PHARMACOLOGY
Anti-Inflammatory
Immune and inflammatory responses protect the body from invading foreign substances.
Certain drug classes can modify these responses:
Antihistamines block the effects of histamine on target tissues.
Corticosteroids suppress immune responses and reduce inflammation.
Uricosurics control the occurrence of gouty arthritis attacks.
Anti-Histamines
Antihistamines primarily block histamine effects in immediate (type I) hypersensitivity reactions (allergic reactions).
Availability: alone or in combination products; prescription or over-the-counter.
H1 receptor antagonists: drugs that act as histamine-1 (H1) receptor antagonists; they compete with histamine for H1-receptor sites throughout the body but do not displace histamines already bound to receptors.
Pharmacokinetics (PK): H1-receptor antagonists are absorbed well after oral or parenteral administration; some can be given rectally.
Distribution: with the exception of loratadine and desloratadine, antihistamines are distributed widely throughout the body and CNS.
Non-sedating antihistamines: fexofenadine, desloratadine, and loratadine; because they minimally penetrate the blood–brain barrier, they are not widely distributed in the CNS and produce fewer sedative effects.
Pharmacodynamics (PD): H1 antagonists compete with histamine for H1 receptors on effector cells, blocking histamine from producing its effects.
Pharmacotherapeutics: used to treat signs and symptoms of type I hypersensitivity reactions, such as:
allergic rhinitis (runny nose and itchy eyes)
vasomotor rhinitis (rhinitis not caused by allergy or infection)
allergic conjunctivitis (eye membranes)
urticaria (hives)
angioedema (submucosal swelling in hands, face, feet)
Drug interactions:
May block/reverse vasopressor effects of epinephrine, causing vasodilation, increased HR, and dangerously low BP at certain doses.
May mask toxic signs of ototoxicity with aminoglycosides or with high doses of salicylates.
May increase sedative and respiratory depressant effects of CNS depressants (tranquilizers, alcohol).
Loratadine may cause serious cardiac effects when taken with macrolide antibiotics (e.g., erythromycin), fluconazole, ketoconazole, itraconazole, miconazole, cimetidine, ciprofloxacin, and clarithromycin.
Adverse reactions:
Most common adverse reaction (except for fexofenadine, loratadine, desloratadine) is CNS depression.
Other CNS effects: dizziness, fatigue, disturbed coordination, muscle weakness.
GI effects: epigastric distress, loss of appetite, nausea/vomiting, constipation, diarrhea, dry mouth/nose/throat.
Nursing considerations (highlights):
Take with meals or snacks to prevent GI upset.
Avoid caffeine, nicotine, and alcohol.
Use warm water rinses, artificial saliva, ice chips, or sugarless gum/candy for dry mouth.
If used for motion sickness, take 30 minutes before travel.
Avoid hazardous activities until CNS effects are known.
Seek medical approval before using alcohol, tranquilizers, sedatives, pain relievers, or sleeping medications.
Stop taking antihistamines 4 days before diagnostic skin tests to preserve accuracy.
Notify prescriber if tolerance develops (a different antihistamine may be needed).
Photosensitivity risk; use sunblock or protective clothing.
Avoid using other products containing diphenhydramine (OTC or topical) during breast-feeding due to risk of adverse reactions.
For insomnia, administer 20 minutes before typical sleep hours.
Corticosteroids
Corticosteroids suppress immune responses and reduce inflammation. They are available as natural or synthetic steroids.
Classifications:
Natural corticosteroids are hormones produced by the adrenal cortex.
Most corticosteroid drugs are synthetic analogues.
Classified by biological activities:
Glucocorticoids (affect carbohydrate, fat, and protein metabolism).
Mineralocorticoids (regulate electrolyte and water balance).
Glucocorticoids:
Most glucocorticoids are synthetic analogues; exert anti-inflammatory, metabolic, and immunosuppressant effects.
Examples include: \text{beclomethasone}, \text{betamethasone}, \text{cortisone}, \text{dexamethasone}, \text{hydrocortisone}, \text{methylprednisolone}, \text{prednisolone}, \text{prednisone}, \text{triamcinolone}
Pharmacokinetics (PK) of glucocorticoids:
Well absorbed orally; after intramuscular (IM) administration, completely absorbed.
Bound to plasma proteins; distributed via blood.
