Introduction to Pharmacology

Phase IV is why drugs get withdrawn after approval. A trial of 3,000 people cannot detect a reaction that occurs in 1 of 50,000 — nurse reporting is how those signals surface.

Which law wins: the FDA regulates development and sale, but local laws further regulate distribution and administration. In most cases the strictest law prevails — and rules vary from state to state and even within a state, so know the ones where you practice.

The pregnancy categories are being phased out. The FDA required a pregnancy category on every new drug starting in 1979. In 2014 it added guidelines covering the drug’s presence in human milk, and in 2015 it moved from letter categories to risk levels. Newly approved and revised labels carry no letter — instead they state risk for fertility, pregnancy, and lactation. High risk in pregnancy means research showed fetal toxicity; high risk in lactation means the drug is known to enter human milk and could harm the infant; low risk means no problems shown so far. Learn the letters as your lecture presents them, but expect risk levels on a current insert.

Every drug has both therapeutic and adverse effects. There is no drug with only the effect you want — that idea underpins the entire second half of this deck.

First-pass effect: an orally absorbed drug travels through the portal vein to the liver and is partly metabolized before it ever reaches systemic circulation. Any route that bypasses the portal system — IV, IM, sublingual, rectal, transdermal — escapes it.

She corrected this in Week 2 because it gets confused: absorption and first-pass are related but not the same thing. “No first-pass” does not mean “no absorption.” IV is the one route with neither. Topical medications are usually intended for a local effect, though some systemic absorption can occur.

Why adverse effects happen at all: drugs act on multiple body systems at once, patients differ in sensitivity, dosing may be wrong for the individual, and individual variation is unavoidable.

The universal first step for any suspected drug allergy is the same: stop the drug, treat the reaction, document it. Severity changes what “treat” means, never the order.

Anticholinergic effects — the classic mnemonic: dry as a bone (dry mouth), red as a beet (flushing), blind as a bat (blurred vision), mad as a hatter (confusion), hot as a hare (hyperthermia). Add urinary retention and constipation.

Why the CJMM exists: it was developed by the NCSBN — the body that writes the NCLEX — as a framework for measuring clinical judgment and decision making. That is why Next Gen NCLEX items are phrased in its language rather than the classic five-step vocabulary.

Her exact caution: the rights help catch errors — they do not replace assessment, clarification, or stopping when something does not make sense. Her warm-up case makes the point: an order for metoprolol 25 mg with a hold parameter of systolic < 100, and a BP of 88/54. The dose is “right.” You still hold it.

Many programs add right documentation, right reason, right response, and right to refuse. This deck teaches five — answer five unless the question says otherwise.

When something does not match: STOP → verify → clarify.

Preventing medication errors: verify the order against the MAR, never give a drug someone else prepared, question any order that is illegible or seems wrong, avoid dangerous abbreviations, and use two identifiers every time. Report errors that reach the patient and near misses — near misses are how systems get fixed.

Since Week 2, two of these came back. Weight-based IV drips and BSA chemotherapy dosing both appeared in course questions, so they have moved into the “know and practice” column and both are drillable below. Slide 19 listed BSA as de-emphasized — treat that as superseded.

This changed the page. The apothecary table and the gtt/min drills below are still here because Karch teaches them and your dosage course may want them — but both are now labelled as outside Week 2’s scope, and D ÷ H × Q is the only setup modelled.

Zeros kill patients. Always write a leading zero before a decimal (0.5 mg, never .5 mg) and never a trailing zero (5 mg, never 5.0 mg). A missed decimal point is a tenfold overdose.

Why metric wins: in 1995 the U.S. Pharmacopeia Convention set standards requiring every prescription to carry the metric measure for quantity and strength, and established that drugs may be dispensed only in metric form. You still need the other two for conversion — finding the equivalent value between two systems.

Why dimensional analysis is worth learning: it carries the units through the arithmetic, so if your units do not cancel to the unit you were asked for, you know you set it up wrong before you get a number.

