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Pharmacology > Cancer and Pain > Flashcards

Cancer and Pain Flashcards

1
Q

Name 2 bisphosphonates

A
  • alendronic acid
  • discodium pamidronate
  • zolendronic acid
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2
Q

Suggest 3 indications for the use of bisphosphonates:

A
  • protection vs. osteoporotic fragility fractures (alendronic acid)
  • treatment of severe hypercalcaemia of malignancy after IV rehydration (pamidronate, zolendronic)
  • protection vs. pathological fractures, cord compression and need for radiotherapy/surgery in pts with myeloma and breast cancer with bone mets
  • 1st line rx for metabolically active Paget’s disease to reduce bone turnover and pain
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3
Q

how do bisphosphonates reduce bone turnover?

A
  • they are readily incorporated into bone, where they accumulate and inhibit the action of osteoclasts
  • and promote apoptosis of osteoclasts so less bone is resorbed and bone mass is improved
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4
Q

2 SEs of bisphosphonates:

how is the most common protected against?

A
  • oesophagitis when taken orally and hypophosphatemia
  • –> swallow whole 30mins before breakfast with plenty of water, stay upright for 30mins after
  • rare: osteonecrosis of jaw (higher risk with IV high doses)
  • atypical femoral fracture
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5
Q

2 CIs and a caution in the administration of bisphosphonates?

A

-CI: SEVERE RENAL IMPAIRMENT (as renally excreted)
-CI: HYPOCALCAEMIA (bisphosphonates bind calcium)
-CI: UPPER GI DISORDERS
Caution: smokers and pts with major dental disease (osteonecrosis risk)

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6
Q

Bisphosphonates bind calcium so absorption is reduced if taken with what?

A
  • calcium salts inc milk
  • antacids
  • iron salts
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7
Q

Name 2 sex hormone antagonists used for breast cancer, which types of breast cancer are they indicated for?

A
  • tamoxifen, anastrozole, letrozole
  • early and locally advanced ER positive breast cancer (as adjuvant post op to reduce recurrence)
  • advanced ER-positive breast cancer to slow disease progression (if HER negative)
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8
Q

What is the difference between tamoxifen and anastrozole and letrozole, in what women are they used?

A
  • tamoxifen is a SERM (selective oestrogen receptor modulator) that prevents oestrogen binding to its receptor (and stimulating cell proliferation) Tamoxifen is used in pre-menopausal women.
  • anastrozole and letrozole are aromatase inhibitors that interfere with oestrogen synthesis outside the ovary (in muscle and fat), used for post-menopausal women but not for used in women with functioning ovaries
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9
Q

anastrozole and letrozole are aromatase inhibitors that interfere with oestrogen synthesis outside the ovary (in muscle and fat), used for post-menopausal women but not for used in women with functioning ovaries, why?

A

-they have little effect on ovarian oestrogen synthesis (may even cause it to rise)

NB: anti-oestrogen therapies are only effective if the tumour expresses oestrogen receptors

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10
Q

Name 4 SEs of tamoxifen and aromatase inhibitors e.g. anastrozole and letrozole
(sx of oestrogen depletion)

A
  • vaginal dryness
  • hot flushes
  • loss of bone density
  • tamoxifen increases risk of VTE and endometrial cancer
  • GI upset
  • headache
  • rarely can –> agranulocytosis and liver failure
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11
Q

2 CIs for tamoxifen and aromatase inhibitors e.g. anastrozole and letrozole

A
  • tamoxifen CI: PREGNANCY
  • tamoxifen CI: LACTATION
  • aromatase inhibitors CI: PRE-MENOPAUSAL WOMEN (unless ovarian function supressed/ablated)
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12
Q

Tamoxifen ____ CYP2C9 enzyme responsible for metabolising ____ so increases the risk of bleeding
The SSRIs fluoxetine and paroxetine ___ hepatic activation of tamoxifen

A
  • inhibits, warfarin

- inhibits

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13
Q

2 Indications for allopurinol

-preventing…..

