Others Flashcards

1
Q

What size do particles need to be in order to be efficiently nebulized to the alveoli? What is the unit used?

A

Between 0.5 - 5 um

Unit is MMD = mass median diameter = particle sizes above and below which 50% of the mass of particles is contained

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2
Q

What are the different types of delivery systems for inhaled medications

A
  1. Jet nebulizers: high-velocity stream of gas (O2) travelling through the medicated solution to comminuted the liquid into an aerosol, then delivered to patient through a spacer and face mask (ideally with one-way inspiratory valve)
  2. Ultrasonic and mesh nebulizers: similar to jet nebulizers but use ultra-high-frequency oscillations or a vibrating aperture plate to aerosolize the liquid
    -> don’t need a high velocity of gas and produce smaller size particles more consistently
  3. Metered dose inhalers: measured dose of medication propelled through nozzle at high velocity to form a spray then delivered through spacer and face mask
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3
Q

What are the 2 main families of bronchodilators and their mechanism of action? What other drugs can cause bronchodilation

A
  1. Beta-agonists (terbutaline, albuterol = salbutamol)
    Stimulation of beta2-adrenergic receptors on bronchi smooth muscle cells -> cAMP pathway (Gs receptor) -> protein kinase activation -> smooth muscle relaxation
  2. Methylxanthines derivatives (theophylline, aminophylline)
    Non-specific phosphodiesterase inhibitors -> increased cAMP and cGMP -> relaxation of bronchi smooth muscle + decreased inflammation
  3. Others:
    - Anticholinergics (inhibit vagally-mediated bronchoconstriction)
    - Calcium antagonists
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4
Q

What nebulized treatment can be used for the treatment of infectious tracheobronchitis in dogs

A

Gentamicin (efficient for B bronchiseptica)

6-7 mg/kg diluted 1:3 with saline nebulizer for 5-10 min q8-12h for at least 3 days

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5
Q

To what chemotherapeutic agents do dogs with the ABCB1 (MDR1) mutation have increased sensitivity

A
  • Doxorubicin
  • Vinblastine, vincristine
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6
Q

What is produced secondary to the catabolism of purines in acute tumor lysis syndrome

A

Uric acide (purines -> hypoxanthine -> xanthine -> uric acid)

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7
Q

What chemotherapeutic carries a high risk of anaphylactic reaction

A

L-asparaginase

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8
Q

What are the main adverse effects of tyrosine kinase inhibitors (eg. toceranib)

A
  • GI with potential GI ulceration / bleed
  • Renal toxicity
  • Possible hepatic toxicity
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9
Q

When does the neutrophil nadir usually happen following chemotherapy? What are some exceptions?

A

Usually 7-10 days

Carboplatin: 10-14 days and 21 days

Lomustine: 7-28 days

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10
Q

Name 2 chemotherapeutics causing severe tissue injury in case of extravasation. What drugs can be administered to mitigate the effects

A
  • Doxorubicin ->apply cold packs and administer IV dexrazoxane at 10 times the extravasated dose (within 3-6h, at 24h, and at 48h)
  • Vinca alkaloids (vincristine, vinblastine) -> apply warm compresses and administer perilesional hyaluronidase (1mL for everyone 1mL of drug extravasated)
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11
Q

Associate these chemotherapeutic agents:
- lomustine (CCNU)
- cyclophosphamide
- doxorubicin
- 5-fluorouracile
- cisplatin
- L-asparaginase
- toceranib

with these adverse effects:
- hemorrhagic cystitis
- hypersensitivity
- nephrotoxicity
- hepatotoxicity
- pancreatitis
- neurotoxicity
- cardiotoxicity
- pulmonary toxicity

(several possible associations)

A
  • Lomustine -> hepatotoxicity, pulmonary toxicity (pulmonary fibrosis - rare)
  • Cyclophosphamide -> hemorrhagic cystitis
  • Doxorubicin -> cardiotoxicity, nephrotoxicity in cats
  • 5-fluorouracile ->neurotoxicity (never use in cats!)
  • Cisplatin -> nephrotoxicity, pulmonary toxicity in cats (never use)
  • L-asparaginase -> hypersensitivity, pancreatitis
  • Toceranib -> nephrotoxicity
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12
Q

List some actions of glucocorticoids on inflammation / immune system

A
  • Inhibit phospholipase A2 -> no release of arachidonic acid -> no initiation of cascade (decreased prostaglandins)
  • Possible direct inhibition of COX-2
  • Inhibition of transcription of NF-kb
  • Inhibition of transcription of several cytokines (IL-1, IL-6, IL-2, IL-8, TNF-alpha, IFN-gamma)
  • Downregulation of cell adhesion molecules (ICAM-1, E-selectin)
  • Inhibition of iNOS
  • Downregulation of Fc receptor expression on macrophages
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13
Q

Compare the glucocorticoid and mineralocorticoid potency of cortisol, hydrocortisone, prednisone, dexamethasone, fludrocorstione, aldosterone

A

See table

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14
Q

Mechanism of action of cyclosporine

A

Calcineurin inhibitor

Binds cyclophilin (cytoplasmic receptor) -> binds to calcineurin -> inhibits transcription of T cell genes, inhibits expression of IL-2

+ directly inhibits IL-3, IL-4, IL-5, IL-8, and TNFα

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15
Q

Mechanism of action of mycophenolate mofetil

A

Inhibitor of inosine monophosphate dehydrogenase (IMPDH) -> inhibit synthesis of purines -> inhibit production of GMP -> anti-metabolite targeting B cells and T cells (prevent proliferation and immunoglobulin synthesis)

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16
Q

Mechanism of action of azathioprine

A

Precursor of 6-thioguanine nucleotides (6-TGNs) which compete with purines for incorporation into DNA / RNA -> inhibits lymphocyte B and T proliferation + antibody synthesis

17
Q

List adverse effects of cyclosporine, mycophenolate, azathioprine

A
  • Cyclosporine: GI (vomiting), gingival hyperplasia, rare hepatotoxicity, allergic reaction when given IV
  • Mycophenolate: GI (diarrhea)
  • Azathioprine: myelosuppression, hepatotoxicity (possibly severe, hepatic necrosis), pancreatitis, GI