Do not let the calculator make the clinical decision for you. The reasonableness check is the step students skip, and it is the one that catches a tenfold error.

Her list of common mistakes: unit mismatch · wrong Q · rounding too early · missing unit on the answer · an implausible result you didn’t stop to question.

Karch’s own Key Points for this chapter: OTC drugs are deemed safe by the FDA when used as directed and need no prescription; they can mask disease, interact with prescriptions, and be taken above the recommended dose to the point of toxicity. Herbal and alternative therapies are dietary supplements and are not tightly regulated; they can produce unexpected effects and toxic reactions, interact with prescription drugs, and contain unknown ingredients that alter effectiveness and toxicity.

Her strongest instruction: never assume “noncompliance” before you assess the barrier. The opening move is “Walk me through how you take your medicines at home.”

On generics: an FDA-approved generic must meet standards for the same active ingredient, strength, dosage form, route, and bioequivalence to the reference product. That makes a generic switch a legitimate cost solution, not a compromise.

Don’t confuse the messenger with the receptor. ACh and norepinephrine are the messages; receptors are the receivers. An agonist mimics or activates; an antagonist blocks.

Alpha-2 is not on your list. Dr. Kaur teaches four receptors — α1, β1, β2 and muscarinic. The textbook also covers α2 agonists (clonidine, dexmedetomidine, guanfacine); those are flagged not required in the medication index so you can skip them.

Then reverse it. Blockers produce the opposite of stimulation — which is how you predict a drug’s adverse effects without memorising them.

The pattern to hold on to: almost every adverse effect of this class looks like too much fight-or-flight. And her closing question after any drug — “what evidence tells me it worked, and what tells me it harmed?”

Her emphasis: clinical judgment beats a memorised cutoff. Do not rely on a single remembered “hold number” — assess the patient, verify the ordered parameters, then act.

Irreversible cholinesterase inhibitors are not therapeutic drugs. Karch covers them because they are nerve agents: absorbed by inhalation or through skin, they bind acetylcholinesterase permanently. ACh floods the system — the heart slows and becomes ineffective, pupils and bronchi constrict, secretions pour, and sustained muscle contraction immobilises the diaphragm so breathing stops. The one exception in clinical use is echothiophate iodide, applied topically to the eye.

Beyond SLUDGE, cholinergic toxicity also brings bradycardia, hypotension, bronchospasm with secretions, and severe weakness. Higher-risk patients: asthma, bradycardia, peptic ulcer disease, and GI or GU obstruction.

Older adults especially: new confusion, constipation, urinary retention or falls may be medication-related. Reduced sweating causes heat intolerance, and several anticholinergic drugs together produce additive “anticholinergic burden.”

Take-home anchors. α1 squeeze · β1 one heart · β2 two lungs · M moist and moving. For every medication: why → how → expected response → safety.

Think it through, don’t memorise it. A patient’s BP is 88/50 on four antihypertensives. Rather than asking “which drug do I hold,” ask which lever is already on the floor. If they are also bradycardic at 48, the rate lever is the problem and the rate-slowing drugs are the suspects. If HR is 96 and they are dry with poor skin turgor, the volume lever is the problem and the diuretic is. Same low BP, two different answers.

The link she wants you to make. Diuretics and RAAS drugs move potassium. Potassium changes the T wave. The T wave reflects the electrical stability of the ventricle. So an electrolyte you drew for “routine monitoring” is really a dysrhythmia risk assessment — that is why K⁺ appears in the monitoring line of nearly every drug in this unit.

Now reverse it — this is the whole safety profile. Block the pathway anywhere and you get the opposite of step 5 and step 7: vasodilation → hypotension, and less aldosterone → less K⁺ excreted → potassium rises. You did not memorise “ACE inhibitors cause hyperkalemia.” You derived it. The same reasoning tells you why spironolactone, which blocks the last step, raises potassium the most.

