyl, amino)
o Converts lipophilic drugs → polar compounds for excretion or prepares for Phase II
o Possible outcomes: active, inactive, or toxic metabolites
Phase II Reactions (Conjugation)
o Adds polar molecules → increases water solubility
o Examples: glucuronidation, sulfation, acetylation
o Often follows Phase I → ensures efficient renal or biliary excretion
Factors Influencing Hepatic Metabolism
• Enzyme induction (rifampin, carbamazepine) → increases metabolism → lowers drug levels
• Enzyme inhibition (fluoxetine, grapefruit juice) → slows metabolism → increases drug levels
• Age: neonates and elderly → reduced metabolism → slower clearance
• Genetics: polymorphisms in CYP enzymes → alter drug metabolism rates (poor or rapid
metabolizers)
• Liver disease: impaired enzyme activity and blood flow → slows metabolism
First-Pass Effect
• Oral drugs absorbed in GI tract → enter portal vein → pass through liver before systemic
circulation
• Extensive metabolism in liver → reduces bioavailability (propranolol, morphine)
Clinical Implications
➢ Adjust dosing for patients with liver impairment (cirrhosis, hepatitis)
➢ Select drugs with minimal hepatic metabolism if liver function compromised
➢ Monitor for drug interactions that affect CYP450 enzymes
➢ Understand genetic differences in metabolism for personalized treatment (pharmacogenetics)
3a) Which liver processes are more, or less affected by aging?
Processes Less Affected by Aging
• Phase II metabolism (conjugation reactions like glucuronidation, sulfation)
• Albumin production (declines modestly but not as significant)
• Hepatic blood flow (may remain sufficient in healthy individuals)
Processes More Affected by Aging
• Phase I metabolism (oxidation, reduction, hydrolysis in P450 enzymes)
o Slower drug clearance due to reduced enzymatic activity
▪ Greater half-life for drugs processed through Phase I (benzodiazepines like
diazepam)
o First-pass metabolism
▪ Reduced efficiency leading to higher bioavailability for drugs with high first-pass
effect (propranolol)
•
Hepatic blood flow in frail or ill elderly individuals
▪ Reduced perfusion affecting metabolism of high-extraction drugs
o Production of clotting factors
▪ May decline, increasing sensitivity to anticoagulants
Clinical Implications
➢ Avoid or reduce doses of Phase I-metabolized drugs in elderly patients
➢ Favor Phase II-metabolized drugs when possible (e.g., lorazepam, oxazepam)
➢ Monitor for prolonged drug effects or toxicity due to slowed metabolism
➢ Consider reduced first-pass metabolism when prescribing drugs with high bioavailability
changes in aging populations
o
4) Why do we care about CYP450 enzymes in psychopharmacology? (Aiken Ch. 10 & 17)
Role in Drug Metabolism
• CYP450 enzymes metabolize most psychotropic medications
• Affect drug clearance, serum levels, and therapeutic effects
• Key enzymes: CYP1A2, CYP2D6, CYP2C19, CYP3A4
Clinical Relevance
• Dosing Adjustments
o Enzyme activity varies by genetics (e.g., poor, intermediate, extensive, ultrarapid
metabolizers)
Poor metabolizers require lower doses; ultrarapid metabolizers need higher doses
• Drug-Drug Interactions
o Inhibitors increase drug levels by blocking metabolism (e.g., fluoxetine inhibits CYP2D6)
o Inducers decrease drug levels by speeding up metabolism (e.g., carbamazepine induces
CYP3A4)
• Prodrugs
o Prodrugs rely on CYP450 enzymes for activation (e.g., codeine, tamoxifen)
o Inhibitors can block activation, reducing therapeutic effects
•
Side Effects and Toxicity
o Impaired metabolism can lead to higher drug levels, increasing side effects (e.g., sedation,
QTc prolongation)
o Examples: Poor CYP2D6 metabolizers experience higher side effects with SSRIs and
antipsychotics
Pharmacogenetic Testing
• Identifies patient-specific enzyme activity
• Guides personalized medication selection and dosing
• Useful for drugs highly dependent on specific CYP450 enzymes (e.g., aripiprazole, tricyclics)
Clinical Implications
➢ Essential for understanding variability in drug response
➢ Helps avoid side effects, toxicity, and treatment failure
Critical in patients with multiple medications or complex conditions
Name the 6 CYP450 enzymes most commonly associated with psychotropics.
