Fa Musculoskeletal And Connective Tissue - Pharmacology

Front 1

What drugs are opiod analgesics? (7)

Back 1

Morphine
Fentanyl
Codeine
Heroin
Methadone
Meperidine
Dextromethorphan

Front 2

MOA of opioid analgesics?

Back 2

Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission.

Front 3

Clinical use of opioid analgesics?

Back 3

-Pain
-Cough suppression (dextromethorphan)
-Diarrhea (loperamide and diphenoxylate),
-Acute pulmonary edema
-Maintenance programs for addicts (methadone).

Front 4

Toxicity of opioid analgesics?

To what does tolerance NOT develop?

Back 4

Addiction
Respiratory depression
Constipation
Miosis (pinpoint pupils)
Additive CNS depression with other drugs

Tolerance does not develop to miosis and constipation.

Front 5

How is opioid analgesic toxicity treated?

Back 5

Toxicity treated with naloxone or naltrexone (opioid receptor antagonist).

Front 6

What is contraindicated in a morphine overdose?

Back 6

Oxygen is contraindicated in morphine overdose, b/c/ it may contribute to respiratory failure.

Front 7

What drugs are NSAIDS? (4)

Back 7

-Ibuprofen
-Naproxen
-Indomethacin
-Ketorolac

Front 8

MOA of NSAIDS? (2)

Back 8

Reversibly inhibit cyclooxygenase (both COX-1 and COX-2).

Block prostaglandin synthesis.

Front 9

Clinical use of NSAIDS? (3)

Back 9

Antipyretic
Analgesic
Anti-inflammatory

Front 10

Toxicity of NSAIDS? (4)

Back 10

Renal damage
Aplastic anemia
GI distress
Ulcers

Front 11

What drugs are COX-2 inhibitors?

Back 11

-Celecoxib
-Valdecoxib

Front 12

MOA of COX-2 inhibitors?

Why are these drugs less corrosive on the GI lining than other NSAIDS?

Back 12

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.

Front 13

Clinical use of COX-2 inhibitors? (2)

Back 13

-Rheumatoid arthritis
-Osteoarthritis

Front 14

Toxicity of COX-2 inhibitors?

Back 14

Similar to other NSAIDs; may have less toxicity to GI mucosa (i.e., lower incidence of ulcers, bleeding).

Front 15

MOA of Acetaminophen?

Where in the body does it act most?

Back 15

Reversibly inhibits cyclooxygenase, mostly in CNS.

Inactivated peripherally.

Front 16

Clinical use of Acetaminophen? (2)

Back 16

Antipyretic, analgesic, but lacking anti-inflammatory properties.

Front 17

Toxicity of Acetaminophen?

What is the antidote?

Back 17

Overdose produces hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in liver.

N-acetylcysteine is antidote––regenerates glutathione.

Front 18

What are 3 drugs used for gout?

Back 18

-Colchicine
-Probenicid
-Allopurinol

Front 19

Colchicine:
-clinical use?
-MOA?
-S/Es?

What drugs is less toxic and thus more commonly used?

Back 19

Acute gout.

Depolymerizes microtubules, impairing leukocyte chemotaxis and degranulation.

GI side effects, especially if
given orally.

(Note: indomethacin is less toxic, more commonly used.)

Front 20

Probenicid:
-use?
-MOA?
what drug does it inhibit the secretion of?

Back 20

Chronic gout.

Inhibits reabsorption of uric
acid

Also inhibits secretion of penicillin.

Front 21

Allopurinol:
-uses? (3)
-MOA?

Back 21

Chronic gout.

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

Also used in lymphoma and leukemia to prevent tumor lysis–associated urate nephropathy.

Front 22

See diagram in Gout drugs section.

Back 22

See diagram in Gout drugs section.

Front 23

MOA of Etanercept?

Back 23

Recombinant form of human TNF receptor that binds TNF-α.

Front 24

Clinical use of Etanercept? (3)

Back 24

Rheumatoid arthritis
Psoriasis
Ankylosing spondylitis

Front 25

MOA of Infliximab?

Back 25

TNF-α antibody.