And the kidney catch. Angiotensin II constricts the efferent arteriole — the vessel leaving the glomerulus — which is how the kidney maintains filtration pressure when perfusion is poor. Remove angiotensin II and that support disappears, so creatinine can rise when you start an ACEI or ARB. A small rise is expected. A large one means the kidney was depending on that support. This is why renal function is checked before and after starting, not just before.

Pregnancy is an absolute stop for all three. Not “use cautiously.” Angiotensin II is required for fetal kidney development; blocking it causes renal failure, oligohydramnios, skull defects and fetal death. Ask about pregnancy and contraception in every patient of childbearing potential before these are started.

The exam trap to rehearse. Given four findings on an ACE inhibitor, the cough feels like the answer because it is the fact you studied. It is not. Rank by airway, then circulation, then comfort — angioedema beats hyperkalemia beats cough beats dizziness beats a normal BP.

The edema question that separates understanding from memorising. A patient on amlodipine has new ankle swelling. Is that fluid overload? No. Amlodipine dilates the arteriole before the capillary, raising capillary hydrostatic pressure and pushing fluid into the tissue. Total body water has not changed — so a diuretic largely will not fix it, and giving one just dehydrates the patient. Distinguish it at the bedside: amlodipine edema is bilateral, dependent, and comes without weight gain, crackles or dyspnea. Heart-failure edema arrives with those. Same swollen ankles, opposite actions.

The heart-failure paradox worth sitting with. Beta blockers reduce contractility — so why give one to a failing heart? Because chronic sympathetic overdrive is itself toxic to myocardium over time. The short-term cost buys a long-term benefit, which is why they are started low, titrated slowly, and only when the patient is stable — never during acute decompensation. If you understand this, you will never be confused by seeing metoprolol on a heart-failure list.

“Hold for HR below 60” is not a rule you should carry. Dr. Kaur is explicit in her sources note: parameters vary by order and policy. A conditioned athlete at 52 who is asymptomatic is not the same patient as someone at 52 who is dizzy and hypotensive. The defensible answer is always assess the patient, compare against the written order, and question or escalate — not recite a number.

Two electrolyte facts that are pure reasoning, not memory. (1) The loop transporter that furosemide blocks is also what drives calcium reabsorption — so loops lose calcium, which is why they are used to treat hypercalcemia. Thiazides work further down and retain calcium, which is why they are chosen for patients who form calcium kidney stones. Same drug family, opposite calcium effects, and you can derive both from where they act. (2) Thiazides also raise glucose and uric acid — so a patient with gout may flare, and a patient with diabetes may need closer glucose monitoring.

Daily weight is the most sensitive measure you have — and the most often done badly. One litre of retained fluid is about 1 kg (2.2 lb), and weight shifts before crackles appear. It only works if the conditions are identical: same scale, same time of day, after voiding, in similar clothing. A 3 lb gain overnight is fluid, not fat — and it is a reportable finding.

Ototoxicity has a mechanism, and therefore a prevention. Furosemide’s risk to hearing rises with rapid IV push and high doses, and compounds with other ototoxic drugs such as aminoglycosides. That is why IV furosemide has an ordered rate limit. “Give it slowly” is not fussiness — it is the entire intervention.

Why this list is a potassium minefield. Look at a realistic heart-failure order set: furosemide (K⁺ down), spironolactone (K⁺ up), lisinopril (K⁺ up), digoxin (dangerous when K⁺ is down). Four drugs pulling potassium in two directions, with a narrow-therapeutic-index drug sitting in the middle. You cannot evaluate any one of them in isolation — which is exactly the clinical judgement Dr. Kaur is testing.

Not every patient gets every drug. The question to carry into the exam is not “what is the heart-failure regimen” but what problem is this particular medication trying to solve in this particular patient — and is that problem still present?

