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Year 2 PODT > Miscellaneous lectures > Flashcards

Miscellaneous lectures Flashcards

1
Q

describe the mode of action of Carbamazepine

A
  • Sodium channel blocker
  • Strong hepatic enzyme inducer (CYP3A4)
  • Hepatic metabolism
  • Auto-induction (over weeks-months) of liver enzymes can fall by 50%.
  • Also used for neuropathic pain.
  • Use slow release preparation - better tolerability
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2
Q

describe some of the side effects of Carbamazepine

A
  • Dose dependent - diplopia (double vision), ataxia (loss of full control of bodily movements), sedation, fatigue.
  • Hyponatraemia - SIADH (SIADH-syndrome of antidiruetic hormone release) : increases ADH release.
  • Idiosyncratic (unpredictibly) - bone marrow suppression, hypersensitivity, hepatic derangement, rash.
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3
Q

describe some of the interactions with Carbamazepine

A

Beware with other sodium channel blockers - compounding of side effects.

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4
Q

describe the mode of action of Phenytoin

A

Sodium channel blocker

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5
Q

describe some of the side effects of Phenytoin

A 
P= P450 interactions
H = Hirsutism - abnormal growth of hair on woman's face or body
E = Enlarged gums
N = Nystagmus - involuntary movement of the eyes
Y = Yellow-browning of the skin
T = Teratogenic
O = Osteomalacia - softening of bones - vitamin D deficiency
I = Interferes with folate metabolism, leads to anaemia 
N = Neuropathies: vertigo, ataxia, headaches
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6
Q

describe some of the interactions of phenytoin

A

Hepatic enzyme inducer.

Phenytoin conc. increased with use of enzyme inhibitors.

Phenytoin conc. can be reduced by carbamazepine and antacids. (i.e. other enzyme inducers)

90% protein bound. Valproate displaces & inhibits metabolism - Increases free phenytoin and toxicity.

Reduced effect of warfarin, anticonvulsants e.g. carbamazepine, oral contraceptive.

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7
Q

describe the mode of action of Sodium Valproate

A

Multiple modes of action: Sodium/calcium channel blocker, GABA, Glutamate

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8
Q

describe the side effects of Sodium Valproate

A

Teratogenicity is the major issue in young women.

Valproate side effects
Appetite increase and weight gain
Liver failure
Pancreatitis
Reversible hair loss
Oedema
Ataxia
Teratogenicity, tremor, thrombocytopenia
Encephalopathy (confusion as elevated ammonia)

spells valproate

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9
Q

describe the interactions of Sodium Valproate

A
  • Antidepressants (reduced anticonvulsant effect) – SSRIs, TCAs, MAOIs
  • Antimalarials (reduced anticonvulsant effect) – mefloquine, chloroquine
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10
Q

describe the mode of action of Levetiracetam

A

Seen as a number one choice for most seizure types.

Acts via SV2A ligand - blocks synaptic vesicle release

Rapid and complete absorption. Little effect from food.

Renal excretion as unchanged drug.

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11
Q

describe the side effects of Levetiracetam

A

Few side effects and no significant interactions.

Common side effects: irritability, anxiety, fatigue, dizziness, behavioral changes and rarely psychosis.

Rare hepatic failure.

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12
Q

describe the interactions of Levetiracetam

A

Few side effects and no significant interactions.

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13
Q

describe the mode of action of Lamotrigine

A

Similar to other sodium channel modulators.

Safer to fetus in terms of congenital malformation. - still not completely safe

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14
Q

describe side effects of Lamotrigine

A

Well tolerated typically

Idiosycratic rash/Stevens-Johnson syndrome can be fatal .

Rash incidence minimized by slow titration. Stop if develop rash.

Other side effects:

  • Insomnia
  • Less cognitive effects
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15
Q

describe the interactions with Lamotrigine

A

Interactions with OCP (oral contraceptive pill), other AEDs

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16
Q

describe the mode of action of Topiramate

A

Multiple modes of action: Sodium/calcium channel blocker, GABA, Glutamate

Enzyme inducer and inhibitor.

17
Q

describe the side effects of Topiramate

A

Side effects: sedation, anorexia, and weight loss, psychiatric. Word finding difficulties.

Rare side effects: kidney stones, and acute angle closure glaucoma.

Teratogenic- avoid in young women if possible.

18
Q

describe AED (Anti-epileptic drug) Hypersensitivity syndrome

A

Rare. Potentially fatal (10%)
First 1-8 weeks of exposure.
Rash, temps, tender nodes, hepatitis (50% mortality), eosinophilia, pharyngitis, organ failure.
Aromatic AEDs Phenytoin/Carbamazepine show Cross reactivity.

19
Q

what is status epilepticus

describe its treatment

A

New operational definition: 5 minutes of continuous seizure activity, of briefer seizures with no recovery of consciousness in between times.

On time with decent doses:

  • T = 5mins : 4 mg Lorazepam. Repeat once at 10-15m. (max 0.1mg/kg)
  • T = 15m : Phenytoin 20mg/kg. 50mg/min. Slower if contraindicated/elderly. - T = 15m : Anaesthetic drugs in ICU with EEG monitoring.

