PPT - Drugs Flashcards by Amy Szuman

Cyclizine

H1 Receptor Antagonist

Actions: sedative (less so than others), antiemetic

MOA: Competitive inhibition of H1 receptor in vestibular nuclei and vomiting centre.

ADE: significant first pass metabolism

Use: nausea in early pregnancy. Motion sickness and other emesis of vestibular origin

Side effects: sedation, confusion in elderly, severe respiratory depression in under 2s, dry mouth (anticholinergic)

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Promethazine

H1 Receptor antagonist

Actions: sedative, antiemetic

MOA: Competitive inhibition of H1 receptors in vestibular nuclei and vomiting centre

ADE: significant first pass metabolism

Use: nausea in early pregnancy. Motion sickness. Meniere’s or other causes of emesis that is vestibular in origin.

Side effects: sedation, confusion in elderly, respiratory depression in under 2s, dry mouth (anticholinergic)

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Ondansetron

5HT3 receptor antagonist

Actions: antiemetic

MOA: competitive inhibition of 5HT3 receptors in chemoreceptor trigger zone (CTZ) and at sensory endings of vagal afferents in GIT

ADE: Metabolised by cytochrome p450

Use: chemotherapy related sickness. Post-op or post-radiotherapy. Limited efficacy in motion sickness.

Side effects: well tolerated. GIT disturbance and headache.

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Metoclopramide

D2 receptor antagonist

Actions: antiemetic. antipsychotic

MOA: Competitive antagonism of D2 receptors in the chemoreceptor trigger zone.

ADE: P450 metabolism

Use: N&V post chemotherapy, radiotherapy and surgery.

Side effects: EPS (Parkinsonian symptoms). Prolactin release (galactorrhoea), hypotension, antihistamine and anitmuscarinic actions.

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Carbemazepine

Sodium channel blocker

Actions: anticonvulsant, relieves neuropathic pain

MOA: blocks Na channels in inhibit action potential initiation and propagation. Acts preferentially on epileptic focus (rapid firing)

ADE: P450 metabolism

Use: epilepsy (partial and generalised), NOT ABSENCE. neuropathic pain, bipolar disorder

Side effects: drowsiness, headache, mental disorientation, motor disturbance
Rare: liver damage, agranulocytosis, aplastic anaemia

P450 INDUCER

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Phenytoin

Sodium channel blocker

Actions: anticonvulsant

MOA: Blocks Na channels to inhibit propagation and initiation of action potentials

ADE: P450 inducer

Use: generalised and focal seizures, not absence. bipolar, neuropathic pain

Side effects: drowsiness, headache, mental disorientation, motor disturbance
Rare: liver damage, agranulocytosis, aplastic anaemia
TERATOGEN - cleft palate

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Lamotrigine

Inhibits glutamate release

Action: anticonvulsant

MOA: inhibits glutamate release and decreases post-synaptic excitation. May be due to Na channel inhibition

Use: partial and generalised seizures. Bipolar.

Side effects: dizziness, headache, double vision, sedation

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Diazepam

Benzodiazepine receptor agonist

Actions: anticonvulsant. hypnotic. anxiolytic

MOA: benzodiazepine receptor agonist on GABA receptor enhancing channel opening by GABA. Increases Cl influx reducing excitability

Use: status epilepticus

Side effects: sedation, tolerance, addiction
Severe respiratory depression

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Clonazepam

Benzodiazepine receptor agonist

Actions: anticonvulsant. hypnotic. anxiolytic

MOA: benzodiazepine receptor agonist on GABA receptor enhancing channel opening by GABA. Increases Cl influx reducing excitability

Use: tonic clonic and absence seizures

Side effects: sedation, tolerance, addiction
Severe respiratory depression

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Phenobarbital

Barbiturate agonist

Actions: anticonvulsant

MOA: binds to barbiturate site on GABA receptor causing increased opening. Increasing Cl- influx decreasing excitability.

Use: tonic clonic and simple partial seizures.

