Learn — Respiratory, GI & other system drugs

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Mydriasis and miotics

Mydriatics dilate the pupil, either by stimulating the radial dilator muscle with a sympathomimetic such as phenylephrine, or by paralysing the circular sphincter with an antimuscarinic such as tropicamide or atropine, which also paralyses accommodation and so produces cycloplegia. Miotics constrict the pupil by stimulating that sphincter with a cholinergic drug such as pilocarpine, which at the same time pulls the iris root away from the trabecular meshwork, and that is exactly why pilocarpine is used in acute angle-closure glaucoma.

Antimuscarinic mydriatics, from longest to shortest acting: atropine 1 per cent lasting 7 to 14 days, used in uveitis and for cycloplegic refraction in small children; homatropine 2 per cent lasting 1 to 3 days; cyclopentolate 1 per cent lasting about a day, the usual agent for cycloplegic refraction; and tropicamide 0.5 to 1 per cent lasting 4 to 6 hours, the routine drop for fundus examination.
Phenylephrine 2.5 or 10 per cent dilates without cycloplegia; the 10 per cent strength is absorbed systemically and can raise the blood pressure, so it is avoided in infants, in the elderly and in cardiac or hypertensive patients.
Miotics: pilocarpine 2 per cent is a direct muscarinic agonist used in acute angle closure and to reverse dilatation, while carbachol and the anticholinesterases act indirectly; their adverse effects are brow ache, dim vision in poor light and induced myopia.
Glaucoma drugs by class: prostaglandin analogues such as latanoprost and bimatoprost, given once at night as first-line and causing iris and periocular darkening with lash growth; beta-blockers such as timolol 0.5 per cent, which reduce aqueous production; the alpha-2 agonist brimonidine, contraindicated in infants because of apnoea; topical carbonic anhydrase inhibitors such as dorzolamide; and oral or intravenous acetazolamide.
Acute angle-closure glaucoma is an emergency treated with intravenous acetazolamide 500 mg, topical timolol, pilocarpine 2 per cent drops, intravenous mannitol 20 per cent, analgesia and an antiemetic, followed by definitive laser peripheral iridotomy to both eyes; pilocarpine only works once the pressure has fallen below about 40 to 50 mmHg, because above that the ischaemic sphincter cannot respond.
Timolol is absorbed systemically through the nasolacrimal duct and can cause bronchospasm, bradycardia and heart block, so it is contraindicated in asthma, chronic obstructive pulmonary disease, bradycardia and heart block, and every patient is taught punctal occlusion by pressing on the inner canthus for 1 to 2 minutes after the drop.
Instillation technique: wash hands, tilt the head back, pull down the lower lid and place a single drop into the conjunctival sac without touching the eye, then occlude the punctum; leave 5 minutes between different drops and instil ointments last.
Warn every dilated patient that vision will be blurred and light painfully bright for hours or days depending on the drug, that they must not drive, and that dark glasses help; in a small child atropine drops can cause systemic anticholinergic toxicity with flushing, fever and delirium, so the ointment is used with punctal occlusion.
Never dilate the pupil of a patient with a head injury or altered consciousness in whom the pupils are the neurological observation, and never dilate an eye with a shallow anterior chamber without ophthalmological advice.

Anticholinergic drugs

Anticholinergic, more precisely antimuscarinic, drugs competitively block acetylcholine at muscarinic receptors, so they dry secretions, dilate the pupil, relax smooth muscle in the gut, bladder and bronchi, and raise the heart rate by removing vagal tone. The same actions become a toxic syndrome when the dose is high or the patient is old, which is why this class is both an emergency treatment and a common ward cause of delirium, urinary retention and falls.