• CYP1A2, CYP2D6, CYP2C19, CYP2C9, CYP3A4, CYP2B6
Explain the relationship between smoking and CYPs.
• Smoking induces CYP1A2, increasing the metabolism of drugs metabolized by this enzyme
• Leads to lower drug levels for medications such as clozapine, olanzapine, and fluvoxamine
• Effect caused by polycyclic aromatic hydrocarbons in cigarette smoke, not nicotine
• Smoking cessation can reverse CYP1A2 induction, causing drug levels to rise
• Careful dose adjustments needed when patients start or stop smoking
What is an example of a food-drug interaction mediated by CYPs?
• Grapefruit juice inhibits CYP3A4 in the gut
• Leads to increased drug levels of medications metabolized by CYP3A4
o Examples: benzodiazepines, statins, calcium channel blockers
• Can cause toxicity (e.g., excessive sedation, muscle pain, or hypotension)
What is the difference between an inducer and an inhibitor?
• Inducers
o Increase the activity or production of CYP enzymes
o Result in faster drug metabolism
o Lower drug levels and potential loss of efficacy
➢ Example: Carbamazepine, St. John’s Wort, smoking
• Inhibitors
o Decrease the activity of CYP enzymes
o Result in slower drug metabolism
o Higher drug levels and potential toxicity
➢ Example: Fluoxetine, Grapefruit juice, Valproate
➢
a)
b)
c)
d)
5) What are your thoughts about pharmacogenetic testing – will you be using it in practice? Why
or why not? Under what circumstances? For which patients, or which medications?
Pharmacogenetic testing can be a valuable tool in certain circumstances, but it may not be something I
use routinely in practice due to limited proven benefits for most patients and a lack of strong evidence for
improved outcomes in all cases. However, I would consider using pharmacogenetic testing in specific
situations, such as when a patient has experienced multiple medication failures or severe side effects, or
in cases where medications with narrow therapeutic windows or significant variability are being
prescribed, such as warfarin or clozapine. It could also be helpful for patients with treatment-resistant
conditions like depression or anxiety or for those who have had unexplained poor responses or adverse
effects to standard treatments.
Pharmacogenetic testing may be particularly relevant for patients requiring high-risk medications, such as
antipsychotics or anticonvulsants, or for those with known genetic predispositions, like the HLA-B*1502
allele, which is associated with a higher risk of Stevens-Johnson syndrome when taking carbamazepine. It
is also useful for medications metabolized by polymorphic CYP enzymes, such as CYP2D6 or CYP2C19, or
for prodrugs like codeine and tamoxifen, where enzyme activity directly affects efficacy and safety.
Despite its potential benefits, I would approach pharmacogenetic testing cautiously and avoid overreliance on commercial testing panels that may lack robust validation. Instead, I would use evidencebased testing selectively and with specific goals in mind, rather than adopting broad, untargeted
approaches. By tailoring its use to high-risk or treatment-resistant cases, pharmacogenetic testing can
serve as a helpful adjunct to clinical decision-making, but it should not replace careful patient monitoring
and clinical judgment.
6) Explain the steps in the process of GI drug absorption and distribution. (Aiken Ch. 3) Where does most of
the absorption happen?
