Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

53 Cards in this Set

  • Front
  • Back
What drugs are opiod analgesics? (7)
MOA of opioid analgesics?
Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission.
Clinical use of opioid analgesics?
-Cough suppression (dextromethorphan)
-Diarrhea (loperamide and diphenoxylate),
-Acute pulmonary edema
-Maintenance programs for addicts (methadone).
Toxicity of opioid analgesics?

To what does tolerance NOT develop?
Respiratory depression
Miosis (pinpoint pupils)
Additive CNS depression with other drugs

Tolerance does not develop to miosis and constipation.
How is opioid analgesic toxicity treated?
Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).
What is contraindicated in a morphine overdose?
Oxygen is contraindicated in morphine overdose, b/c/ it may contribute to respiratory failure.
What drugs are NSAIDS? (4)
MOA of NSAIDS? (2)
Reversibly inhibit cyclooxygenase (both COX-1 and COX-2).

Block prostaglandin synthesis.
Clinical use of NSAIDS? (3)
Toxicity of NSAIDS? (4)
Renal damage
Aplastic anemia
GI distress
What drugs are COX-2 inhibitors?
MOA of COX-2 inhibitors?

Why are these drugs less corrosive on the GI lining than other NSAIDS?
Selectively inhibit cyclooxygenase (COX) isoform 2, which is found in inflammatory cells and mediates inflammation and pain; spares COX-1, which helps maintain the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDs on the GI lining.
Clinical use of COX-2 inhibitors? (2)
-Rheumatoid arthritis
Toxicity of COX-2 inhibitors?
Similar to other NSAIDs; may have less toxicity to GI mucosa (i.e., lower incidence of ulcers, bleeding).
MOA of Acetaminophen?

Where in the body does it act most?
Reversibly inhibits cyclooxygenase, mostly in CNS.

Inactivated peripherally.
Clinical use of Acetaminophen? (2)
Antipyretic, analgesic, but lacking anti-inflammatory properties.
Toxicity of Acetaminophen?

What is the antidote?
Overdose produces hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in liver.

N-acetylcysteine is antidote––regenerates glutathione.
What are 3 drugs used for gout?
-clinical use?

What drugs is less toxic and thus more commonly used?
Acute gout.

Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.

GI side effects, especially if
given orally.

(Note: indomethacin is less toxic, more commonly used.)
what drug does it inhibit the secretion of?
Chronic gout.

Inhibits reabsorption of uric

Also inhibits secretion of penicillin.
-uses? (3)
Chronic gout.

Inhibits xanthine oxidase,
↓ conversion of xanthine to uric acid.

Also used in lymphoma and leukemia to prevent tumor lysis–associated urate nephropathy.
See diagram in Gout drugs section.
See diagram in Gout drugs section.
MOA of Etanercept?
Recombinant form of human TNF receptor that binds TNF-α.
Clinical use of Etanercept? (3)
Rheumatoid arthritis
Ankylosing spondylitis
MOA of Infliximab?
TNF-α antibody.
Clinical use of Infliximab? (3)
Crohn’s disease
Rheumatoid arthritis
Ankylosing spondylitis
Immunosuppresive agent: Prednisone

It blocks what parts of the inflamm pathway? (2)
-tissue injury
Immunosuppresive agent: Cyclosporine

It blocks what parts of the inflamm pathway? (2)
-differentiation to T-cells or antibody
Immunosuppresive agent: Azathioprine

It blocks what parts of the inflamm pathway? (1)
Immunosuppresive agent: Methotrexate

It blocks what parts of the inflamm pathway? (1)
Immunosuppresive agent: Dactinomycin

It blocks what parts of the inflamm pathway? (2)
-differentiation synthesis
Immunosuppresive agent: Cyclophosphamide

It blocks what parts of the inflamm pathway? (1)
Immunosuppresive agent: Antilymphocytic globulin and monoclonal T-cell antibodies

It blocks what parts of the inflamm pathway? (3)
-antigen recognition (B and T-cells)
-differentiation synthesis
Immunosuppresive agent: Rh3(D) immune globulin

It blocks what parts of the inflamm pathway? (1)
-antigen recognition (B and T-cells)
Immunosuppresive agent: Tacrolimus

It blocks what parts of the inflamm pathway? (1)
cytokine secretion!
MOA of Cyclosporine?
Binds to cyclophilins. Complex blocks the differentiation and activation of T cells
by inhibiting calcineurin, thus preventing the production of IL-2 and its receptor.
Clinical use of Cyclosporine? (2)
-Suppresses organ rejection after transplantation
-Selected autoimmune disorders.
Toxicity of Cyclosporine? (3)
Predisposes patients to viral infections and lymphoma

Nephrotoxic (preventable with mannitol diuresis).
MOA of Tacrolimus (FK506)?
Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.
Clinical use of Tacrolimus (FK506)?
Potent immunosuppressive used in organ transplant recipients.
Toxicity of Tacrolimus (FK506)? (5)
Peripheral neuropathy
Pleural effusion,
MOA of Azathioprine?
What is it toxic to?
Antimetabolite derivative of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids.

Toxic to proliferating lymphocytes.
Clinical use of Azathioprine? (2)
Kidney transplantation

Autoimmune disorders (including glomerulonephritis and
hemolytic anemia).
Toxicity of Azathioprine?

What drug may increase toxic effects if used in combo?
Bone marrow suppression.

Active metabolite mercaptopurine is metabolized by xanthine oxidase; thus, toxic effects may be ↑ by allopurinol.
Clinical use of Aldesleukin (IL-2)? (2)
-Renal cell carcinoma
-Metastatic melanoma
Clinical use of Erythropoietin (epoetin)?
anemias (especially in renal failure)
Clinical use of Filgrastim (granulocyte colony-stimulating factor)?
Recovery of bone marrow
Clinical use of Sargramostim (granulocyte-macrophage colony-stimulating factor)?
Recovery of bone marrow
Clinical use of α-interferon? (4)
Hepatitis B and C
Kaposi’s sarcoma
Malignant melanoma
Clinical use of β-interferon?
Multiple sclerosis
Clinical use of γ-interferon?
Chronic granulomatous disease
Clinical use of Oprelvekin (interleukin-11)?
Clinical use of Thrombopoietin?