Metabolized in the liver; excreted by the kidneys.
Pharmacodynamics (PD):
Suppress hypersensitivity and immune responses through mechanisms not fully understood.
Suspected actions:
Inhibit cell-mediated immune reactions; reduce leukocytes, monocytes, eosinophils.
Decrease binding of immunoglobulins to cell-surface receptors.
Inhibit interleukin synthesis.
Drug interactions with glucocorticoids:
Barbiturates, phenytoin, rifampin, and aminoglutethimide may reduce glucocorticoid effects.
Amphotericin B, chlorthalidone, ethacrynic acid, furosemide, and thiazide diuretics may enhance potassium-wasting effects.
Erythromycin and troleandomycin may increase effects by reducing metabolism.
Glucocorticoids reduce serum concentrations and effects of salicylates.
NSAIDs and salicylates increase peptic ulcer risk when taken with corticosteroids.
Vaccines may have reduced response in patients taking glucocorticoids.
Estrogen-containing birth control increases corticosteroid effects.
Antidiabetic drug effects may be reduced, causing higher blood glucose.
Adverse reactions (systemic effects, esp. long-term/high-dose):
Insomnia, sodium and water retention, increased potassium excretion, immunosuppression, osteoporosis, gut ulcers, impaired wound healing, cataracts, hypertension, personality changes, increased infection risk.
Endocrine: diabetes mellitus, hyperlipidemia, adrenal atrophy, hypothalamic-pituitary axis suppression, Cushingoid signs (buffalo hump, moon face), hyperglycemia.
Nursing considerations:
Give early in the day to mimic circadian rhythm; with food to prevent GI irritation.
Prevent infection; monitor for adverse reactions; adjust dose during physiologic stress (surgery, trauma, infection).
Do not stop abruptly; avoid prolonged use in children; notify prescriber of severe adverse reactions.
Mineralocorticoids
Mineralocorticoids affect electrolyte and water balance.
Example: fludrocortisone acetate, a synthetic analogue of adrenal cortex hormones.
Pharmacokinetics:
Absorbed well; distributed broadly.
Metabolized in the liver; excreted by the kidneys.
Pharmacodynamics:
Increase sodium reabsorption and increase potassium and hydrogen secretion in the distal renal tubule.
Pharmacotherapeutics:
Replacement therapy for adrenocortical insufficiency (reduced glucocorticoids, mineralocorticoids, and androgens).
Drug interactions similar to glucocorticoids.
Uricosurics
Uricosurics and other antigout drugs act on uric acid metabolism.
Hyperuricemia leads to gout (increased uric acid in blood) due to overproduction or decreased renal excretion.
Major uricosurics: probenecid and sulfinpyrazone (two first-line NSAIDs for gout in this context).
Pharmacokinetics:
Absorbed from GI tract.
75–95% of probenecid and 98% of sulfinpyrazone are protein-bound.
Metabolized in the liver; excreted primarily by the kidneys; small amounts excreted in feces.
Pharmacodynamics:
Probenecid and sulfinpyrazone reduce reabsorption of uric acid at the proximal convoluted tubule, promoting uric acid excretion in urine and lowering serum urate.
Pharmacotherapeutics:
Indicated for symptoms of gout, gouty arthritis (joint inflammation due to urate crystals), and abarticular gout (under-skin urate deposits).
Note: Should not be given during an acute gout attack; can prolong inflammation if started during an attack. Colchicine is used during the first 3–6 months of therapy to prevent attacks when initiating uricosurics.
Drug interactions:
Probenecid can significantly increase and prolong effects of cephalosporins, penicillins, and sulfonamides.
Serum urate levels may rise when probenecid is used with antineoplastic drugs.
Adverse reactions:
Uricosurics can cause uric acid stone formation and blood abnormalities.
Probenecid: headache, anorexia, nausea/vomiting, hypersensitivity.
Sulfinpyrazone: nausea, indigestion, GI pain, GI bleeding.
Nursing considerations:
Encourage fluid intake to maintain at least 2 L/day; urine alkalinization with sodium bicarbonate or potassium citrate as needed to prevent hematuria, renal colic, uric acid stones.
Begin therapy after an acute attack subsides; not useful during an acute attack.
Expect increased frequency, severity, and duration of acute attacks during the first 12 months; prophylactic colchicine or another anti-inflammatory is given during the first 3–6 months.