• Oral drugs swallowed → dissolve in stomach → form solution for absorption
• Solution moves to small intestine → primary site of absorption (large surface area, rich blood
supply, optimal pH)
• Passive diffusion through intestinal epithelial cells (lipid-soluble drugs) or active transport (watersoluble drugs) → enter bloodstream
• Bloodstream → portal vein → liver for first-pass metabolism (reduces bioavailability)
• Liver → systemic circulation → distribution to target tissues
a) Where most absorption happens
o Stomach → small intestine → large surface area (villi and microvilli) → efficient absorption
b) Routes bypassing hepatic metabolism
o Sublingual/buccal → absorbed via oral mucosa → direct venous drainage → systemic
circulation
o Rectal → lower rectum drains to systemic veins (bypasses liver partially); upper rectum →
portal vein → liver (first-pass metabolism)
c) Considerations for bariatric surgery patients
o Altered GI anatomy (e.g., smaller stomach, bypassed intestine) → reduced surface area for
absorption
o Reduced gastric acid → affects solubility and dissolution of acid-dependent drugs
o Shortened transit time → limits contact with absorption sites
o Use alternative forms: liquid formulations → crushable tablets → non-oral routes
o Monitor therapeutic level → adjust doses as needed
o Avoid extended-release formulations → altered transit impacts release mechanisms
7) Tell me what you know about excretion of medications (Aiken Ch. 9):
Primary Routes of Excretion
• Renal Excretion (Kidney): Main pathway for most medications and their metabolites. Drugs are
filtered through the glomerulus, secreted into renal tubules, and excreted in urine. Requires watersoluble forms for effective clearance
• Biliary/Fecal Excretion (Liver): Drugs are metabolized in the liver and excreted into bile, which
enters the gastrointestinal tract and is eliminated in feces. Important for lipid-soluble drugs
Key Renal Processes in Drug Excretion
• Filtration: Glomeruli filter small molecules like free (unbound) drugs into the urine. Protein-bound
drugs are not filtered
•
Reabsorption: Lipophilic drugs can be passively reabsorbed into the bloodstream in the renal
tubules. This process is minimized when drugs are converted to water-soluble metabolites
• Secretion: Active transport systems in the renal tubules move drugs from the blood into the urine
Factors Affecting Renal Excretion
• Kidney function (e.g., age-related decline, renal disease) impacts drug clearance
• pH of urine influences ionization and reabsorption of weak acids/bases
• Drug-drug interactions may affect tubular transport
Biliary Excretion and Enterohepatic Recycling
• Drugs excreted into bile may undergo enterohepatic recirculation, where they are reabsorbed in the
intestines and returned to the liver, prolonging their effects
• Impaired biliary excretion (e.g., liver disease) can lead to accumulation and toxicity.
Clinical Implications
➢ Adjust dosing for patients with renal or hepatic impairment
➢ Monitor renal function (e.g., GFR, creatinine) and liver enzymes to ensure safe drug clearance
➢ Be cautious with drugs heavily reliant on excretion, like lithium (renal) and hydroxyzine (biliary)
8) What are the advantages and disadvantages of various drug formulations? (A chart might be
helpful for this question.) For each, list a situation in which you would prescribe a given
formulation (e.g. ODT vs. tablet, IR vs. MR etc.).
