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QUM (Core Concept)

Ensuring the right patient receives the right medicine, at the right dose, for the right reason, while minimising harm (appropriate, safe, effective use)

Medication Errors

Preventable events causing inappropriate medication use or harm (e.g. wrong drug, dose, patient, route, omission)

Systems Approach

Focus on improving systems (e.g. eMeds, standardisation) rather than blaming individuals to reduce errors

Pharmacodynamics Definition

What the drug does to the body via interactions with biological targets

Drug Targets

Receptors, ion channels, enzymes, and transporters that drugs interact with to produce effects

Receptor Theory

Drug binds receptor --> forms complex -->produces biological response

Agonists vs Antagonists

Agonists activate receptors; antagonists bind but block without activating

Affinity vs Efficacy

Affinity = binding strength; efficacy = ability to produce effect

Dose-Response Relationship

Increasing dose increases effect up to a maximum; relates to potency and efficacy

Potency

Amount of drug needed to produce an effect (higher potency = lower dose required)

Efficacy

Maximum effect a drug can produce regardless of dose

Adverse Drug Reactions (ADRs)

Harmful effects from drugs due to dose, allergy, or interactions; higher risk in elderly/polypharmacy

Pharmacokinetics Definition

What the body does to the drug

Absorption

Movement of drug into bloodstream; depends on route, blood flow, and drug properties

First-Pass Metabolism

Liver metabolises oral drugs before systemic circulation, reducing bioavailability

Distribution

Drug movement through body; influenced by blood flow, protein binding, and barriers

Metabolism

Liver (CYP450) alters drugs to be more water-soluble; can activate or inactivate drugs

Excretion

Removal of drugs, mainly by kidneys; depends on renal function

Routes of Administration

Oral, IV, IM, SC, inhalation, sublingual, transdermal; affect onset and bioavailability

Half-Life (t½)

Time for drug concentration to reduce by 50%; determines dosing and steady state

CYP450 Pathway

Liver enzyme system; inhibition increases drug levels, induction decreases drug levels

ANS Overview

Controls involuntary functions and maintains homeostasis via two opposing systems

ANS pathway

Two-neuron pathway: preganglionic (CNS-->ganglion) and postganglionic (ganglion-->organ)

Parasympathetic System

Rest and digest; long preganglionic, short postganglionic fibres

Sympathetic System

Fight or flight; short preganglionic, long postganglionic fibres

Neurotransmitters & Receptors

Parasympathetic uses acetylcholine (muscarinic); sympathetic uses noradrenaline (a, B)

Muscarinic Receptors

Parasympathetic receptors causing decrease HR, increases digestion, bronchoconstriction

Adrenergic Receptors

a1 (vasoconstriction), B1 (increases HR), B2 (bronchodilation)

Sympathomimetics

Drugs that mimic sympathetic activity (e.g. B2 agonists --> bronchodilation)

Sympatholytics

Drugs that block sympathetic receptors (e.g. beta-blockers --> decrease HR)

Parasympathomimetics

Drugs that mimic ACh --> increases digestion, decrease HR

Anticholinergics

Block muscarinic receptors --> increases HR, bronchodilation

Mechanism-Based Thinking

Predict drug effects by receptor type, location, and agonist/antagonist action

Neurotransmitters & Function

ACh = rest/digest; noradrenaline = fight/flight

Liver Function Importance

Impaired liver --> decreases metabolism --> increases drug levels and toxicity

Causes of CLD

Alcohol, hepatitis B/C, NAFLD, autoimmune disease, drugs/toxins

Signs of CLD

Early fatigue/nausea; advanced jaundice, ascites, oedema, bleeding, encephalopathy

Portal Hypertension

Increased resistance --> increases portal pressure --> ascites and varices

Ascites

Fluid accumulation due to increase pressure and decrease albumin

Hepatic Encephalopathy

Ammonia buildup affects brain due to liver failure

Coagulopathy

Reduced clotting factors --> increased bleeding risk

CLD Management

Treat cause, manage complications, monitor LFTs and INR

Kidney Functions

Excretion, fluid/electrolyte balance, acid-base control, hormone production

Serum Creatinine

Marker of kidney function; increase indicates impairment

eGFR

Best indicator of kidney filtration ability

Urea

Waste product, increases in renal dysfunction

Electrolytes in kidney failure

Imbalance (especially increase K+)