Other antigout drugs
Allopurinol and colchicine are also used in gout management.
Allopurinol reduces uric acid production and can be used with uricosurics at lower dosages.
Colchicine reduces inflammation by affecting white blood cells’ (WBCs) role in inflammation.
Allopurinol pharmacokinetics:
Oral absorption; allopurinol and its metabolite oxypurinol widely distributed except in brain
Metabolized in liver; excreted in urine.
Colchicine pharmacokinetics:
Oral absorption; partially metabolized in the liver; biliary resecretions; reabsorption from intestines; distributed to tissues; excreted mainly in feces; some in urine.
Pharmacodynamics:
Allopurinol inhibits xanthine oxidase, the enzyme responsible for uric acid production.
Pharmacotherapeutics:
Allopurinol treats primary gout, hyperuricemia with blood abnormalities or during tumor treatment; treats primary/secondary uric acid nephropathy; prevents recurrent uric acid stone formation; can be used with uricosurics for lower dosages.
Drug interactions:
Colchicine has minimal interactions with many drugs, but allopurinol interactions can be serious:
Potentiates effects of oral anticoagulants.
Increases mercaptopurine and azathioprine levels, increasing toxicity risk.
ACE inhibitors increase hypersensitivity risk with allopurinol.
Allopurinol can raise theophylline levels.
Bone marrow suppression risk increases when cyclophosphamide is used with allopurinol.
Adverse reactions:
Allopurinol commonly causes a rash.
Colchicine long-term may cause bone marrow suppression.
Common across allopurinol/colchicine: nausea, vomiting, diarrhea, abdominal pain.
Salicylates (for context):
Salicylates (e.g., aspirin and related compounds) inhibit prostaglandin synthesis; have antipyretic effects via prostaglandin mediation at the hypothalamus; low-dose aspirin reduces platelet aggregation via thromboxane A2; high-dose inhibition of prostacyclin reduces anti-platelet effects.
Indications: mild-to-moderate pain, fever, various inflammatory conditions; mesalamine/balsalazide for ulcerative colitis; sodium thiosalicylate for arthritis/pain.
Contraindications and cautions: allergy to salicylates/NSAIDs; bleeding abnormalities; renal impairment; risk of Reye Syndrome in children with influenza or chickenpox; perioperative risk; pregnancy/lactation cautions.
Adverse effects: GI upset; hematologic abnormalities; salicylism (dizziness, tinnitus, hearing loss, nausea, vomiting, confusion, lassitude); acute toxicity at doses of about 20-25\,\text{g} in adults or 4\,\text{g} in children.
Interactions: anticoagulants; NSAIDs; activated charcoal; antacids; carbonic anhydrase inhibitors.
Nursing considerations: take with food; check all medicines for salicylate ingredients; monitor for severe reactions; provide supportive care; ensure hydration; educate about adverse effects and warning signs.
Vaccines and Sera (Immunization)
Immunization is the process of artificially stimulating active immunity by exposing the body to weakened or less toxic proteins from disease-causing organisms.
Goal: to provoke an immune response without causing disease.
Types of immunity:
Active Immunization: stimulates host to produce antibodies or cellular responses to protect against/eliminate disease.
Passive Immunization: administration of antibodies to neutralize a pathogen around exposure.
Vaccines provide an antigenic stimulus that does not cause disease but can produce long-lasting protective immunity.
Types of vaccines and their characteristics: 1) Live (attenuated) vaccines: include viral vaccines (polio oral Sabin, mumps, measles, rubella, varicella) and some bacterial (BCG for TB).
Advantages: induce both humoral (Abs) and cellular (CTLs) responses; long-lasting immunity often with one or two doses.
Limitations: risk for immunocompromised persons; thermolabile/instability.
2) Inactivated (killed) vaccines: include pertussis, typhoid, polio (Salk), influenza.Advantages: greater stability; safety (no infection risk).
Limitations: shorter-lasting immunity; require boosters; lower immunogenicity (often need adjuvant).
3) Subunit (antigenic) vaccines: use structural antigens (proteins or polysaccharides) or toxoids.Examples: pertussis (acellular), tetanus/diphtheria toxoids, influenza (Hemagglutinin/Neuraminidase), hepatitis B (HBsAg), HPV (L1 protein/virus-like particles), pneumococcal and meningococcal polysaccharide vaccines.