By use: atropine for bradycardia and organophosphate poisoning; hyoscine for motion sickness and to dry secretions; glycopyrrolate, which does not cross the blood-brain barrier and is therefore paired with neostigmine to reverse neuromuscular blockade; ipratropium and tiotropium by inhalation in chronic obstructive pulmonary disease; oxybutynin, tolterodine and solifenacin for overactive bladder; trihexyphenidyl and benztropine for drug-induced parkinsonism and acute dystonia; and dicyclomine for intestinal colic.
Predictable effects: dry mouth, blurred near vision and photophobia from cycloplegia, tachycardia, constipation, urinary hesitancy and retention, reduced sweating with heat intolerance, and confusion in the elderly.
The toxidrome is remembered as hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter and full as a flask: hyperthermia, dry skin and mouth, flushing, dilated pupils, delirium with visual hallucinations and plucking movements, and urinary retention.
Contraindications: narrow-angle glaucoma, benign prostatic hyperplasia or any bladder outflow obstruction, paralytic ileus and toxic megacolon, myasthenia gravis, and cardiac disease with tachyarrhythmia.
Poisoning, including Datura seed poisoning which is the common cause in India, is treated supportively with intravenous fluids, active cooling, benzodiazepines for agitation and catheterisation for retention; physostigmine 1 to 2 mg slowly intravenously with cardiac monitoring is reserved for severe central delirium and is avoided if the QRS is wide or tricyclic poisoning is suspected.
In the elderly the anticholinergic burden of several small drugs together, an antihistamine with an antidepressant, an antispasmodic and a bladder drug, adds up to falls, confusion and retention, and these drugs feature prominently on the Beers list of potentially inappropriate medicines.
Ward monitoring: pulse, temperature, bowel sounds and, above all, whether the patient has passed urine, because a distended bladder in a confused elderly patient on an anticholinergic is the diagnosis until proved otherwise.

Antidiarrhoeal agents

Antidiarrhoeal agents slow intestinal motility, reduce secretion or adsorb toxins, but they treat a symptom and never the cause: in acute diarrhoea the treatment that saves life is oral rehydration solution with zinc, and in dysentery an antimotility drug is dangerous. The examination and the ward both turn on knowing when such a drug is legitimate, which is the adult with watery traveller's diarrhoea, and when it is forbidden, which is the child, the febrile patient and the patient passing blood.

The standard of care in acute diarrhoea is low-osmolarity oral rehydration solution of 245 mOsm/L, containing sodium 75, glucose 75, chloride 65, potassium 20 and citrate 10 mmol/L, with zinc 20 mg daily for 14 days in children over 6 months and 10 mg daily under 6 months, alongside continued feeding and breastfeeding.
WHO Plan A treats no dehydration at home with extra fluids, zinc and food; Plan B treats some dehydration with 75 mL/kg of oral rehydration solution over 4 hours; Plan C treats severe dehydration with 100 mL/kg of Ringer lactate intravenously, given as 30 mL/kg in the first hour then 70 mL/kg over 5 hours in infants under 12 months, and as 30 mL/kg in 30 minutes then 70 mL/kg over 2.5 hours above that age.
Loperamide is a peripherally acting mu-opioid agonist that slows motility without central effects at normal doses: 4 mg initially and then 2 mg after each loose stool, to a maximum of 16 mg a day in adults, and for a short course only.
Loperamide is contraindicated in children under 5 years and is not recommended in childhood diarrhoea at all, in bloody diarrhoea or dysentery with fever, in suspected Clostridioides difficile infection, and in ulcerative colitis, where it can precipitate toxic megacolon; deliberate high-dose misuse causes QT prolongation and torsades de pointes.
Diphenoxylate with atropine behaves like loperamide but crosses into the brain in overdose; the atropine is added to discourage misuse, and children are especially vulnerable to the combined opioid and anticholinergic toxicity.
Racecadotril is an enkephalinase inhibitor that reduces intestinal secretion without slowing motility, given as 1.5 mg/kg three times a day in children; it is an adjunct only and never a substitute for oral rehydration solution and zinc.
Other agents: bismuth subsalicylate for traveller's diarrhoea, which blackens the tongue and stool and is avoided in children because of Reye syndrome; bulk agents such as ispaghula; cholestyramine for bile-acid diarrhoea; and octreotide for secretory and carcinoid diarrhoea.
Antibiotics are for specific indications only: cholera, shigellosis, amoebiasis and giardiasis with metronidazole, enteric fever, and Clostridioides difficile infection, which is treated with oral vancomycin or fidaxomicin after stopping the offending antibiotic. Routine antibiotics for viral gastroenteritis do harm.
Nursing monitoring: weigh the patient, classify dehydration by the WHO chart using sunken eyes, skin pinch, thirst and level of consciousness, record stool frequency and character, watch for hypokalaemia and metabolic acidosis, and protect the perianal skin.