FORMULATION
IMMEDIATE RELEASE (IR)
ADVANTAGES
o
o
Rapid onset of action
Easier titration of dosage
DISADVANTAGES
o
o
MODIFIED RELEASE (MR)
ORALLY
DISINTEGRATING
TABLETS (ODT)
o
o
o
o
o
o
Prolonged drug effect
Reduces dosing frequency
Lower risk of peak-related
side effects
Convenient for patients with
swallowing difficulties or
limited access to water
Rapid absorption
Useful for improving
adherence in psychiatric
conditions
o
o
o
o
WHEN TO USE
Requires frequent
dosing
Shorter duration
of action
o
Delayed onset
Potential for dose
dumping with
improper
administration
o
Limited
availability for
some
medications
May be more
expensive
o
o
o
o
Acute situations
(e.g., panic attack)
When short-term
effects are desired
Chronic conditions
(e.g., depression
requiring sustained
effects)
When adherence to
dosing schedule is a
concern
Patients with
dysphagia or when
water is unavailable
Children or geriatric
patients
LIQUID FORMULATIONS
o
o
o
INJECTABLES
o
o
o
PATCHES
(TRANSDERMAL)
o
o
Easy to administer for
pediatric or geriatric
populations
Allows flexible dosing
Useful for patients with
feeding tubes
o
o
Rapid onset of action (e.g.,
intramuscular)
Long-acting injectables
improve adherence
Steady plasma levels over
weeks to months
o
Sustained release over time
Avoids gastrointestinal
metabolism
o
o
o
SUBLINGUAL/BUCCAL
o
o
Rapid absorption through
mucosa
Avoids first-pass metabolism
o
o
Shorter shelf life
Difficult to
transport and
store
o
Invasive, requires
medical
administration
Risk of local
irritation or
infection
o
Limited drugs
available in this
form
Skin irritation
o
Taste may be
unpleasant
Limited availability
of drugs
o
o
o
o
o
Patients unable to
swallow tablets
Patients requiring
precise dosing
adjustments
Emergency
situations (e.g.,
agitation, psychosis)
Nonadherent
patients with chronic
conditions
Patients with
adherence issues or
GI intolerance
When steady drug
levels are important
Situations requiring
fast onset without
injections
Patients with GI
absorption issues
ODT: Use in nonadherent schizophrenic patients who avoid swallowing pills.
• MR: Prescribe for generalized anxiety disorder requiring steady medication levels.
• Liquid: Administer in pediatric ADHD patients needing titration.
• Injectables: Employ for patients with severe psychosis nonadherent to oral antipsychotics.
• Patches: Utilize in patients unable to tolerate GI side effects from oral medications.
Sustained Release (SR):
o Gradually releases the drug over time
o Reduces dosing frequency (e.g., once daily)
o Used for maintaining consistent blood levels in chronic conditions
Delayed Release (DR):
o Releases the drug at a specific location (e.g., intestine)
o Protects the drug from stomach acid or reduces gastric side effects
o Often used for acid-sensitive drugs or targeted delivery
•
9) Why do we order labs in psychiatry?
Labs are ordered to monitor medication safety, assess for potential side effects, and guide treatment
decisions. They help identify metabolic, liver, kidney, or thyroid dysfunctions that can mimic or exacerbate
psychiatric symptoms. Labs also track therapeutic drug levels and screen for substance use or medical
conditions affecting mental health.
10) Optional, but encouraged – make a chart of the components of a CBC, CMP, and UA. For
each, include a note about what an abnormal finding may indicate that could be relevant to psychiatry.
(see below)
11) Draw a table/chart about the common liver diseases seen in practice, the lab abnormalities
you would expect in each & their implication for prescribing.
Common Liver Diseases, Lab Abnormalities, and Prescribing Implications: alcohol liver disease, drug
induced liver injury, chronic hepatitis (hepatitis B/C), non-alcoholic fatty liver disease, cirrhosis
Liver Disease
Alcoholic Liver Disease
o
Lab Abnormalities
Elevated AST/ALT (AST/ALT
ratio >2:1)
Elevated GGT
Implications for Prescribing
o Typically, no dose adjustments
unless cirrhosis is present
o Avoid hepatotoxic drugs
o Consider oxazepam or lorazepam
for alcohol detox due to reduced
liver metabolism
Drug-Induced Liver
Injury
o
o
Elevated ALT/AST
Possible elevated bilirubin
Hepatitis B/C (chronic)
o
o
Mildly elevated ALT/AST
Chronic Hepatitis C: higher
likelihood of progression to
severe disease
o Discontinue offending drug
o Avoid reintroduction of the
offending drug
o No adjustments unless cirrhosis
is present
o Monitor hepatic function regularly
during treatment