Advantages: safety; same general benefits as inactivated.
Limitations: sometimes lower immunogenicity (similar to inactivated vaccines).
Toxoids: inactivated toxins used as vaccines (e.g., tetanus and diphtheria toxoids) requiring booster injections every ~10 years.
Serum preparations (passive antibodies):
Types include homogeneous serum (from immunized human donors) and heterogeneous serum (animal sources, e.g., horse antisera such as tetanus antitoxin, diphtheria antitoxin, rabies immune globulin).
Immune globulins (human) and various immune globulins (e.g., hepatitis B immune globulin, rabies immune globulin).
Hypersensitivity reactions to heterogeneous serum can occur (type I/anaphylactic reactions within 2–30 minutes).
Anaphylaxis: systemic reactions causing shock and breathing difficulties; can be fatal; localized reactions include hay fever, asthma, hives.
Serum sickness: systemic hypersensitivity occurring 7–12 days after a high-concentration foreign serum injection.
Psychopharmacology: Neurotransmitters, Drugs, and Concepts
Neurotransmitters are chemical messengers that can be excitatory or inhibitory; after release into the synapse and receptor activation, they are removed by reuptake or breakdown by enzymes (primarily MAO).
Dopamine: located mainly in brainstem; generally excitatory; synthesized from tyrosine.
Antipsychotics work by blocking dopamine receptors (D1–D5; D2 most linked to psychosis and EPS).
Norepinephrine (noradrenaline) and Epinephrine (adrenaline):
Norepinephrine is the most prevalent CNS neurotransmitter; involved in mood regulation.
Epinephrine has limited CNS distribution; controls fight-or-flight responses in the periphery.
Serotonin (5-HT): in brain; derived from tryptophan; mostly inhibitory; involved in sleep, mood, appetite, pain control, sexual behavior, temperature regulation, etc.
Some antidepressants block serotonin reuptake, increasing serotonin in the synapse.
Acetylcholine: in brain, spinal cord, PNS; excitatory or inhibitory; involved in sleep-wake cycle and muscle activation; decreased acetylcholine noted in Alzheimer's disease.
Glutamate: excitatory amino acid; high levels can be neurotoxic.
GABA (gamma-aminobutyric acid): major inhibitory neurotransmitter; modulates other neurotransmitters; benzodiazepines increase GABA function to treat anxiety and aid sleep.
Pharmacodynamics and clinical notes:
Efficacy: maximal therapeutic effect a drug can achieve.
Potency: amount of drug needed to achieve maximal effect; low-potency requires higher doses; high-potency achieves efficacy at lower doses.
Half-life: the time it takes for half of the drug to be removed from the bloodstream; denoted as t_{1/2}.
The FDA may issue a black-box warning when a drug has serious or life-threatening side effects; boxed warnings appear prominently in package inserts.
Antipsychotic Drugs
Also known as neuroleptics; used to treat psychosis (e.g., schizophrenia, schizoaffective disorder, manic phase of bipolar).
Mechanism: primarily block dopamine receptors (D2, D3, D4).
Generations: 1) First Generation (Conventional): strong D2 blockade; high risk of extrapyramidal symptoms (EPS).
Examples: chlorpromazine, thioridazine, fluphenazine, haloperidol.
High-potency agents often used for positive symptoms (e.g., hallucinations); associated with EPS; contraindicated in older adults (>65 years) in some contexts.
2) Second Generation (Atypical): lower D2 blockade with greater effects on serotonin receptors; more effective for negative symptoms; lower EPS but risk of metabolic side effects.Examples: olanzapine, quetiapine, clozapine, risperidone, ziprasidone, lurasidone, molindone.
3) Third Generation: dopamine system stabilizers; partial agonists that balance dopamine activity.Examples: aripiprazole, brexpiprazole.
Depot therapy: long-acting injectable formulations for noncompliance.
Extrapyramidal side effects (EPS): major adverse effects include:
Acute dystonia (prolonged involuntary muscle contractions), pseudoparkinsonism, akathisia (restlessness).
D2 receptor blockade in midbrain causes EPS; features include torticollis, opisthotonus, and oculogyric crisis; acute treatment with anticholinergic drugs.
Pseudoparkinsonism features: rigid/stiff posture, mask-like face, reduced arm swing, shuffling gait, tremor, drooling, bradykinesia; managed with anticholinergics or amantadine (dopamine agonist).