Proton pump inhibitors (PPI)

Proton pump inhibitors are prodrugs that accumulate in the acid space of the gastric parietal cell, are converted there to an active sulphenamide and bind irreversibly to the H+/K+-ATPase, the final common pump of acid secretion, so a single daily dose suppresses acid for far longer than the short plasma half-life suggests. Because they can only bind pumps that are actively secreting, they must be taken 30 to 60 minutes before a meal, and the commonest reason a proton pump inhibitor appears not to work is that the ward gave it after breakfast.

Members and standard adult doses: omeprazole 20 mg, esomeprazole 40 mg, pantoprazole 40 mg, rabeprazole 20 mg and lansoprazole 30 mg once daily, doubled or given twice daily for erosive oesophagitis, Zollinger-Ellison syndrome and eradication regimens.
Indications: gastro-oesophageal reflux disease, peptic ulcer, Helicobacter pylori eradication, prophylaxis against NSAID ulcers, stress ulcer prophylaxis in the ventilated or coagulopathic critically ill patient, Zollinger-Ellison syndrome and upper gastrointestinal bleeding.
In upper gastrointestinal bleeding after endoscopic haemostasis the regimen is pantoprazole 80 mg intravenously as a bolus followed by 8 mg per hour for 72 hours, which reduces rebleeding.
Onset and duration: acid suppression begins within an hour, but the maximum effect needs 3 to 5 days of daily dosing and the inhibition lasts 24 to 48 hours because new pumps must be synthesised, so a proton pump inhibitor is not a rescue drug for immediate symptoms, for which an antacid or an H2 blocker is used.
Adverse effects that decide nursing action: hypomagnesaemia with tetany, tremor and arrhythmia on long-term use, vitamin B12 and iron deficiency, an increased risk of Clostridioides difficile and other enteric infections and of pneumonia, acute interstitial nephritis with a rising creatinine, and reduced bone density with fractures.
Interactions: omeprazole and esomeprazole inhibit CYP2C19 and reduce the activation of clopidogrel, so pantoprazole is the preferred agent in a stented patient; proton pump inhibitors also reduce the absorption of ketoconazole, itraconazole, atazanavir and iron salts, and raise methotrexate levels.
Helicobacter pylori is now treated for 14 days, and because clarithromycin resistance is high in India, bismuth-based quadruple therapy with a proton pump inhibitor, bismuth, tetracycline and metronidazole, or concomitant therapy, is preferred to the old clarithromycin triple regimen; the proton pump inhibitor is given twice daily throughout.
Nursing administration: give 30 to 60 minutes before the first meal of the day; do not crush enteric-coated tablets, but use the dispersible form or open the capsule into a small amount of acidic juice or soft food for a nasogastric tube and flush well; give the intravenous form slowly through a flushed line, because it is incompatible with many drugs.
Deprescribe deliberately: review at 4 to 8 weeks, step down to the lowest effective or on-demand dose, and warn the patient about rebound acid hypersecretion for a week or two after stopping a long course.
Alarm features mean endoscopy rather than a longer prescription: dysphagia, unintentional weight loss, anaemia, haematemesis or melaena, persistent vomiting, a palpable mass, and new dyspepsia over the age of 45 to 55.

