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Step 1 Pharm > Musculoskeletal Drugs > Flashcards

Musculoskeletal Drugs Flashcards

1
Q

What is the pathways for AA?

What is the starting product?

Where does it go to next?

A

Start with membrane lipid ( phophatidylinositoly)

lipid—> (Phospholipase A2) –> Arachidonic Acid

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2
Q

What different paths can Arachidonic Acid head down?

What enZs do that?

What drugs inhibit those enzymes?

A

AA—> (Lipoxygenase)—> Hydorperoxidase ( HPETES) that go to LeukoT

Zieluton inhibits Lipoxygenase

OR

AA–> (COX1 and 2)–> Endoperoxides (PGG2, PGH2)

NSAIDs/aspirin/actaminophen/ COX-2 inhitors block COX1 and 2

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3
Q

What drugs inhibit COX 1 and COX 2?

A

Corticosteroids

NSAIDS, aspirin, acetominophen, COX-2 inhibitors

Thus can’t make Prostacyclines (PGI2)

Can’t make Prostaglandins (PGE2, PGF2)

Can’t make Thormoboxane (TXA)

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4
Q

What is the Starting point of the AA cycle

What does it genererate?

Via what pathways

A

Start with lipid membrane —> Phospholipase A2 to AA

Then can head down lipoxygeanse path to make Leukotrienes

OR

Head down the COX1 and 2 path to amke TXA2, Prostaglandins: PGE2, PGF2 and Prostacyclines: PGI2

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5
Q

What drug can inhibit the progression for LTC4, LTD4 and LTE4 which causes

INCREASED bronchial tone

A

Zarfirlukast and Montelukast block receptor for LCT, LTD and LTE

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6
Q

What is the role of the following:

LTB4:

LTC4, LTD4, LTE4:

A

LTB4: Neutrophil chemotaxis

LTC4, LTD4, LTE4: Increase bronchial tone (blocked by Zeiluton or Monteclast)

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7
Q

What are the restuls of the following products

Prostacyclin : PGI2

Prostaglandin: PGE2 and PGF2

Thromboxane: TXA

A

Prostacyclin : PGI2 –> Low plat aggregation, low vascular tone, low bronchial tone, low uterine tone

Prostaglandin: PGE2 and PGF2–> Increased uterine tone and decrease bronchial tone

Thromboxane: TXA: Increase plat aggregation, increase vascular tone, increase bronchial tone

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8
Q

______ is a neutrophil chemotactic agent.
_____ inhibits platelet aggregation and promotes vasodilation.

A

LTB4

PGI2

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9
Q

what is the mechanism of Acetaminophen?

Where does it act?

What is it used for?

A

Reversibly inhibits cyclooxygenase, mostly in CNS. Inactivated peripherally.

Antipyretic, analgesic, but not anti-inflammatory.

Used instead of aspirin to avoid Reye syndrome in children with viral infection

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10
Q

What drug would we use for child with fever and aches?

What’s it’s mechanims?

A

Use Acetominophen

irreversible inhibits COX and safer choice over aspirin

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11
Q

What toxicity is associated with Acetominophen?

What organ?

What is the antidote?

A

Overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue byproducts in liver.

N-acetylcysteine is antidote—regenerates glutathione.

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12
Q

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) via acetylation, which􏰀 decreases synthesis of TXA2 and prostaglandins.􏰁

Increased bleeding time. No effect on PT, PTT. A type of NSAID.

A

Aspirin

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13
Q

What is the difference between low dose, intermediate dose and high dose Aspirin

A

Low dose (< 300 mg/day): 􏰀 platelet aggregation.

Intermediate dose (300–2400 mg/day): antipyretic and analgesic.

High dose (2400–4000 mg/day): anti-inflammatory.

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14
Q

What is the mechanism of Aspirin?

A

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) via acetylation, which􏰀 increase synthesis of TXA2 and prostaglandins.􏰁bleeding time. No effect on PT, PTT. A type of NSAID.

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15
Q

What toxicity is associated with Aspirin?

A

Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, GI bleeding.

Risk of Reye syndrome in children tr_eated with aspirin for viral in_fection. Causes respiratory alkalosis early, but transitions to mixed metabolic acidosis-respiratory alkalosis

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16
Q

What is the mechanism and use of Celcoxib?

A

Reversibly inhibits specifically the cyclooxygenase (COX) isoform 2,

which is found i_n inflammatory cells and vascular endothelium_ and mediates inflammation and pain; spares COX-1, which helps maintain gastric mucosa.

17
Q

What pathways in the AA path are spared by Celecoxib?

A

spares COX-1, which helps maintain gastric mucosa.

Thus, does not have the corrosive effects of other NSAIDs on the GI lining. Spares platelet function as TXA2 production is dependent on COX-1.