A
  • preventing recurrent attacks of gout
  • preventing uric acid and calcium oxalate renal stones
  • preventing hyperuricaemia and tumour lysis syndrome associated with chemo
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14
Q

Allopurinal MOA

  • it is a ____ ____ inhibitor
  • ____ ____ metabolises ___ (produced from purines) to ____ ___
  • so inhibition of it lowers plasma ___ ___ concentrations and reduces ______ of it in the ____ or ____
A
  • xanthine oxidase
  • xanthine oxidase metabolises xanthine to uric acid
  • lowers plasma uric acid and reduces precipitation of it in the joints and kidneys
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15
Q

3 SEs of allopurinol

A
  • starting can trigger/worsen an acute gout attack (risk reduced if NSAID or colchicine co-prescribed)
  • skin rash (can be mild or Steven-Johnson’s or toxic epidermal necrolysis
  • allopurinol hypersensitivity syndrome: rare: fever, eosinophiliia, lymphadenopathy and other organ involvement
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16
Q

3 CIs to allopurinol (relate directly to the 3 SEs) and 1 caution

A
  • CI: DURING ACUTE GOUT ATTACK
  • CI: RECURRENT SKIN RASH
  • CI: SIGNS OF SEVERE HYPERSENSITIVITY
  • Caution in severe renal or hepatic impairment
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17
Q

Describe the interaction of allopurinol (a xanthine oxidase inhibitor) with azathioprine and ACE inhibitor and with amoxicillin:

A
  • mercaptopurine the active metabolite of azathioprine is metabolised by xanthine oxidase so use of both increases risk of toxicity
  • co-prescription with ACEi or thiazide diuretics increases risk of hypersensitivity reactions
  • co-prescription w Amoxicillin increases risk of the rash
18
Q

when starting allopurinol NSAID/colchicine should also be prescribed for how long for what?

A

-continue for 1 month+ after serum uric acid levels return to normal to avoid triggering an acute attack

19
Q

Ondansetron and Granistron are anti-emetics useful in prophylaxis and rx of what? esp. in what context? They are antagnoists of which receptor?

A
  • of N&V esp in context of general anaesthesia and chemotherapy
  • 5-HT3-receptor antagonists

NB: unsilenced but effective for hyperemesis gravidarium where benefits > risks

20
Q

Explain MOA of 5-HT3-R antagonists e.g. ondansetron

A
  • there is a high density of these receptors in the CTZ (senses emetogenic substances in blood)
  • 5-HT is a key NT released by gut in response to emetogenic stimuli
  • Ondansetron blocks these effects
21
Q

5-HT3-R antagonists e.g. ondansetron SEs / 1 adverse consequence

A
  • rare but constipation, diarrhoea, headaches are possible
  • rarely high doses can cause QT prolongation so avoid in pts with this already and avoid if pt is on other drugs that also have this effect e.g. anti-psychotics, quinine, SSRIs…
22
Q

Typical starting dose for 5-HT3-R antagonists e.g. ondansetron is ___mg 12-hrly can be oral, IV or?

A

8-12mg

-also rectal and injectable IM preparations are available

23
Q

Paracetamol is a weak inhibitor of ____ the enzyme involved in ____ metabolism. This increased pain threshold and decreases _____ E2 (PGE2) conc in thermoreg area of _____ therefore controls fever

A
  • COX (cox-2 selective)
  • prostaglandin
  • decreases prostaglandin E2
  • hypothalamus
24
Q

paracetamol is cox-2 selective, it is v safe with few SEs, what difference to NSAIDs mean it doesn’t cause peptic ulcers/renal impairment/risk of CVS event?

A

-lack of cox-1 inhibition

25
Q

In paracetamol OD what toxic metabolite builds up due to insufficient _____for safe conjugation before elimination?