Neuroleptic Malignant Syndrome (NMS): potentially fatal idiosyncratic reaction; 10–20% mortality; symptoms include rigidity, high fever, autonomic instability, delirium, elevated CK; treat with stopping antipsychotic and supportive care.
Tardive Dyskinesia (TD): irreversible syndrome of involuntary movements, especially of tongue and facial muscles; no definitive cure; risk increases with long-term use.
Agranulocytosis risk with certain antipsychotics (e.g., clozapine); requires monitoring of WBC; discontinuation if severe leukopenia.
Antidepressants
Mechanism: interact with monoamine neurotransmitters (norepinephrine, serotonin, dopamine).
Groups:
MAO Inhibitors (MAOIs): e.g., tranylcypromine, isocarboxazid, phenelzine, selegiline.
Note: MAOIs carry high risk of hypertensive crisis if tyramine-containing foods are ingested (aged cheeses, aged meats, tofu, beer, sauerkraut, soy sauce, yogurt, etc.).
MAOIs require caution or avoidance with other antidepressants and CNS depressants; overdose risk is high.
Selective Serotonin Reuptake Inhibitors (SSRIs): e.g., fluoxetine, sertraline, citalopram, escitalopram, fluvoxamine, paroxetine, etc.
Often preferred when suicide risk is a concern due to lower overdose risk than cyclic antidepressants or MAOIs; effective for mild-to-moderate depression.
Tricyclic Antidepressants (TCAs) and related cyclics: e.g., imipramine, amitriptyline, nortriptyline, clomipramine, desipramine, etc.
Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): e.g., venlafaxine, duloxetine, desvenlafaxine (and others).
Other antidepressants: venlafaxine, bupropion, duloxetine, trazodone, nefazodone.
Quickest antidepressants effects: roughly 1 week; examples reported as effective: \text{Zoloft} (sertraline), \text{Lexapro} (escitalopram), \text{Paxil} (paroxetine), \text{Luvox} (fluvoxamine), \text{Prozac} (fluoxetine).
Antidepressants act on monoamine systems; reuptake inhibitors increase synaptic serotonin or norepinephrine depending on class:
SSRIs block serotonin reuptake (primary action to improve mood and anxiety symptoms).
TCAs and SNRIs block reuptake of norepinephrine to varying degrees and also affect serotonin.
MAOIs inhibit enzyme monoamine oxidase, affecting breakdown of monoamines.
Memory trick (mnemonics):
MAOIs: insomnia; morning dosing.
TCAs: sedation; evening dosing.
SSRIs/SNRIs: anorexia; take with food.
Antidepressants are hepatotoxic; monitor AST/ALT whether indicated.
St. John’s wort should not be combined with antidepressants due to risk of seizures and serotonin syndrome.
Mood Stabilizers
Mood stabilizers are used to treat bipolar disorder to stabilize mood and prevent manic/depressive episodes.
Lithium:
First-line agent.
Normalizes reuptake of serotonin, norepinephrine, acetylcholine, and dopamine; reduces norepinephrine release via calcium competition.
Mechanism of action largely intracellular.
Therapeutic serum level: 1.0\ \text{mEq/L}.
Therapeutic range: typically 0.6-1.2\ \text{mEq/L}; toxicity concerns begin above ~3.0\ \text{mEq/L} where dialysis may be indicated.
Effects may take weeks to manifest.
Anticonvulsants used as mood stabilizers: valproic acid, topiramate; gabapentin; pregabalin; lamotrigine; lithium.
Valproic acid and topiramate increase GABA activity, thought to stabilize mood by inhibiting kindling (recurrent seizures or subclinical activity that could contribute to mania).
Kindling concept: snowball effect where minor seizures lead to more severe episodes; mood stabilization may raise seizure threshold similarly.
Nursing considerations for lithium:
Therapeutic level typically 0.6-1.2\ \text{mEq/L}; common side effect is fine tremor.
Polyuria and polydipsia may indicate toxicity.
Severe toxicity signs require management with mannitol (osmotic diuretic) and careful sodium management; monitor sodium levels because low sodium can precipitate lithium toxicity.
Normal sodium range: 135-145\ \text{mmol/L}.
Diet: moderate sodium intake; avoid excessive sweating; monitor hydration.