18
Q

What are the big effects of aspirin?

A

Analgesic: central and peripheral action

Antipyrietic: acts in hypothal to lower the set point of temperature control elevated by fever—causes sweating

Anti-inflammatory: INhibits peripheral prostaglandin synthesis

Respiratory stimulation: Direct action on repiratory center thus indirectly increaese CO2 production

19
Q

This drug can be used for pain relief but doen’st fuck with the gastric mucosa.

What are some risks associated with it?

A

High risk of thrombophelbeitis because leaves the TXA pathway alone as well as SULFA allergy

20
Q

Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac.

All are examples of what type of drug and all have what MOA?

A

NSAIDs

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

21
Q

These drugs REVERSIBLY inhibit COX 1 and COX2 to block PG synthesis.

What is their use?

What drugs are they?

What is a specific use of Indomethacin?

A

Use: Antipyretic, analgesic, anti-inflammatory.

Indomethacin is used to close a PDA.

These are NSAIDS: Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac.

22
Q

Pt experiences chronic low back pain so takes ibuprofen on a daily basis at double the recommended dose..

What is he putting himself at risk for?

Why?

A

Interstitial nephritis

gastric ulcer (prostaglandins protect gastric mucosa)

renal ischemia (prostaglandins vasodilate afferent arteriole).

23
Q

What are examples of Bisphosphonates?

How do they work?

A

Alendronate, other -dronates.

Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity

24
Q

When would you prescribe Aldeondronate?

What is it’s mechanism?

A

Osteoporosis, hypercalcemia, Paget disease of bone.

Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity.

25
Q

YOu have a pt with Pagets disease and have her on a medication that binds hydroxyapetite and limits osteoclast activity.

What negative side effects do we worry about?

A

Corrosive esophagitis (patients are advised to take with water and remain upright for 30 minutes), osteonecrosis of jaw.

26
Q

What is Teriparatide and what is it’s MOA?

A

Recombinant PTH analog given subcutaneously daily.􏰁

INCREAES osteoblastic activity.

27
Q

Drug used for Osteoporosis. Causes 􏰁 bone growth compared to antiresorptive therapies (e.g., bisphosphonates).

What neg affect do we worry about?

A

Teriparatide

Transient hypercalcemia. May increase risk of osteosarcoma

28
Q

What is the MOA of allopurinol and why is it beneficial for Gout pts?

A

Inhibits Xanthine Oxidase to Decrease conversion of Xanthine–> Uric Acid

Thus lower Uric acid that ppt into crystals

29
Q

What are some other uses of allopurinol and their role in lymphoma

A

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

Increases 􏰁concentrations of azathioprine and 6-MP (both normally metabolized by xanthine oxidase).

30
Q

Why would you take allopurinol with 6MP or Azothioprine?

A

Will increase the concentrations of azothiprine and 6MP in pts

azothioprine and 6-MP are metabolized by xanthine oxidase

31
Q

What is the use and Mechanism of Febuxostat

A

Inhibits xanthine oxidase.

Preventative Gout medication

32
Q

What is Peglioticase?

What’s it’ use?

A

Recombinant uricase that c_atalyze metabolism of uric acid_ to allantoin (a more water-soluble product).

Use to prevent Gout

33
Q

What is the use of PRobenecid?

What’s is MOA?

A

Inhibits reabsorption of uric acid in proximal convoluted tubule (also inhibits secretion of penicillin). Can precipitate uric acid calculi.

34
Q

What drugs are recommended to prevent gout flare?

A

Allopurinol

Febuxostat

Probenecid

35
Q

What is a problem associated with TNF-alpha inhibitors?

A

All TNF-α inhibitors predispose to infection, including reactivation of latent TB, since TNF is important in granuloma formation and stabilization.

36
Q

What is Etanercept?

What is it’s MOA?

Uses?

A

Fusion protein (receptor for TNF-α + IgG1 Fc), produced by recombinant DNA.

Etanercept is a TNF decoy receptor.

Rheumatoid arthritis, psoriasis, ankylosing spondylitis

37
Q

Fusion protein (receptor for TNF-α + IgG1 Fc), produced by recombinant DNA.

TNF decoy receptor.

What drug is this?

What is it used for?

A

Etanercept (receptor decoy)

Rheumatoid arthritis, psoriasis, ankylosing spondylitis

38
Q

What is the MOA of Infliximab, adalimumab

When do we Rx them?

A

Anti-TNF-α monoclonal antibody.

Inflammatory bowel disease, rheumatoid arthritis, ankylosing spondylitis, psoriasis

39
Q

Anti-TNF-alhpa antibody used to tx Inflammatory bowel disease, rheumatoid arthritis, ankylosing spondylitis, psoriasis

A

Infliximab, adalimumab

Step 1 Pharm (15 decks)

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