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Year 4 > PPT - Drugs > Flashcards

PPT - Drugs Flashcards

1
Q

Cyclizine

A

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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2
Q

Promethazine

A

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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3
Q

Ondansetron

A

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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4
Q

Metoclopramide

A

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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5
Q

Carbemazepine

A

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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6
Q

Phenytoin

A

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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7
Q

Lamotrigine

A

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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8
Q

Diazepam

A

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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9
Q

Clonazepam

A

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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10
Q

Phenobarbital

A

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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11
Q

Vigabatrin

A

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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12
Q

Gabapentin

A

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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13
Q

Pregabalin

A

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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14
Q

Sodium valproate

A

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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15
Q

Ethosuximide

A

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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16
Q

Topiramate

A

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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17
Q

Side effects of amlodipine

A

Postural hypotension

Peripheral oedema

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18
Q

Side effects of furosemide

A

AKI
Dehydration
Postural hypotension
Hypokalaemia

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19
Q

AMTS

A 
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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20
Q

Symptoms of hyponatraemia

A

Off legs
Instability
Confusion
Immobility

Nausea and vomiting
Postural hypotension
Decreased appetite

Very low - seizures

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21
Q

Causes of hyponatraemia

A

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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22
Q

Treatment of hyponatraemia

A

IV fluids
TRICKLE and check every 4 hours

Too quick an increase can cause CENTRAL PONTINE MYELINOSIS

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23
Q

Treatment of hypernatraemia

A

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

24
Q

Causes of hyperkalaemia

A 
Sando K
ACEi
ARBs
Potassium sparing diuretics
Haemolysed blood sample
Thrombocytosis
25
Q

ECG changes in hyperkalaemia

A

Tented T waves
Broad QRS –> sine
Hyperdynamic T waves

26
Q

Treatment for hyperkalaemia

A

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

27
Q

Causes of hypokalaemia

A

Diuretics
Vomiting
Chronic diarrhoea
Bullaemia

28
Q

Symptoms and ECG changes in hypokalaemia

A

Achy
Nausea
Fatigue
Unwell

ECG: u waves

29
Q

Treatment for hypokalaemia

A

IV 20-40mmol/L
Sando K
Stop diuretics

30
Q

Symptoms of hypercalcaemia

A 
Headache
Aches and pains
Bone pain
Constipation
Renal stones
Polyuria
Polydipsia
Confusion
Depression
31
Q

ECG changes in hypercalcaemia

A

shortened QT interval

32
Q

Treatment of hypercalcaemia

A

IV fluids
Loop diuretic
Bisphosphonates
Prednisolone if due to malignancy

33
Q

Causes of hypercalcaemia

A

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

34
Q

Symptoms of hypocalcaemia

A

periorbital tingling

muscle twitching

35
Q

What is the dollshead reflex?

A

When you roll the head

Eyes should move together in opposite direction to head movement

36
Q

Aetiology of coma

A

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

37
Q

Investigations in coma

A 
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
38
Q

Management of coma

A 
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
39
Q

Drugs contraindicated in breast feeding

A

Almost all drugs pass into breast milk but these are contraindicated

Amiodarone
Chloramphenicol
Chemotherapy agents
Iodine
Methotrexate
Lithium
Tetracycline
Pseudoephedrine
Ergotamine
Cabergoline
Ergot alkaloids
40
Q

Drugs that decrease milk production

A

progestins
oestrogens
ethanol
bromocriptine

41
Q

MOA of local anaesthetics

A

Reversible blockade of voltage gated sodium channels

42
Q

Stages of Na+ channels

A

Resting - closed but able to open

Open - allow rapid influx

Inactivated - rapid change at cytoplasmic end. Resistant to depolarisation.

43
Q

Factors that influence local anaesthetic action

A

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

44
Q

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

A

A delta
C fibres

Blocked quicker than motor and sensory nerves
Most rapidly affected by LA
Have longest LA effect

45
Q

What determines the intrinsic and clinical potency of local anaesthetics

A

Intrinsic

  • pH and kPa
  • Lipophilic hydrophilic balance

Clinical

  • vasoconstrictor use
  • fibre size, type, myelination
  • frequency of nerve stimulation (increase = increased potency)
  • Electrolyte concentration
46
Q

Describe components of local anaesthetic

A

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
47
Q

Relationship between kPa and pH (onset and block)

A

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

48
Q

What can be added to local anaesthetic

A

Bicarbonate to increase speed of onset

Adrenaline to increase duration time (not in digits)

49
Q

Differences between epidural and spinal

A

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

50
Q

Side effects of local anaesthesia

A

Irritiation and inflammation
Iscahemia (if using vasoconstrictor)

CV

  • myocardial depression
  • vasodilation and hypotension
  • arrhythmia

CNS

  • agitation
  • confusion
  • tremor
  • convulsions
51
Q

What dose is in 10ml of 1% lidocaine?

A

1g in 100ml

100mg in 10ml

52
Q

Steps in general anaesthetic?

A
  1. premedication
  2. induction
  3. muscle relaxant and intubation
  4. maintenance of anaesthesia
  5. analgesia
  6. reversal
53
Q

Action of IV anaesthetics

A

Potent amnesics
Potent sedatives
Weak muscle relaxants

Enhance activity at GABA A receptors

54
Q

Factors affecting inhalation anaesthesia

A

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

55
Q

What is MAC?

A

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

Year 4 (7 decks)

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