Side effects: highly sedative. megaloblastic anaemia. hypersensitivity reactions
OD = coma, respiratory and cardiac failure

P450 INDUCER

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Vigabatrin

GABA transaminase inhibitor

Actions: anticonvulsant

MOA: inhibits GABA transaminase which breaks down GABA. Increase synaptic GABA, increase Cl- influx, reduce excitability

Use: adjunct to other anticonvulsants

Side effects: sedation, fatigue, hyperactivity in children
Visual field defects if long-term use

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Gabapentin

Calcium channel blocker

Actions: anticonvulsant, analgesic

MOA: Blocks voltage activated Ca channels to block calcium entry and prevent exocytosis of glutamate

Use: adjunct for partial seizures, neuropathic pain

Side effects: sedation, dizziness, unsteadiness

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Pregabalin

Calcium channel blocker

Actions: anticonvulsant, analgesia

MOA: blocks voltage gated calcium channels to prevent calcium influx therefore restricting exocytosis of glutamate

Use: adjunct for partial seizures, neuropathic pain

Side effects: dizziness, sedation, unsteadiness

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Sodium valproate

Na channel antagonist & inhibits GABA transaminase

Action: anticonvulsant, mood stabiliser

MOA: blocks voltage gated sodium channels to inhibit action potential initiation and propagation.
Inhibits GABA transaminase to decrease GABA breakdown, increase synaptic GABA, decreased excitation

Use: epilepsy. Manic phase of bipolar. Migraine

Side effects: nausea and vomiting, tremor, weight gain, reproductive dysfunction, hepatic and pancreatic toxicity
TERATOGEN: neural tube defects

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Ethosuximide

Calcium channel blocker (neuronal)

Action: anticonvulsant

MOA: blocks T type sodium channels in thalamic neurons to counteract slow 3Hz spike and wave firing

Use: absence seizures

Side effects: anorexia, GI upset, rash, drowsiness, fatigue

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Topiramate

Glutamate receptor antagonist

Actions: anticonvulsant

MOA: block AMPA receptors for glutamate and sodium channels and potentiates GABA actions

Use: generalised tonic clonic seizures, partial seizures. Migraine

Side effects: psychomotor slowing, memory impairment, paraesthesia, sedation, fatigue, confusion, decreased appetite and weight.
Rare: vision loss

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Side effects of amlodipine

Postural hypotension

Peripheral oedema

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Side effects of furosemide

AKI
Dehydration
Postural hypotension
Hypokalaemia

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AMTS

Age
DOB
Place
Time
Year
Give 42 West Street
WWII 
Current monarch 
Recognise 2 people
Recall 42 West Street
Count 20-1

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Symptoms of hyponatraemia

Off legs
Instability
Confusion
Immobility

Nausea and vomiting
Postural hypotension
Decreased appetite

Very low - seizures

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Causes of hyponatraemia

Heart failure, liver failure, renal failure
Infection
Drugs - diuretics, SSRIs, PPIs, phenytoin
SIADH - lung cancer, infection
Stroke
Brain tumour
Primary aldosteronism (Addison’s)

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Treatment of hyponatraemia

IV fluids
TRICKLE and check every 4 hours

Too quick an increase can cause CENTRAL PONTINE MYELINOSIS

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Treatment of hypernatraemia

IV 5% dextrose
Drop slowly - check regularly
No more than 8 mmol/L drop in 24 hourss

Causes of hyperkalaemia

Sando K
ACEi
ARBs
Potassium sparing diuretics
Haemolysed blood sample
Thrombocytosis

ECG changes in hyperkalaemia

Tented T waves Broad QRS --> sine Hyperdynamic T waves

Treatment for hyperkalaemia

Calcium carbonate/gluconate - to stabilise myocardium Insulin and dextrose infusion Repeat - if it fails then renal haemofiltration