Carminatives

A carminative is an agent given to relieve flatulence and the discomfort of trapped gas, either by acting as a defoaming agent that coalesces small gas bubbles into larger ones that can be passed, or by relaxing gastrointestinal smooth muscle and the lower oesophageal sphincter so that gas can be belched out. They are among the most used and least effective preparations in Indian practice, and their real clinical importance is the discipline of proving that a distended, colicky abdomen is wind and not an obstruction.

Simethicone, also called activated dimethicone, is the standard agent: a silicone polymer that lowers the surface tension of gas bubbles, is not absorbed from the gut and has no systemic effect, given as 40 to 125 mg after meals and at bedtime in adults and 20 to 40 mg with feeds in infants.
Simethicone is also given before endoscopy and abdominal ultrasound to clear the gas that obscures the view, and it is combined with antacids and antispasmodics in many Indian preparations.
The evidence is weak: controlled trials of simethicone in infantile colic show no benefit over placebo, so the honest advice to parents is reassurance, attention to feeding and winding technique and a review of the mother's diet, rather than an escalating list of drops.
Traditional carminatives include peppermint oil, which relaxes smooth muscle through calcium channel blockade and is given as enteric-coated capsules in irritable bowel syndrome, along with fennel, ajwain, ginger, dill water, asafoetida, cardamom and clove.
Peppermint oil worsens gastro-oesophageal reflux by relaxing the lower oesophageal sphincter, and menthol-containing preparations must never be applied to an infant's face or nostrils, because they can cause apnoea and laryngospasm.
Gripe water is not a regulated medicine: preparations vary and have contained alcohol, sugar, sodium bicarbonate and herbs; it can displace breast milk, cause hyponatraemia and carry contaminated water, and Indian paediatric practice advises against it.
Infantile colic is defined by the rule of threes, crying for more than 3 hours a day on more than 3 days a week for more than 3 weeks in a thriving infant under 3 months, and it resolves spontaneously by 3 to 4 months; management is parental support, holding and soothing, feeding technique and winding.
The nursing responsibility is to exclude what imitates colic: intussusception, an incarcerated hernia, volvulus, obstruction, cow's milk protein allergy, urinary tract infection and a hair tourniquet around a digit.

Antiemetics — MOA and use

Vomiting is coordinated by the vomiting centre in the medulla, which receives input from the chemoreceptor trigger zone in the area postrema, where dopamine D2, serotonin 5-HT3 and neurokinin NK1 receptors sit outside the blood-brain barrier, from the vestibular apparatus through histamine H1 and muscarinic receptors, from the cortex, and from vagal afferents in the gut. Antiemetics are therefore chosen by matching the drug to the receptor driving that particular patient's vomiting, which is why an antihistamine works for motion sickness and a 5-HT3 blocker does not.

5-HT3 antagonists such as ondansetron 4 to 8 mg orally or intravenously every 8 hours, granisetron and palonosetron are first-line for chemotherapy-induced and postoperative vomiting and for vomiting in gastroenteritis; they prolong the QT interval and cause headache and constipation, and the maximum single intravenous dose of ondansetron is 16 mg.
Dopamine D2 antagonists: metoclopramide 10 mg up to three times a day is also a prokinetic through 5-HT4 agonism, but is limited to about 5 days because of extrapyramidal reactions and is contraindicated in bowel obstruction, perforation and phaeochromocytoma; domperidone does not cross the blood-brain barrier and so causes fewer extrapyramidal effects, but it prolongs the QT interval.
Phenothiazines such as prochlorperazine, promethazine and chlorpromazine act at D2, H1 and muscarinic receptors and are useful in vertigo and palliative care; promethazine causes severe tissue injury and even gangrene if it extravasates or is injected into an artery.
H1 antihistamines and antimuscarinics, including promethazine, cinnarizine, meclizine, dimenhydrinate and transdermal hyoscine, are the drugs for motion sickness and vestibular vertigo, and they are taken before the journey because they prevent far better than they treat.
NK1 antagonists such as aprepitant and fosaprepitant are added for highly emetogenic chemotherapy in combination with a 5-HT3 antagonist and dexamethasone, often with olanzapine; dexamethasone is a potent adjunct in its own right and olanzapine is used for breakthrough vomiting.
Nausea and vomiting of pregnancy is treated first with doxylamine plus pyridoxine, with dietary advice and ginger, and ondansetron is reserved for when these fail.
Postoperative nausea and vomiting risk, raised by female sex, non-smoking, previous postoperative vomiting or motion sickness and postoperative opioids, guides prophylaxis, usually ondansetron 4 mg with dexamethasone 4 to 8 mg given during surgery.
The adverse effects that decide nursing action are acute dystonia with metoclopramide and the phenothiazines, seen as oculogyric crisis, torticollis, trismus and tongue protrusion, mostly in young women and children and treated with intravenous promethazine or an anticholinergic; and QT prolongation with torsades from ondansetron and domperidone, so potassium and magnesium are checked and the ECG reviewed in patients on other QT-prolonging drugs.
Before giving any antiemetic, look for the cause: raised intracranial pressure, bowel obstruction, myocardial infarction, diabetic ketoacidosis, pregnancy, uraemia and drug toxicity such as digoxin all present with vomiting, and an antiemetic simply masks them.