Nonalcoholic Fatty Liver
Disease
o
Mildly elevated ALT/AST
(AST/ALT ratio <1)
Associated with obesity,
diabetes, and
hyperlipidemia
o
o
o No dose adjustments unless
cirrhosis is present
o Avoid weight-gain inducing
medications
Cirrhosis
o
o
o
o
Notes:
•
•
•
•
•
•
Mild AST/ALT elevation;
AST/ALT ratio >1
Elevated bilirubin
Low albumin, elevated
prothrombin time (PT)
Hypoalbuminemia leading to
higher free drug levels
o Adjust doses for medications
metabolized by the liver
o Avoid drugs with a high risk of
hepatotoxicity
o Avoid drugs that worsen hepatic
encephalopathy (benzodiazepines,
valproate)
o Use medications metabolized by
Phase II glucuronidation when
possible (lorazepam, oxazepam,
temazepam)
o Reduce doses of drugs with
prolonged half-lives in cirrhosis
(diazepam, zolpidem)
Avoid drugs with high hepatotoxic risk in all forms of liver disease (e.g., acetaminophen >3 g/day,
isoniazid, methotrexate, amiodarone)
Monitor liver enzymes regularly for patients on psychotropics with hepatic metabolism
Cirrhosis: always monitor liver function and adjust doses for drugs metabolized by the liver
Phase II metabolism (e.g., glucuronidation) is preserved in liver disease, making drugs like
lorazepam, oxazepam, and temazepam safer choices
Avoid valproate and disulfiram in cirrhosis due to high hepatotoxic risk and potential to worsen
encephalopathy
Lithium, gabapentin, and topiramate are preferred options in severe liver disease due to renal
excretion and minimal hepatic metabolism
12) Regarding urine drug screening (article, lab text), why do benzodiazepines & opioids frequently
have false negative results? What can you do if you suspect this?
False Negatives for Benzodiazepines and Opioids
Benzodiazepines and opioids often produce false negatives on urine drug screens due to differences in
drug metabolites and test specificity, as some immunoassays are not designed to detect certain
formulations or metabolites. If a false negative is suspected, confirmatory testing with gas
chromatography-mass spectrometry (GC-MS) or high-performance liquid chromatography (HPLC) can
provide accurate results.
False Positive Example
Bupropion is a psychiatric medication that can cause false positives for amphetamines on urine drug
screening, likely due to structural similarities between bupropion metabolites and amphetamine
compounds.
Use of Urine Drug Screenings in Practice
In practice, urine drug screenings will be used to monitor adherence to prescribed medications, detect
illicit substance use, and ensure safe prescribing practices, particularly before initiating medications like
stimulants or benzodiazepines. They will also aid in identifying potential substance use disorders and
guiding appropriate referrals for treatment.
13) Regarding iron deficiency (lecture, lab text):
What is the difference between iron deficiency without anemia, and iron deficiency
anemia? What is the difference between their symptoms?
Iron deficiency without anemia involves depleted iron stores but normal hemoglobin levels, often
presenting with fatigue and mild symptoms. Iron deficiency anemia occurs when iron depletion progresses
to reduced hemoglobin, leading to more pronounced symptoms like pallor, shortness of breath, and
dizziness.
Which populations of people are at risk for iron deficiency, and should therefore be
considered for routine screening?
Populations at higher risk include menstruating individuals, pregnant individuals, vegetarians/vegans,
those with chronic blood loss (e.g., gastrointestinal issues), infants/children, and older adults. These
groups may benefit from routine screening.
What labs would you order to assess iron deficiency, in which situations?
Initial labs include ferritin (low in early deficiency), serum iron, total iron-binding capacity (TIBC), and
transferrin saturation. A complete blood count (CBC) helps identify anemia if present. Use ferritin in earlystage deficiency and add CBC if symptoms suggest anemia.
The symptoms of iron deficiency might mimic which psychiatric conditions/diagnoses might?
Iron deficiency can mimic symptoms of depression (fatigue, low energy), anxiety (restlessness), and
attention-deficit disorders (poor concentration). Screening for iron deficiency is essential to rule out
physiological causes of psychiatric symptoms.
14) Regarding B vitamin deficiencies (lecture, lab text):
Why do you think we end up ordering these tests more often than other specialties?