Anticonvulsants for mood stabilization:
Carbamazepine (Tegretol), valproic acid (divalproex), etc.
Benzodiazepines as anxiolytics and sedatives are often used adjunctively:
They act on GABA to provide CNS inhibition; examples: alprazolam, chlordiazepoxide, clonazepam, diazepam, lorazepam, oxazepam, triazolam.
Note: benzodiazepines can be used for anxiety, seizures, sedation; caution about dependence and withdrawal.
Pharmacokinetics: rapidly absorbed; high protein binding (~85–90%); liver metabolism; renal excretion; cross placenta and present in breast milk.
Pharmacodynamics: anticonvulsants, anti-anxiety, sedative-hypnotics, muscle relaxants.
Special notes: avoid long-term daily use; abrupt withdrawal may cause seizures; monitor for CNS depression when coadministered with other CNS depressants; ensure safety when giving IV benzodiazepines.
Stimulants
Primary use today: ADHD in children/adolescents; residual adult ADHD; narcolepsy.
Mechanism: indirectly acting amines; increase norepinephrine, dopamine, and serotonin by releasing them from presynaptic terminals and/or blocking reuptake.
Common stimulants: dextroamphetamine, methylphenidate, mixed amphetamine salts.
PK/PD:
Well absorbed from GI tract; methylphenidate undergoes significant first-pass metabolism.
Metabolized in liver; excreted mainly in urine.
Effects include increased synaptic norepinephrine and dopamine; improved attention, reduced impulsivity and hyperactivity.
Nursing considerations:
Give at least 6 hours before bedtime to avoid sleep interference.
Long-term use may cause psychological dependence or habituation, especially in those with prior drug history.
After prolonged use, taper to prevent rebound depression.
Avoid hazardous activities until CNS effects are known.
Avoid caffeine-containing drinks as they increase stimulant effects.
Report adverse effects (excess stimulation, tolerance) to prescriber.
Anesthesia
General anesthesia aims: analgesia, unconsciousness, amnesia.
Risk factors: cardiovascular (CV) and respiratory risk, renal and hepatic considerations; also potential for CNS depression.
Balanced anesthesia: combine several agents to achieve required effects while minimizing adverse effects (e.g., NMJ blockers, sedatives, antiemetics, antihistamines, narcotics).
Phases of anesthesia:
1) Induction: start of anesthesia to stage 3.
2) Maintenance: stage 3 until completed.
3) Recovery: emergence from anesthesia.General anesthetic agents:
Barbiturate and non-barbiturate IV anesthetics, gas anesthetics, and IV liquids.
Barbiturate class example: Thiopental (Pentothal) – most widely used IV anesthetic; no analgesic properties; may require additional analgesia after surgery.
Methohexital (Brevital) – lacks analgesic property; rapid onset; recovery 3–4 minutes; lipophilic; diffuses rapidly to brain.
Contraindications/precautions: Methohexital should not contact silicone; ensure readiness for intubation; rapid onset may cause respiratory depression.
Pregnancy and lactation: avoid unless benefits clearly outweigh fetal risk; CNS depressant risk to fetus.
Adverse effects: decreased pulse, hypotension, suppressed respiration, decreased GI activity, nausea/vomiting.
Drug interactions: barbiturates can affect theophylline, oral anticoagulants, beta blockers, corticosteroids, hormonal contraceptives, etc.; barbiturate anesthesia plus narcotics can cause apnea more commonly.
Non-barbiturate IV anesthetics:
Midazolam (Versed); Droperidol (Inapsine); Etomidate (Amidate); Fospropofol (Lusedra); Ketamine; Propofol (Diprivan).
Pharmacokinetics: varies by agent; e.g., midazolam onset rapid but peak effectiveness around 30–60 minutes; etomidate ~1 minute onset; propofol rapid onset; ketamine ~30 seconds onset.
Pharmacodynamics: sedative, amnestic, anticonvulsant, anxiolytic, etc.
Indications: premedication, induction, sedation for intubated patients, continuous sedation.
Contraindications/precautions: midazolam can cause nausea/vomiting and respiratory depression; monitor; droperidol caution with renal/hepatic failure and prolonged QT risk; etomidate not recommended for children under 10; etc.
Adverse effects: various CNS, respiratory, GI, and cardiovascular effects depending on agent.
