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Pulmonology Exam > Pulmonary Pharmacology 2 > Flashcards

Pulmonary Pharmacology 2 Flashcards

1
Q

targets for drug therapy of pulmonary arterial hypertension

A
  1. endothelin-1 pathway
  2. prostacyclin (PGI2) pathway
  3. nitric oxide pathway
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2
Q

PH tx: nitric oxide (NO) - MOA

A

*activates guanylyl cyclase to increase cGMP in vascular smooth muscle (receptor for NO is sGC [soluble guanylate cyclase])
*pulmonary VASODILATOR:
-increased blood flow to lung and decreased pulmonary vascular resistance
-reduced pulmonary artery pressure and improved perfusion of ventilated areas of the lung

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3
Q

nitric oxide (NO) - uses

A

*cardiac surgery
*variety of pediatric respiratory conditions
*ARDS?
*pulmonary arterial hypertension?

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4
Q

nitric oxide (NO) - ADEs

A

*hypotension
*methemoglobinemia
*note - not used much in pulmonary hypertension due to difficultly in administration

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5
Q

Riociguat - drug class, MOA

A

*drug class: oral “guanylate cyclase stimulant” (sGC stimulator)
*MOA: increases cGMP → vasodilation
-directly stimulates the nitric oxide receptor (sGC)
-increases the sensitivity of sGC to endogenous NO

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6
Q

Riociguat - ADEs

A

*hypotension
*dizziness
*headache
*contraindicated in pregnancy

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7
Q

Riociguat - uses

A

*pulmonary arterial hypertension

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8
Q

PDE-5 inhibitors (phosphodiesterase 5 inhibitors) - MOA, examples

A

*MOA: inhibits PDE-5 → increased cGMP → smooth muscle relaxation → increased blood flow
*examples: sildenafil, tadalafil
*ADEs: flushing, headache, indigestion, nasal congestion, insomnia
*contraindicated in patients on nitrates or riociguat

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9
Q

sildenafil - drug class, MOA, ADEs

A

*drug class: PDE-5 inhibitor
*MOA: inhibits PDE-5 → increased cGMP → smooth muscle relaxation → increased blood flow
*used for pulmonary hypertension
*ADEs: flushing, headache, indigestion, nasal congestion, insomnia
*contraindicated in patients on nitrates or riociguat

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10
Q

tadalafil - drug class, MOA, ADEs

A

*drug class: PDE-5 inhibitor
*MOA: inhibits PDE-5 → increased cGMP → smooth muscle relaxation → increased blood flow
-used to treat pulmonary hypertension
*ADEs: flushing, headache, indigestion, nasal congestion, insomnia
*contraindicated in patients on nitrates or riociguat

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11
Q

prostaglandins & prostacyclin analogues to treat pulmonary arterial hypertension

A

*prostacyclin (PGI2) lowers peripheral, pulmonary, and coronary vascular resistance
*examples: esoprostenol (PGI2), trepostinil, iloprost, selexipag)
*ADEs: flushing, headache, hypotension, dizziness, bleeding (inhibits platelet aggregation)

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12
Q

endothelin receptor antagonists

A

*endothelin-1 (ET-1) is a potent vasoconstrictor
*there is increased ET-1 in PAH, so we want to block the receptor
*MOA - competitively antagonize endothelin-1 receptors → decreased pulmonary vascular resistance
*examples: bosentan, macitentan, ambrisentan
*ADEs: HEPATOTOXICITY, peripheral edema, flushing, contraindicated in pregnancy

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13
Q

categories of therapies for pulmonary hypertension

A

*endothelin receptor antagonists
*PDE-5 inhibitors
*prostacyclin analogs

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14
Q

drugs used for treatment of fibrotic interstitial lung diseases

A

*pirfenidone
*nintedanib
*azathioprine
*mycophenolate
*tocilizumab
*methotrexate, rituximab, cyclophosphamide
*adalimumab, abatacept
*infliximab

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15
Q

algorithm for management of pulmonary fibrosis

A
  1. glucocorticoids
  2. prophylaxis for PCP (TMP-sulfa)
  3. other anti-inflammatories
  4. antifibrotic agents
  5. non-pharmacologic treatments (supplemental oxygen, psychosocial support, smoking cessation, end-of-life care)
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16
Q

nintedanib - drug class, MOA, ADEs

A

*drug class: antifibrotic agent used in pulmonary fibrosis
*MOA: KINASE INHIBITOR that prevents proliferation, migration, and transformation of fibroblasts in the lungs
*reduces annual FVC decline and # of acute exacerbation
*ADEs: diarrhea, increased LFTs, cannot use if fully anticoagulated

17
Q

pirfenidone - drug class, MOA, ADEs

A

*drug class: antifibrotic agent used in pulmonary fibrosis
*MOA: not clearly known; inhibits various growth factors and cytokines; anti-fibrotic effect
*ADEs: rash, PHOTOSENSITIVITY, increased LFTs, lots of CYP450 drug interactions