Drug allergy — first sign

A drug allergy is an immune-mediated adverse reaction to a medicine — quite separate from a dose-related side effect — and because it needs prior sensitisation it appears on a second or later exposure rather than the first. It matters at the bedside because the first sign is almost always cutaneous, and the nurse who acts on itching and urticaria, before the wheeze and the fall in blood pressure, is the one who prevents an anaphylactic death.

The first and commonest sign is cutaneous: itching of the palms, soles and scalp, flushing, urticarial weals and angio-oedema of the lips and eyelids, present in about 80–90% of anaphylactic reactions.
The sequence to watch is skin, then gut (cramps, vomiting), then airway (hoarseness, stridor from laryngeal oedema, wheeze), then circulation (tachycardia, hypotension, collapse). By the time the blood pressure falls the airway is often already closing.
Gell and Coombs types: Type I is immediate IgE-mediated within minutes to an hour (urticaria, bronchospasm, anaphylaxis); Type II is cytotoxic IgG (penicillin-induced haemolysis, drug-induced thrombocytopenia); Type III is immune-complex at 1–3 weeks (serum sickness, vasculitis); Type IV is delayed T-cell mediated at 48–72 hours or later (contact dermatitis, maculopapular rash, Stevens–Johnson syndrome).
The drug that treats it is adrenaline 0.3–0.5 mg intramuscularly (0.01 mg/kg; 1:1000 = 1 mg/mL) into the mid-anterolateral thigh, repeated every 5–15 minutes if there is no response. Intramuscular thigh, not subcutaneous and not deltoid; antihistamine and hydrocortisone are second-line and must never delay the adrenaline.
The usual culprits are beta-lactams (penicillins and cephalosporins), sulphonamides, NSAIDs including aspirin, radiocontrast media, neuromuscular blockers and vancomycin.
Vancomycin red-man syndrome is direct histamine release from a rapid infusion, not IgE-mediated allergy — the answer is to slow the infusion to at least 60 minutes per gram and pre-treat with an antihistamine, not to abandon the drug.
Cross-reactivity between penicillins and cephalosporins is far lower than the old 10% teaching; it depends on a shared R1 side chain and is under about 2% for later-generation cephalosporins, so a documented mild penicillin rash rarely bars every beta-lactam.
Monitoring and prevention: ask about drug allergy before every first dose, record the drug AND what happened in the case sheet, the drug chart and the wrist band, keep the patient in view for the first 15–30 minutes of any parenteral drug, and keep adrenaline within reach of the trolley.
Every suspected reaction is reported on the suspected adverse drug reaction form to the nearest ADR Monitoring Centre under the Pharmacovigilance Programme of India, and the allergy is carried forward into the discharge summary.

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