Why low potassium causes digoxin toxicity — the actual mechanism. Digoxin and potassium compete for the same binding site on the Na⁺/K⁺-ATPase pump. When potassium is low, there is less competition, so more digoxin binds — the drug’s effect intensifies even though the serum digoxin level has not moved. This is why a patient can be “therapeutic” on paper and toxic at the bedside, and why the potassium result matters as much as the digoxin result. Now connect it forward: furosemide lowers potassium. Furosemide and digoxin appear on heart-failure lists together constantly. That pairing is the single most testable interaction in this week.

How to rank when every option is abnormal. Work in this order: (1) airway — angioedema beats everything. (2) circulation — a rhythm-threatening potassium or a symptomatic bradycardia. (3) a trend heading somewhere bad — a 3 lb overnight weight gain, a creatinine climbing. (4) genuine discomfort — cough, constipation, gynecomastia. And discard anything that is simply the drug working: a BP of 128/74 on an antihypertensive is never the answer to “which finding concerns you most.”

The habit worth building now. When you see a CV medication, do not ask “what do I remember about this drug.” Ask: which lever does it pull, what else on this list pulls the same lever, and what single lab tells me whether it is going wrong? Three questions, and they work on drugs you have never seen.

Read it across, not down. The reason this unit is hard is that the classes interact. Open ACE inhibitors, spironolactone and loop diuretics together and read only the labs rows: every one of them says potassium, for opposite reasons. That single lab is the thread running through the whole chapter, and it is where the exam questions live.

Sources. Karch’s Focus on Nursing Pharmacology, 10th ed. (Tucker), Ch 42–44 and 51; Dr. Kaur’s NURS-11 Week 6 deck and her cited references (NCSBN 2026 NCLEX-RN® test plan, DailyMed prescribing information, ACC/AHA/HFSA guideline principles for medication-role context); AGS Beers Criteria® for the older-adult notes. No commercial study sites were used.

Why it is built by class, not by drug. Karch teaches prototypes — the model drug its class is compared against. Learn epinephrine and you can reason about any adrenergic agonist; learn atropine and every anticholinergic follows the same dry–dilated–retained–confused pattern.

Exam weighting. Every class here except the β1 agonists appears in Dr. Kaur’s decks. textbook only marks a class that is in Karch but not in her slides — learn it for completeness and for the α1 / β1 / β2 symmetry, but weight your revision toward the lecture classes.

Sources. Karch’s Focus on Nursing Pharmacology, 10th ed. (Tucker), Ch 29–33; Dr. Kaur’s NURS-11 lecture decks; the AGS Beers Criteria® and FDA prescribing information for the special-population notes. No commercial study sites were used.

How to use this. Study the both rows first — a drug her slides and the textbook name is the most likely to be tested. Then lecture. The textbook rows are worth recognising by class rather than memorising individually.

The four questions that replace memorising a class. Her pearl: do not memorise a class in isolation. For any antiarrhythmic ask — what does it do to rate, to conduction, to blood pressure, and to repolarisation? Answer those four and the monitoring plan writes itself: rate and conduction → apical pulse and rhythm; blood pressure → BP before dosing; repolarisation → QT and the electrolytes that govern it.

The paradox at the centre of this class. Every antiarrhythmic is also proarrhythmic — a drug that changes electrical behaviour to fix one rhythm can create another. That is why “the rhythm looks different” is never automatically good news, and why potassium and magnesium appear in the monitoring line: low K⁺ or low Mg²⁺ destabilises repolarisation and makes drug-induced dysrhythmia far more likely. Notice that this is the same potassium thread running through Day 1.

Why the toxicity is multi-organ. Amiodarone is intensely lipophilic. It leaves the blood and loads into fat, lung, liver, thyroid and skin, giving it an enormous volume of distribution and a half-life measured in weeks to months. Two consequences follow directly: toxicity is cumulative rather than dose-by-dose, and stopping the drug does not stop the exposure — it lingers for months. On top of that, the molecule contains iodine, which is why the thyroid is involved at all. Every item below is downstream of those two facts.