Causes of hypokalaemia

Diuretics Vomiting Chronic diarrhoea Bullaemia

Symptoms and ECG changes in hypokalaemia

Achy Nausea Fatigue Unwell ECG: u waves

Treatment for hypokalaemia

IV 20-40mmol/L Sando K Stop diuretics

Symptoms of hypercalcaemia

``` Headache Aches and pains Bone pain Constipation Renal stones Polyuria Polydipsia Confusion Depression ```

ECG changes in hypercalcaemia

shortened QT interval

Treatment of hypercalcaemia

IV fluids Loop diuretic Bisphosphonates Prednisolone if due to malignancy

Causes of hypercalcaemia

Bony mets (BBKTP) Breast Bowel Kidney Thyroid Prostate Myeloma PTH secreting tumours Primary hyperparathyroidism (most common) Thiazide diuretics Iatrogenic (Calcium supplements) Milk alkali syndrome

Symptoms of hypocalcaemia

periorbital tingling | muscle twitching

What is the dollshead reflex?

When you roll the head | Eyes should move together in opposite direction to head movement

Aetiology of coma

Vascular - cerebral hypoperfusion (cardiac), cerebrovascular accident, hypertensive encephalopathy Infection - meningitis, encephalitis, abscess, malaria, toxoplasmosis Trauma - SAH, SDH, depressed skull fracture Autoimmune - vasculitis Metabolic - hypo/hyperglycaemia, hypercalcaemia, hyper/hyponatraemia, hypopituitarism, hypothyroid, hypoxia, hypercapnia Neoplasm - brain tumour, SOP Drugs - over dose sedative, alcohol Carbon monoxide poisoning

Investigations in coma

``` Blood glucose ABG Bloods - FBC, U&Es, LFTs, TFTs, troponin Urine dip and pregnancy test Paracetamol and salicylate levels Blood cultures Blood films for malaria Ethanol levels ECG CXR Head CT/MRI EEG LP ```

Management of coma

``` Resuscitation - intubation and ventilation if needed IV thiamine and glucose if cause unclear Trial naloxone and flumazenil Mannitol if raised ICP Fluid rehydration Prevention of pressure sores Adequate nutrition ```

Drugs contraindicated in breast feeding

Almost all drugs pass into breast milk but these are contraindicated ``` Amiodarone Chloramphenicol Chemotherapy agents Iodine Methotrexate Lithium Tetracycline Pseudoephedrine Ergotamine Cabergoline Ergot alkaloids ```

Drugs that decrease milk production

progestins oestrogens ethanol bromocriptine

MOA of local anaesthetics

Reversible blockade of voltage gated sodium channels

Stages of Na+ channels

Resting - closed but able to open Open - allow rapid influx Inactivated - rapid change at cytoplasmic end. Resistant to depolarisation.

Factors that influence local anaesthetic action

Local concentration of LA Size of nerve fibre Nerve myelination Length of nerve exposed to LA

Which nerve fibres carry pain? How are they affected by LA

A delta C fibres Blocked quicker than motor and sensory nerves Most rapidly affected by LA Have longest LA effect

What determines the intrinsic and clinical potency of local anaesthetics

Intrinsic - pH and kPa - Lipophilic hydrophilic balance Clinical - vasoconstrictor use - fibre size, type, myelination - frequency of nerve stimulation (increase = increased potency) - Electrolyte concentration

Describe components of local anaesthetic

Lipophilic end - allows for transfer across nerve membrane Amide bond Hydrophilic end - allows binding to sodium channels once across lipid membrane - LAs are weak bases -

Relationship between kPa and pH (onset and block)

The closer the pKa is to physiological pH then faster onset due to high concentration of non-ionised base (when non-ionised it is lipid soluble) The higher the kPa the slower the onset but the more effective the block

What can be added to local anaesthetic

Bicarbonate to increase speed of onset Adrenaline to increase duration time (not in digits)

Differences between epidural and spinal

Epidural is above dura, leave in catheter for top ups, 15-30 minute onset Spinal - Into subarachnoid space - much lower drug doses (especially opioids) Both between L3 and 4 Spread depends on density of solution and posture post event

Side effects of local anaesthesia

Irritiation and inflammation Iscahemia (if using vasoconstrictor) CV - myocardial depression - vasodilation and hypotension - arrhythmia CNS - agitation - confusion - tremor - convulsions

What dose is in 10ml of 1% lidocaine?

1g in 100ml | 100mg in 10ml

Steps in general anaesthetic?

1. premedication 2. induction 3. muscle relaxant and intubation 4. maintenance of anaesthesia 5. analgesia 6. reversal

Action of IV anaesthetics

Potent amnesics Potent sedatives Weak muscle relaxants Enhance activity at GABA A receptors

Factors affecting inhalation anaesthesia

Absorption of alveolar membranes Solubility Cardiac output Relative concentration at brain in equilibrium

What is MAC?

Minimum alveolar concentration Measures potency concentration of a vapour in the lungs that is needed to prevent movement (motor response) in 50% of subjects in response to surgical (pain) stimulus