Geriatric and Paediatric Pharmacology and Nervous System

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Lecture Five: Geriatric and Paediatric Pharmacology/ Autonomic Nervous System

Absorption

Slower peristalsis and gastric emptying = greater degree of drug absorption

Infants: bile secretion slower – impaired absorption of some fat-soluble drugs. Also,

gastric acid secretion is erratic = less absorption of some acidic drugs. Sometimes

advantageous eg. Penicillin.

Parenteral administration limited – poor peripheral tissue perfusion and less muscle

mass.

Topical administration- thinner skin and SA/body mass ratio is higher = fast delivery

of drug.

Distribution

Lower concentration of plasma proteins in blood AND proteins have decreased

capacity to bind with drugs = greater chance of toxicity.

Bilirubin may be displaced from albumin by drugs that bind strongly to proteins –

bilirubin may cross BBB in infants = neurotoxicity.

Fat deposits increase with age, influencing distribution of fat soluble drugs. In

elderly, drug effects may decrease in magnitude but have prolonged effects.

Extracellular body fluid decreases with age – in neonates, lower concentration of

some water soluble drugs = diminished response.

Metabolism and Excretion

Certain enzymes do not reach max levels until 3 years of age – lower metabolic

clearance = prolonged half-life.

Some drugs, however, induce cytochrome p450 levels. These are anticonvulsants,

corticoids, antibiotics and barbiturates. This = higher levels of microsomal enzymes

which will increase drug metabolism.

Metabolism decreases with age.

GFR is less in neonates (<1 year) and elderly.

Paediatric Dosage Rules

Young’s Rule:

Age x adult dose / Age + 12 = Dose

*This rule does not consider BMI

Clarke’s Rule (body weight):

Weight x adult dose / 68 = Dose

*Considers BMI

Clarke’s Rule (SA)

SA x adult dose / 1.73 = Dose.

*Uses a ‘nomo-gram-style’ chart to determine SA. This rule is the most accurate.

Anti-inflammatory Drugs

Two types: steroid origin (anti-immune effects), and NSAID (prostaglandin inhibitors).

PROSTAGLANDINS:



Enhance histamine action.



Stimulate nociceptors directly.



Stimulate hypothalamus and raise body temp. Increased temp = increased enzyme

activity and increased Ab activity.



May stimulate neutrophil diapedesis (WBC movement).

NSAID’s

Usually acidic.

Decrease gastric acid mucous production, increase gastric digestive secretions.

As PGs control renal flow rate, NSAIDs may decrease GFR, causing electrolyte

imbalance (sodium and fluid retention) = hypertension.

Salicylates:

Analgesic, anti-inflammatory, anti-pyretic and anti-platelet. Aspirin.

Salicylate Derivatives:

Direct derivatives: Suldinac and Diflunisal. Often prescribed with paracetamol.

Have less gastric effects, and can cause diarrhoea.

Methyl salicylate: oil of wintergreen. Topical – promotes anaesthesia, anti-

inflammatory and warming.

Copper salicylate: promotes salicylates in skin. Eg. copper bangles.

Propionic Acid Derivatives:

Chemical modifications of acetic acid:-

Naproxen – longer t ½ therefore requires fewer doses.

Ibuprofen and Ketoprofen – these, along with Naproxen, are aggressive to stomach

lining.

Indolacetic Acid

Been around since 1960’s. V. effective prostaglandin E2 inhibitors, however high incidences

of GI disturbances and CNS effects have been noted. Rectal administration often prescribed.

Indomethacin and Suldinac

Fenamates

Late 1980’s. For pain associated with muscle, connective tissue and arthritis. Often

prescribed with a prostaglandin analogue misoprostol – acts as a protective drug for people

on long term NSAIDs.

Diclofenac.

Oxicams

Late 1980’s. T ½ 2 days – takes around 10 days to reach a steady state. Potent gastric

irritants.

Piroxicam and Tenoxicam

Pyrazolones

*No longer available – causes anaemias.

Phenylbutazone

NSAIDs as COX Inhibitors

COX1 iso enzyme: stomach – involved in prostaglandin synthesis.

COX2 iso enzyme: joints.

Drugs available that target only COX2: Celecoxib and Rofecoxib. These are weak

acidic compounds unrelated to other NSAIDs.

Celecoxib: affects heart in high doses.

Rofecoxib: affects enzymes in heart = MIs and disease. No longer available!

COX2 Inhibitors: Pro’s and Con’s

Studies by pharmaceutical companies claim significant reduction in arthritic pain, and

in ulcer complications as opposed to Naproxen and Ibuprofen.

Incidence of severe GI problems is low and comparable to placebos.

Benefits no greater than other drugs, except for decreased irritation.

Corticosteroids

Glucocorticoids – ‘metabolic switches’ – penetrates into cell as this is where the

receptors for steroids lie, and switches off machinery related to inflammation.

Stabilize lysosomes and mast cells.

Inhibit protein synthesis.

Decrease neutrophil and macrophage responsiveness.

Inhibit T helper cell function – impacts immune system = problematic in long term

users.

Inhibit fibroblasts.

Other actions:

Hypernatraemia (high sodium levels).

Substrate (triglyceride) mobilizing – fat mobilizer, meaning fat may redeposit in

unwanted areas.

Synergistic with adrenaline.

Insulin antagonist – contraindicated for diabetes.

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