Front 26

Clinical use of Infliximab? (3)

Back 26

Crohn’s disease
Rheumatoid arthritis
Ankylosing spondylitis

Front 27

Immunosuppresive agent: Prednisone

It blocks what parts of the inflamm pathway? (2)

Back 27

-proliferation
-tissue injury

Front 28

Immunosuppresive agent: Cyclosporine

It blocks what parts of the inflamm pathway? (2)

Back 28

-proliferation
-differentiation to T-cells or antibody

Front 29

Immunosuppresive agent: Azathioprine

It blocks what parts of the inflamm pathway? (1)

Back 29

proliferation

Front 30

Immunosuppresive agent: Methotrexate

It blocks what parts of the inflamm pathway? (1)

Back 30

proliferation

Front 31

Immunosuppresive agent: Dactinomycin

It blocks what parts of the inflamm pathway? (2)

Back 31

-proliferation
-differentiation synthesis

Front 32

Immunosuppresive agent: Cyclophosphamide

It blocks what parts of the inflamm pathway? (1)

Back 32

proliferation

Front 33

Immunosuppresive agent: Antilymphocytic globulin and monoclonal T-cell antibodies

It blocks what parts of the inflamm pathway? (3)

Back 33

-antigen recognition (B and T-cells)
-proliferation
-differentiation synthesis

Front 34

Immunosuppresive agent: Rh3(D) immune globulin

It blocks what parts of the inflamm pathway? (1)

Back 34

-antigen recognition (B and T-cells)

Front 35

Immunosuppresive agent: Tacrolimus

It blocks what parts of the inflamm pathway? (1)

Back 35

cytokine secretion!

Front 36

MOA of Cyclosporine?

Back 36

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.

Front 37

Clinical use of Cyclosporine? (2)

Back 37

-Suppresses organ rejection after transplantation
-Selected autoimmune disorders.

Front 38

Toxicity of Cyclosporine? (3)

Back 38

Predisposes patients to viral infections and lymphoma

Nephrotoxic (preventable with mannitol diuresis).

Front 39

MOA of Tacrolimus (FK506)?

Back 39

Similar to cyclosporine; binds to FK-binding protein, inhibiting secretion of IL-2 and other cytokines.

Front 40

Clinical use of Tacrolimus (FK506)?

Back 40

Potent immunosuppressive used in organ transplant recipients.

Front 41

Toxicity of Tacrolimus (FK506)? (5)

Back 41

Significan:
Nephrotoxicity
Peripheral neuropathy
Hypertension
Pleural effusion,
Hyperglycemia

Front 42

MOA of Azathioprine?
What is it toxic to?

Back 42

Antimetabolite derivative of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids.

Toxic to proliferating lymphocytes.

Front 43

Clinical use of Azathioprine? (2)

Back 43

Kidney transplantation

Autoimmune disorders (including glomerulonephritis and
hemolytic anemia).

Front 44

Toxicity of Azathioprine?

What drug may increase toxic effects if used in combo?

Back 44

Bone marrow suppression.

Active metabolite mercaptopurine is metabolized by xanthine oxidase; thus, toxic effects may be ↑ by allopurinol.

Front 45

Clinical use of Aldesleukin (IL-2)? (2)

Back 45

-Renal cell carcinoma
-Metastatic melanoma

Front 46

Clinical use of Erythropoietin (epoetin)?

Back 46

anemias (especially in renal failure)

Front 47

Clinical use of Filgrastim (granulocyte colony-stimulating factor)?

Back 47

Recovery of bone marrow

Front 48

Clinical use of Sargramostim (granulocyte-macrophage colony-stimulating factor)?

Back 48

Recovery of bone marrow

Front 49

Clinical use of α-interferon? (4)

Back 49

Hepatitis B and C
Kaposi’s sarcoma
Leukemias
Malignant melanoma

Front 50

Clinical use of β-interferon?

Back 50

Multiple sclerosis

Front 51

Clinical use of γ-interferon?

Back 51

Chronic granulomatous disease

Front 52

Clinical use of Oprelvekin (interleukin-11)?

Back 52

thrombocytopenia

Front 53

Clinical use of Thrombopoietin?

Back 53

thrombocytopenia