A
  • toxic NAPQI

- glutathione

26
Q

What damage does accumulated toxic NAPQI have on liver in paracetamol OD?
-prevention is with giving the glutathione precursor a_____

A
  • hepatocellular necrosis

- precursor = acetylcysteine

27
Q

give 2 cautions for use of paracetamol/when you’d consider lower dose
(relates to likelihood of toxic NAPQI buildup)

A
  • chronic excessive alcohol use
  • reduced glutathione stores e.g. malnutrition, low BMI
  • severe hepatic impairment (esp. if paracetamol being given IV)
28
Q

What medications increase the rate of NAPQI production and hence risk of liver toxicity after paracetamol OD?

A

-CYP inducers (e.g. phenytoin, carbamazepine)

29
Q

Name 2 blood tests to do after paracetamol OD?

A

-INR
-serum ALT
-creatinine concentration
(to establish efficacy of acetylcysteine rx and need for further rx)

30
Q

NSAIDs inhibit prostaglandin synthesis from arachidonic acid by inhibiting COX
COX-1 (constitutive) stimulates prostaglandin synthesis and is essential for what?
COX-2 (inducible) is expressed in response to inflammatory stimuli -> pain
(so SEs are related to COX1 inhibition, therapeutic effects from cox2)

A

COX1 prostaglandin needed to:

  • preserve integrity of gastric mucosa
  • maintain renal perfusion by dilating afferent glomerular arterioles
  • inhibits thrombus formation at vascular endothelium
31
Q

Give 3 CIs to NSAID use and 2 cautions

A 
CI: SEVERE RENAL IMPAIRMENT
CI: HEART FAILURE 
CI: LIVER  FAILURE
CI: KNOWN NSAID HYPERSENSITIVITY
Cautions: peptic ulcer disease, GI bleeding, cardiovascular disease, renal impairment
32
Q

why is NSAID use CI in heart failure?

A
  • increased risk of cardiovascular events (MI, stroke)

- also risk of fluid retention which can worsen hypertension and heart failure

33
Q

What advice should you give someone when prescribing NSAIDs?

in terms of safety netting and when to stop taking

A
  • warn that most common SE is indigestion and to stop rx and seek advice if occurs
  • for pts with acute pain explain long-term use >10days is not recommended due to SEs
  • advise (if on long-term rx) to stop taking if: become acutely unwell/dehydrated to reduce risk of damage to kidneys
34
Q

Quinine sulphate is used for the treatment and prevention of night-time what? only if regularly disrupting sleep and non-pharm methods have failed.

A

Leg-cramps

35
Q

Quinine sulfate as well as rx for leg-cramps is the 1st-line option for what disease?

A

-P. falciparum Malaria

NB: kills parasites in the schizont stage in the blood

36
Q

Quinine is safe at recommended doses but overdose carries many severe risks, suggest 2

A
  • tinnitus, deafness
  • blindness (can be permanent)
  • GI upset
  • hypersensitivity reactions
  • prolongs QT interval (arrhythmia risk)
  • Hypoglycaemia
37
Q

Suggest 2 cautions for prescription of quinine:

A
  • hearing/visual loss pre-existing
  • avoid in 1st trimester pregnancy as teratogenic (risk/benefit)
  • avoid in people with G6PD deficiency (can precipitate haemolysis)
38
Q

Naloxone has few intrinsic adverse effects but opioid reversal can -> severe withdrawal reaction, what are 3 symptoms of withdrawal?

A
  • pain
  • restlessness
  • N&V
  • dilated pupils
  • cold, dry skin with piloerection
39
Q

Activated charcoal reduces absorption of certain poisons and increases elimination of them. Benzos and methotrexate are adsorbable.
What are risks esp in pts with reduced conciousness?
(NB: protect airway with endotracheal intubation, and give with NG tube)

A
  • aspiration –> pneumonitis, bronchospasm, airway obstruction
  • intestinal obstruction
  • black stools, vomiting
40
Q

What mild/mod opioid lowers seizure threshold?

NB: this med can increase the risk of seratonin syndrome with other seratonergic drugs

A

Tramadol

Pharmacology (14 decks)

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