Benzodiazepines:

  • Different benzodiazepines used in status epilepticus.
  • Diazepam, Midazolam, Lorazepam - lorazepam is the best
  • GABA agonists
  • Multiple routes
  • IV most definitive. IM in pre hospital status epilepticus.
  • Pharmacokinetics of lorazepam make it drug of choice.
20
Q

what 3 things increase and what 1 thing decreases the action of the proton pump in the stomach and the control of acid secretion

A

increase:

  • acetylcholine
  • histamine
  • gastrin

decrease:
- prostaglandin

21
Q

what is a peptic ulcer and what causes it

A

Defect in the gastric or duodenal mucosa

Due to an imbalance in the peptic acid secretion and gastroduodenal mucosal defence

22
Q

how are peptic ulcers treated

A
  • Remove gastric irritants especially NSAIDs
  • Test and treat for H Pylori infection
  • 1st Line – Proton pump inhibitors
  • 2nd Line – H2 antagonist

Must investigate anyone at increased risk of gastric carcinoma as treatment may mask early symptoms.

23
Q

describe how antacids work in treating peptic ulcers

A

Produce symptomatic relief by raising gastric pH and reducing proteolytic activity.

Most are ALUMINIUM and MAGNESIUM SALTS often in combination.

Sodium bicarbonate is a rapidly acting antacid but is well absorbed and can cause a metabolic alkalosis, sodium and water retention and renal stone formation.

24
Q

what is the ending for proton pump inhibitors and give 2 examples

A

-prazole

Omeprazole
Lansoprazole
Pantoprazole
Esomeprazole

25
Q

describe the mode of action and clinical indications and some adverse drug reactions of omeprazole

A

mode of action:
Targeted irreversible proton pump inhibitor

Clinical Indications:

  • Peptic ulcer disease (PUD)
  • Reflux oesophagitis (GORD)

ADRs:

  • GI disturbance e.g. nausea, vomiting, abdominal pain, flatulence, diarrhoea, constipation
  • Headache

Important ADRs:

  • Increased risk of Clostridium difficile infection,
  • electrolyte disturbance: Hyponatraemia, Hypomagnesaemia,
  • Hepatitis, Interstitial nephritis, Blood disorders – leucopenia, leucocytosis, pancytopenia, thrombocytopenia,
  • Observational studies suggest small increase in risk of community acquired and hospital acquired pneumonia
  • Observational studies have also suggested a small increase risk in developing CKD
26
Q

name some of the interactions of omeprazole

A

Slight variation between different PPIs

Warfarin (Omeprazole and esomeprazole are weak CYP450 enzyme inhibitors, therefore they can increase anticoagulant effect)

Clopidogrel (Pro-drug) (Omeprazole and esomeprazole are weak CYP450 enzyme inhibitors reduce antiplatelet effect)

27
Q

what is the ending for Histamine2 Receptor Antagonists

name 2

A
  • tidine

Cimetidine
Ranitidine

28
Q

what is the mode of action, clinical indications, adverse effects and interactions of cimetidine

A

Mode of Action:
Competitive antagonist at the H2 receptor in gastric parietal cells.

Clinical Indications:
2nd line agent for peptic ulcer disease and reflux oesophagitis.

Adverse Effects:
Diarrhoea, confusion, gynaecomastia.

Interactions:
A potent inhibitor of cytochrome P450 dependent metabolism.

29
Q

what is the mode of action, clinical indications, adverse effects and interactions of ranitidine

A

Mode of Action:
Competitive antagonist at the H2 receptor in gastric parietal cells.

Clinical Indications:
2nd line agent for peptic ulcer disease and reflux oesophagitis.

Adverse Effects:
Diarrhoea, fewer than cimetidine.

Interactions:
A mild inhibitor of cytochrome P450 dependent metabolism, of little clinical importance.

30
Q

how would you treat a helicobacter infection

A
  • PPI (or H2 blocker)
  • Clarithromycin
  • Amoxicillin (or Metronidazole if penicillin allergic)
  • Triple therapy for 7 days
31
Q

when should you do an urgent upper GI endoscopy

A
  • Acute bleeding suspected
  • Chronic bleeding / Fe def Anaemia
    > Upper and Lower as 10% dual pathology
  • Weight loss
  • Dysphagia
  • Persistent vomiting
  • Anyone with unexplained, persistent dyspepsia
    >Especially if 55+ years
32
Q

briefly describe how you would manage nausea

A
  • identify underlying causes and correct these if you can
  • treat the symptoms
    > anti-emetics selected according to the inferred underlying mechanisms
  • prevent nausea
    > anti-emetic regimen if nausea prolonged
    > prevent constipation
  • if one agent not completely effective then review, add another or replace it
33
Q

name three anti-emetics

A

Metoclopramide - Anti-dopamine agent

Ondansetron - 5HT3 antagonist

Cyclizine - Antihistamine

Year 2 PODT (14 decks)

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