Drug interactions: CNS depressants increase toxicity; cimetidine and hormonal contraceptives increase CNS depression with benzodiazepines; etc.
Inhaled gas anesthetics (gas):
Nitrous oxide: potent analgesic; fast onset and offset; usually combined with other agents; does not cause muscle relaxation; watch for hypoxia risk due to reuptake-blocking effects; avoid in pregnancy unless benefits outweigh risks; nursing mothers should wait 4 hours before nursing after administration.
Halogenated volatile liquids (inhaled anesthetics): Halothane, Desflurane, Enflurane, Isoflurane, Sevoflurane.
Prototypes and characteristics:
Halothane: rapid onset; maintenance; rare hepatic toxicity (recovery syndrome); avoid repeated use beyond 3 weeks.
Desflurane: may cause respiratory irritation; avoid in some patients with respiratory problems.
Enflurane: caution with known cardiac/respiratory disease or renal dysfunction.
Isoflurane: may cause hypotension, hypercapnia, sour taste; use with caution in respiratory depression.
Sevoflurane: minimal adverse effects; rapidly cleared; commonly used for induction.
Pharmacokinetics: onset and recovery times vary; Halothane 1–2 minute onset, ~20 minutes recovery; Desflurane/Enflurane/Isoflurane 1–2 minute onset, 5–20 minute recovery; Sevoflurane ~30 second onset, ~10 minute clearance. All are eliminated via the lungs.
Contraindications/precautions: hepatic impairment with Halothane; respiratory/cardiac risks with Desflurane/Enflurane; caution with respiratory depression for Isoflurane/Sevoflurane; potential malignant hyperthermia risk; have dantrolene available.
Adverse effects: Halothane recovery syndrome; Desflurane respiratory reactions; Isoflurane hypotension and dysgeusia; Enflurane renal impairment; Sevoflurane minimal effects.
Drug interactions: caution with other CNS depressants.
Local anesthesia
Topical: lotion, cream, ointment, eye drops for mucous membranes.
Infiltration: injection into tissues to be treated.
Field block: injection around the area to be affected; more intense than infiltration.
Nerve blocks: peripheral sensory/motor block; central nerve blocks along spinal roots; includes:
Epidural: from the word epidural (space around spinal nerves) used in obstetrics.
Caudal epidural.
Spinal: injection into the subarachnoid space.
IV regional anesthesia: tourniquet to isolate limb circulation; inject anesthetic into a limb vein.
Local anesthetic agents: esters or amides.
Pharmacokinetics:
Ester-type locally: rapidly hydrolyzed in plasma by esterases.
Amide-type locally: slower metabolism in the liver; potential toxicity if accumulated.
Therapeutic actions/indications: to prevent pain during procedures; can be used for infiltration, nerve block, spinal anesthesia, and local pain relief.
Contraindications: allergy history, decreased plasma esterases, pregnancy/lactation (balance risk vs benefit).
Adverse effects: local numbness, loss of temperature, touch, proprioception, muscle tone; CNS effects (headache, dizziness, tremors); GI effects (nausea, vomiting); cardiovascular effects (vasodilation, myocardial depression, arrhythmias); potential fatal cardiac or respiratory arrest in severe cases.
Drug interactions:
Local anesthetics + succinylcholine: increased neuromuscular blockade.
Local anesthetics + epinephrine: reduced systemic absorption, increased local effect.
Heart block risk with certain combinations.
Reminders on Practice and Safety
Many drug interactions require careful review of all medications the patient is taking.
For anesthesia, ensure monitoring systems and resuscitation equipment are ready; avoid rapid changes in drug administration without confirming airway/ventilation support.
For antipsychotics, monitor for EPS, TD, NMS, and agranulocytosis; Clozapine requires regular WBC monitoring.
For corticosteroids, consider the physiologic stress response and potential HPA axis suppression; taper rather than abrupt withdrawal.
For salicylates, monitor for signs of salicylism and toxicity; exercise caution in populations at risk (children, overweight, comorbidities).
For vaccines, be aware of hypersensitivity risks and the difference between live attenuated and inactivated products as described above.
For mood stabilizers and antidepressants, monitor therapeutic levels, liver function, and potential suicidal risk if using certain agents; avoid drug interactions that raise toxicity risk.
LaTeX notes used where applicable:
Lithium