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Pharmacology for FRCR CO1 > 2.5 Clinical pharmacology of supportive therapies > Flashcards

2.5 Clinical pharmacology of supportive therapies Flashcards

1
Q

What are the 8 classes of antiemetics?

A
  1. H1 antagonists
  2. Dopamine antagonist
  3. 5HT3 antagonist
  4. NK1 Inhibitor (can combine with 5HT3)
  5. Levomepromazine
  6. Olanzapine
  7. Nabilone
  8. Lorazepam
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2
Q

Where do H1 agonists act?

A

Vestibular nuclei

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3
Q

What are some examples of H1 agonists?

A
  • Cyclizine
  • Promethazine
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4
Q

Where do dopamine antagonists act?

A
  • Centrally - medulla and chemoreceptor trigger zone

or

  • Gut
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5
Q

What is an example of a centrally acting dopamine antagonist?

A

Haloperidol

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6
Q

What are examples of a gut-acting dopaine antagonist?

A

Domperidone
Olanzapine

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7
Q

What dopamine antagonist works both centrally and on the gut?

A

Metoclopramide

Combined D2 antagonist and 5HT4 agonist

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8
Q

Where do 5HT3 antagonists work?

A

Centrally and gut

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9
Q

What are some examples of 5HT3 antagonists?

A
  • Ondansetron
  • Granisetron
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10
Q

Where do NK1 inhibitors act?

A

Central - block substance P in CTZ

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11
Q

What are some examples of NK1 inhbitors?

A
  • Aprepitant
  • Fosaprepitant
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12
Q

What is an example of a combined 5HT3 antagonist and NK1 inhibitor?

A

Akynzeo

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13
Q

Where does Levomepromazine act?

A
  • 5HT2
  • Dopamine
  • Acetylcholine
  • Histamine antagonist

broad spectrum, acts centrally

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14
Q

What is Nabilone?

A

Synthetic cannaboid

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15
Q

What are the indications for steroids in cancer?

A
  1. Treatment
  2. Chemotherapy Induced Nausea and Vomiting
  3. Pain and inflammation
  4. Hypersensitivity
  5. Immune mediated
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16
Q

What are the acute side effects of steroid use?

A
  1. Hypernatraemia
  2. Fluid retention
  3. Hyperglycaemia
  4. HTN
  5. Immunosuppression
  6. Modd changes, psychosis
17
Q

What are the delayed side effects of steroid use?

A
  1. Osteoporosis
  2. Peptic ulcers
  3. Thrombocytopenia
  4. Myopathy
  5. Adrenal suppression
  6. Cushing’s
18
Q

What do haemopoetic growth factors do? (GCSF)

A

Stimulate proliferation and differentiation of neutrophil progenitors and release neutrophils from bone marrow into blood

19
Q

Indications for prophylactic GSCF?

A
  • > 65
  • Pre-existing neutropenia
  • Extensive prior chemotherapy
  • Poor ps
  • Poor neutritional
20
Q

When should GCSF be given?

A

5-7 days from day 5 (or depending on timing of Nadir)

21
Q

What is the dose of filgrastim?

A

<70kg 30 million units (300mcg)
>70kg 40 mu (480 mcg)

22
Q

What is the mechanism of action of Vitamin K Agonists?

A

Inhibits vitamin K epoxide reductase, reducing activation of clotting factors II, VII, IX, and X, and proteins C and S

23
Q

What is the mechanism of action of Unfractionated Heparin?

A

Activates antithrombin III, inhbiting thrombin (factor IIa) and factor Xa

24
Q

What is the mechanism of action of Low Molecular Weight Heparins?

A

Preferentially inhbits factor Xa via antithrombin activation

25
Q

What are some examples of LMWH?

A
  • Enoxaparin
  • Dalteparin
  • Tinsaparin
26
Q

What are the mechanisms of action for Direct Oral Anticoagulants?

A

Direct thrombin inhibitors: Dabigatran (inhbits thrombin IIa)

Direct factor Xa inhibitors

27
Q

What are the direct factor Xa inhbitors?

A

Apixaban
Rivaroxaban
Edoxaban

28
Q

What is Fondaparinux?

A

Synthetic pentasaccharide that selectively inhbitors factor Xa via antithrombin

29
Q

Pharmacological properties

A
30
Q

What are the indications of anticoagulation in oncology?

A
  1. Prevention of VTE e.g. surgery, high risk chemo
  2. Cancer Associated Thrombosis
  3. Palliative care
31
Q

What are some adverse events associated with anticoagulation in oncology patients?

A
  1. Bleeding - big risk with cancer especially luminal
  2. Heparin-induced thrombocytopneia (HIT) - usually unfractionated
  3. Warfarin - skin necrosis, purple toes
  4. DOACs - dyspepsia, elevated LFTS
32
Q

What drugs potentiate VKAs?

A
  • antibiotics e.g. fluconazole, metronidaole
  • amiodarone
  • NSAIDs
33
Q

What drugs reduce VKAs?

A
  • Leafy greens
  • Barbituates (barbitals)
34
Q

What drugs affect DOACs?

A

CYP3A4/P-gp inhbitors potentiate e.g. ketoconazole

CYP3A4/P-gp inducers e.g. carbamazepine, phenytoin

35
Q

What are some special considerations for oncology patients when considering anticoagulating them?

A
  1. Renal impairment - LMWH and DOACs will need dose adjustment. Use UFH if severe renal impairment as half-life is short
  2. Mucin-producing adenocarcinomas e.g. pancreas, stomach higher thrombotic risk
  3. S/C injections might be difficult if cachexic
36
Q

What are the clinical recommendations for anticoag in oncology?

A

LMWH first line in CAT
Should be considered beyond 6 months

Pharmacology for FRCR CO1 (7 decks)

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