Two more that students miss. Photosensitivity and a slate-grey or bluish skin discolouration with long-term use — same lipophilic loading, this time into skin. And amiodarone raises digoxin and warfarin levels, so if either is on the MAR, anticipate toxicity and a dose reduction. That is a Day 1 drug and a Day 2 drug colliding on one medication list.

The number that explains everything: a half-life of roughly 10 seconds. Adenosine is taken up by red blood cells and endothelium almost immediately. Give it slowly and it is destroyed before it reaches the heart — the dose simply fails. So: rapid IV push, through the port closest to the patient, followed immediately by a saline flush to drive the drug centrally before it disappears. The technique is not a ritual; it is the only way the drug can work.

The judgement this drug tests. A brief pause or a few seconds of asystole on the monitor after adenosine is the expected mechanism, not a complication — the drug is deliberately stopping conduction so the rhythm can restart cleanly. Recognising that is the difference between calmly watching the monitor and calling a code on a working drug. That said, “expected” is exactly why continuous ECG and resuscitation readiness are required: you have to be able to tell a two-second pause from one that is not ending. Caution in asthma — adenosine can provoke bronchospasm.

Her pearl, and the distinction the exam will test. Beta blockers and calcium channel blockers are prevention and control — not rapid rescue. A patient with chest pain right now does not take their metoprolol early; they take sublingual nitroglycerin and follow the emergency plan. Confusing a maintenance drug for a rescue drug is the same error as confusing salmeterol with albuterol — and you have already met that pattern in the autonomic unit.

When chest pain is not angina. Chest pain that is new, worsening, prolonged, or occurring at rest may be acute coronary syndrome and needs urgent evaluation, not another nitroglycerin tablet and a wait. Stable angina is predictable: same trigger, same duration, relieved by rest or nitrate. Anything that breaks that pattern is a change in condition.

The absolute interaction — and why “separate them by an hour” is wrong. Never combine nitrates with PDE-5 inhibitors (sildenafil, tadalafil, vardenafil). Both act on the same pathway: nitrates raise cGMP, PDE-5 inhibitors block its breakdown. Stacking them produces profound, refractory hypotension. Her slide 30 makes the point precisely — a patient-chosen one-hour gap is not safe teaching, because sildenafil persists around 24 hours and tadalafil up to 36. Ask about these drugs before giving a nitrate, and ask plainly: patients often do not consider them medication, and may be embarrassed to volunteer them.

Why “muscle pain + dark urine” is the pairing she keeps repeating. In rhabdomyolysis, skeletal muscle breaks down and releases myoglobin into the blood. Myoglobin is filtered by the kidney and turns the urine dark brown or tea-coloured — that is not blood, it is muscle protein — and it is directly toxic to renal tubules. So the dark urine is not an incidental extra symptom: it is the sign that muscle injury has become kidney injury. Muscle ache alone is common and often benign; muscle pain with weakness with dark urine is the emergency.

Pregnancy. Cholesterol is required for fetal development, so statins are stopped in pregnancy — which is why “report pregnancy promptly” is on her teaching list rather than being an afterthought.

Why arterial and venous get different drugs — the reasoning, not the list. Arterial clots form in fast, high-pressure flow where platelets dominate — a pale, platelet-rich “white clot.” So you attack platelets: aspirin, clopidogrel. Venous clots form in slow, stagnant flow where the cascade dominates — a fibrin-and-red-cell-rich “red clot.” So you attack the cascade: heparin, warfarin, DOACs. That single distinction explains why a patient in atrial fibrillation gets apixaban rather than aspirin, and why a stent patient gets clopidogrel rather than warfarin.