Renal Impairment

Reduced clearance --> drug accumulation and toxicity

Dose Adjustment

Required in reduced eGFR to prevent toxicity

Renal Disease Overview

Disrupts fluid, electrolytes, waste removal, and drug clearance

AKI Definition

Sudden decline in kidney function --> decrease GFR and increase waste products

Pre-Renal AKI

Reduced blood flow to kidneys (e.g. dehydration)

Intrinsic AKI

Damage to kidney tissue (e.g. toxins, ischemia)

Post-Renal AKI

Urinary obstruction (e.g. stones)

AKI Risk Factors

Elderly, CKD, dehydration, nephrotoxic drugs

AKI Symptoms

Oliguria, fluid overload, increase creatinine, electrolyte imbalance

AKI Management

Treat cause, correct fluids, manage electrolytes

Drug Considerations in AKI

Reduced clearance --> dose adjustment required

CKD Definition

Progressive, irreversible loss of kidney function

CKD Causes

Diabetes, hypertension, cardiovascular disease

CKD Staging

Based on declining eGFR

CKD Symptoms (Uraemia)

Fatigue, nausea, fluid retention, toxin buildup

CKD Complications

CVD, hyperkalaemia, anaemia, bone disease

CKD Management

Control BP/glucose, manage complications, slow progression

Renal Replacement Therapy (RRT)

Needed in ESKD or severe AKI

Haemodialysis

Blood filtered externally to remove waste and fluid

Peritoneal Dialysis

Uses peritoneum to filter waste via diffusion

Dialysis Drug Considerations

Some drugs removed; adjust dose/timing

Renal Transplant

Best long-term option; requires immunosuppression

AKI vs CKD

AKI = sudden/reversible; CKD = gradual/irreversible

Pharmacology Link

Renal disease decreases excretion --> increase drug levels and toxicity risk

GI Overview

GI system balances acid secretion and mucosal protection; disease occurs when aggressive factors overpower protection

Gastric Acid Secretion

Parietal cells produce acid stimulated by histamine (H2), acetylcholine, and gastrin

Protection Mechanisms

Mucus, bicarbonate, and blood flow protect gastric lining from acid damage

Pathophysiology of GORD

Reflux of gastric acid into oesophagus due to weak LES, delayed emptying, or increase abdominal pressure

Clinical Features of GORD

Heartburn, regurgitation, chest pain; complications include oesophagitis, Barrett’s oesophagus, cancer

Risk Factors for GORD

Obesity, pregnancy, smoking, alcohol, trigger foods, certain drugs (e.g. NSAIDs, anticholinergics)

Lifestyle Management of GORD

Weight loss, avoiding triggers, elevating head of bed

Antacids

Neutralise stomach acid for rapid symptom relief

H2 Receptor Antagonists

Block histamine receptors --> decrease acid secretion

Proton Pump Inhibitors (PPIs)

Irreversibly inhibit proton pumps --> most effective acid suppression

What is PUD?

Ulceration of gastric or duodenal lining due to acid damage and reduced mucosal protection

Cause of PUD (H. pylori)

Produces urease --> damages mucosa and causes inflammation

Cause of PUD (NSAIDs)

Inhibit prostaglandins --> decreases mucus/bicarbonate --> increases acid damage

Clinical Features of PUD

Epigastric pain, nausea, possible bleeding

Diagnosis of PUD

Urea breath test for H. pylori detection

Management of H. pylori PUD

Triple therapy: PPI + 2 antibiotics

Management of NSAID-Induced PUD

Stop NSAID if possible; use PPI or misoprostol

Mucosal Protection Drugs

Misoprostol increases mucus; sucralfate forms protective barrier

Definition of UI

Involuntary leakage of urine; not a normal part of ageing

Normal Bladder Function

Coordination of detrusor muscle, sphincter, pelvic floor, and nervous system

Pathophysiology of UI

Occurs when bladder control mechanisms fail

Stress Incontinence

Leakage with increased pressure (coughing, sneezing) due to weak pelvic floor

Urge Incontinence

Sudden urge with leakage due to overactive detrusor muscle

Overflow Incontinence

Dribbling and incomplete emptying due to obstruction or weak bladder

Functional Incontinence

Normal bladder but inability to reach toilet

Mixed Incontinence

Combination of multiple types

Risk Factors for UI

Age, pregnancy, obesity, prostate disease, neurological conditions

Consequences of UI

UTIs, falls, skin breakdown, social isolation

Non-Pharmacological Management

Pelvic floor exercises, bladder training, lifestyle changes