Psychiatrists often order B vitamin tests because deficiencies in B12 or folate can mimic or exacerbate
psychiatric conditions like depression, cognitive impairment, or psychosis. These vitamins are critical for
neurological function, and addressing deficiencies can improve psychiatric symptoms.
What patient demographic factors and signs or symptoms would lead you to order a test for B12 and/or
folate?
Demographics: Older adults, vegetarians/vegans, individuals with malabsorption syndromes (e.g., celiac
disease, bariatric surgery), or those on medications like metformin or PPIs.
Symptoms: Fatigue, cognitive decline, memory issues, depression, neuropathy, or macrocytic anemia on
CBC results.
Which test(s) would you order if B12 or folate levels are borderline?
For borderline B12: Order methylmalonic acid (MMA) and homocysteine levels (both elevated in B12
deficiency). For borderline folate: Check homocysteine levels (elevated in folate deficiency).
15) Which psychiatric medications do we routinely check drug serum levels for?
Lithium: Monitor for therapeutic levels (typically 0.6–1.2 mEq/L), and prevent toxicity (above 1.5 mEq/L)
Valproate (Depakote): Target range 50–125 µg/mL, monitoring for efficacy and hepatotoxicity
Carbamazepine (Tegretol): Therapeutic range 4–12 µg/mL, monitoring for toxicity and interactions
Clozapine: Check levels to assess adherence, efficacy, and risk for agranulocytosis; therapeutic range
350–600 ng/mL
Tricyclic Antidepressants (TCAs): Monitor for therapeutic range (varies by medication) to avoid toxicity
16) Regarding medications in the perinatal period: (podcasts, lecture, resources, article)
Why is the first trimester a particularly vulnerable time?
• Organs form during weeks 3–8 (organogenesis), making the fetus highly susceptible to teratogens
• Teratogens can lead to congenital malformations
What are the 3 questions to consider when deciding whether or not to use a medication during pregnancy?
• What are the risks of untreated illness to the mother and fetus?
• What are the risks of medication exposure to the fetus?
• Are there safer alternatives or non-pharmacological interventions available?
What is relative infant dose (RID) and when/why does it matter?
• The percentage of maternal medication dose transferred to the infant via breast milk
• Important for assessing medication safety during breastfeeding; RID <10% is generally considered
low risk
Why did the FDA do away with pregnancy category ratings for medications?
• Categories (A, B, C, D, X) were oversimplified and often misleading
• Replaced by narrative summaries to provide more nuanced, evidence-based information
Where can you find information on the safety of medications in the perinatal period?
• LactMed Database (National Library of Medicine)
• MotherToBaby (Organization of Teratology Information Specialists)
1) Explain the steps in the process of GI drug absorption and distribution. (Aiken Ch. 3)
• Oral drugs swallowed → dissolve in stomach → form solution for absorption
• Solution moves to small intestine → primary site of absorption (large surface area, rich blood
supply, optimal pH)
• Passive diffusion through intestinal epithelial cells (lipid-soluble drugs) or active transport (watersoluble drugs) → enter bloodstream
• Bloodstream → portal vein → liver for first-pass metabolism (reduces bioavailability)
• Liver → systemic circulation → distribution to target tissues
d) Where most absorption happens
o Stomach → small intestine → large surface area (villi and microvilli) → efficient absorption
e) Routes bypassing hepatic metabolism
o Sublingual/buccal → absorbed via oral mucosa → direct venous drainage → systemic
circulation
o Rectal → lower rectum drains to systemic veins (bypasses liver partially); upper rectum →
portal vein → liver (first-pass metabolism)
f)
Considerations for bariatric surgery patients
o Altered GI anatomy (e.g., smaller stomach, bypassed intestine) → reduced surface area for
absorption
o Reduced gastric acid → affects solubility and dissolution of acid-dependent drugs
o Shortened transit time → limits contact with absorption sites
o Use alternative forms: liquid formulations → crushable tablets → non-oral routes
o Monitor therapeutic level → adjust doses as needed
o Avoid extended-release formulations → altered transit impacts release mechanisms