Her warning, and it is the one students fail. Do not normalise clinically important bleeding simply because the patient is on an antiplatelet or anticoagulant. “Of course they are bruising, they are on heparin” is how a GI bleed gets missed for a shift. The medication explains a tendency; it never explains away melena, hematemesis, a severe headache, or a falling blood pressure. Assess severity, review the last dose and every other bleeding-risk drug on the list, get the ordered labs, and escalate.

INR belongs to warfarin alone. Her slide 34 tests exactly this: an apixaban patient with an INR of 1.1 is not concerning, because INR is not used to dose DOACs — reading it as “subtherapeutic” is the trap. Warfarin needs INR because it works indirectly, by reducing production of vitamin K–dependent clotting factors, and each patient’s response differs. DOACs inhibit a single factor directly and predictably, so they are dosed by patient characteristics — renal function, age, weight — not by a titration lab.

Heparin-induced thrombocytopenia — the counterintuitive one. Platelets fall, so the instinct is to think bleeding. It is the opposite. HIT is an immune reaction in which antibodies activate platelets, consuming them while driving new clot formation. The patient becomes thrombocytopenic and prothrombotic at once — which is why her case presents as a platelet drop plus new leg pain. If suspected: stop all heparin (including flushes) and escalate; a non-heparin anticoagulant is started. Giving platelets would be the wrong reflex. Her wording is worth keeping: HIT is a prothrombotic complication, not simply “low platelets = bleeding.”

Why the screening is so strict. These drugs cannot tell the difference between the clot causing the stroke and a clot that is holding something closed — a recent surgical site, a healing ulcer, a small vessel in the brain. That is the entire reason for the eligibility checklist: recent surgery, recent bleeding, uncontrolled hypertension, prior intracranial hemorrhage. And it is why an ischemic stroke must be distinguished from a hemorrhagic one by imaging first — giving a thrombolytic into a brain bleed is catastrophic.

The one-line distinction to carry into the exam. Anticoagulants prevent a clot forming or extending. Thrombolytics dissolve a clot that is already there. Aspirin stops platelets clumping in the first place. Three drugs, three different moments in the life of a clot.

Dark stool versus melena — the discrimination she tests twice. Iron makes stool dark or greenish-black but formed and otherwise normal, in a patient who feels fine. Melena from GI bleeding is black, tarry, sticky and foul-smelling, and it comes with dizziness, weakness, pallor or tachycardia. Her pearl: dark stool can be expected with iron; black tarry stool plus dizziness and weakness is a different clinical picture. The stool colour alone does not decide it — the patient’s symptoms do.

The folate trap — genuinely important. Folate and B12 deficiency look identical on a blood count: both cause megaloblastic anemia with large red cells. Give folate to someone who is actually B12 deficient and the anemia improves — the count normalises, everyone is reassured — while the neurologic damage continues silently and can become permanent. The discriminator is neurologic: numbness, tingling, balance problems point to B12. That is why her slide says identify the underlying cause, and why B12 may need injection when absorption is the problem — as in pernicious anemia or after gastric surgery, where oral replacement cannot be absorbed at all.

Her framing is the exam point: safe erythropoiesis, not maximal. More hemoglobin sounds better, but raising it too high thickens the blood and drives clotting events — which is why there is a target range rather than a target of “normal.” And the drug is useless without iron: you can tell the marrow to build red cells, but it cannot build them out of nothing. That is why iron studies are monitored alongside hemoglobin.

Her pearl about antidotes, which is the right way to hold them. Do not memorise an antidote alone — connect it to the toxicity or bleeding pattern that tells you reversal may be needed. “Heparin → protamine” is a flashcard. “Falling BP, rising HR, black stool, patient on heparin → this may need reversal” is nursing.

How she tells you to study, and it is worth following. Build a prototype card for each drug — why · action · common adverse effect · danger · check · teach. Then practise give versus question against real vital signs, labs and symptoms. Then explain every wrong answer: why is that distractor less safe or less relevant? Her final line: do not copy the slide word for word — retrieve it and apply it to a patient.