18
Q

azathioprine - drug class, MOA, ADEs

A

*drug class: purine antimetabolite (derivative of 6-mercaptopurine) used in pulmonary fibrosis and others
*MOA: reduces intracellular purine nucleotide synthesis; decreased numbers of T and B lymphocytes
*ADEs: bone marrow suppression, pancreatitis, teratogenic
*do NOT give with allopurinol or febuxostat

19
Q

mycophenolate mofetil - drug class, MOA, ADEs

A

*drug class: IMP inhibitor; drug for interstitial lung disease and transplants
*MOA: inhibits Inosine Monophosphate Dehydrogenase (IMP), which inhibits de novo purine synthesis; blocks proliferation of T and B lymphocytes
*ADEs: nausea, diarrhea, constipation, leukopenia, teratogenic

20
Q

tocilizumab - drug class/MOA

A

IL-6 inhibitor

21
Q

pulmonary embolism treatment

A

anticoagulants!

22
Q

big picture treatment differences in lung cancers

A

*small cell lung cancer: chemo (surgery is difficult because it is usually disseminated at presentation)
*non-small cell lung cancer: surgical resection is best chance if caught early; some have sensitive mutations that can be treated with targeted chemo

23
Q

Small Cell Lung Cancer - treatment regimen

A

*cisplatin + etoposide or carboplatin + etoposide

24
Q

Non-Small Cell Lung Cancer - treatment regimen

A

*resect if you can
*most chemo regimens have a backbone of cisplatin or carboplatin
*PD-1/PD-L1 inhibitors are playing an expanding role
*use other agents to target various mutations and other tumor characteristics if present

25
Q

platinums (cisplatin & carboplatin)

A

*traditional chemotherapy
*MOA: cross-link DNA (cell-cycle nonspecific)
*ADEs:
-cisplatin: NEPHROTOXICITY, N/V
-carboplatin: neurotoxicity, vomiting, hypersensitivity
-oxaliplatin: peripheral neuropathy

26
Q

ironotecan

A

*topoisomerase I inhibitor
*class: camptothecin
*ADEs: SEVERE DIARRHEA, myelosuppression

27
Q

etoposide

A

*topoisomerase II inhibitor
*class: epipodophyllotoxins
*ADEs: myelosuppression

28
Q

programmed cell death protein 1 (PD-1) & PD-Ligand-1 (PD-L1) inhibitors - why do these work?

A

*we have a “checkpoint” to keep T cells from attacking normal cells: PD-1 ligands interact with PD-1 (receptor) to downregulate T cell activation
*many tumors express PD-1 ligands and inactivate T cells from killing the tumor cells
*interrupting this PD-L1/PF-1 interaction removes the inhibition of T cells, restoring their anti-tumor immune response
*our medications are antibodies to either PD-1 or PD-L1

29
Q

PD-1 receptor blockers used in lung cancer

A

*pembrolizumab
*nivolumab

30
Q

PD-L1 ligand blockers used in lung cancer

A

*atezolizumab
*durvalumab

31
Q

PD-1/PD-L1 inhibitor toxicities

A

*derm: rash, vitiligo
*diarrhea, colitis
*pneumonitis
*fatigue
*anemia
*cardiotoxicities (including myocarditis)

32
Q

4 drugs used for tuberculosis

A
  1. isoniazid
  2. rifampin
  3. ethambutol
  4. pyrazinamide (PZA)
33
Q

isoniazid - MOA, ADEs, info

A

*part of the regimen for treating TUBERCULOSIS
*MOA: inhibits mycolic acid synthesis, which interferes with cell wall synthesis
*it is a prodrug (resistance can occur)
*metabolized by ACETYLATION (there is a lot of genetic diversity to see how fast they can do this)
*inhibits CYP450
*ADEs: HEPATOTOXICITY, peripheral neuropathy, ataxia, paresthesia, rash, fever, drug-induced SLE, myelosuppression

34
Q

rifampin - MOA, ADEs, info

A

*part of the regimen for treating TUBERCULOSIS
*MOA: block RNA synthesis by inhibiting bacterial DNA-dependent RNA polymerase
*metabolized by the liver
*ADEs: orange/red discoloration of body fluids, GI, flu-like syndrome, derm reactions, hepatitis
*POTENT INDUCER OF CYP450 (need to look over every med before giving)

35
Q

ethambutol

A

*part of the regimen for treating TUBERCULOSIS
*ADEs: OPTIC NEUROPATHY, hepatotoxicity, GI

36
Q

pyrazinamide

A

*part of the regimen for treating TUBERCULOSIS
*ADEs: hepatotoxicity, inhibits uric acid excretion, GI, etc

37
Q

TB treatment regimen: latent infection

A

*rifampin for 4 months

38
Q

TB treatment regimen: active infection

A

*INH + rifampin + ethambutol + PZA for 2 months
*INH + rifampin for 4 more months

Pulmonology Exam (36 decks)

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