PHARM WEEK 4 THURSDAY

Why is gastric acid considered a barrier defense?

It destroys many swallowed or ingested pathogens.

What does chemotaxis do?

Attracts + activates neutrophils and macrophages at the injured area.

What are neutrophils?

WBCs that rapidly attack and engulf pathogens during acute inflammation.

What do B cells provide?

Humoral immunity → become plasma cells → produce antibodies.

What do T cells provide?

Cell-mediated immunity → directly attack infected or abnormal cells.

How can B cells versus T cells be remembered?

B = antibodies in Body fluids; T = Target abnormal cells.

What additional effect does interleukin-1 produce besides activating T and B cells?

Fever + muscle/joint pain + slow-wave sleep (conserves energy).

How do corticosteroids decrease inflammation?

Suppress the inflammatory + immune responses.

What are examples of systemic corticosteroids?

Prednisone + dexamethasone.

What are examples of topical corticosteroids?

Hydrocortisone + betamethasone.

How do antihistamines reduce inflammation?

Block histamine’s effects during the inflammatory response.

Which antihistamine is first generation and sedating?

Diphenhydramine (Benadryl).

Which antihistamine is second generation and mildly sedating?

Cetirizine (Zyrtec).

How do salicylates decrease pain

fever

What is aspirin used to treat?

Pain + fever + inflammatory conditions.

What is the priority adverse effect of aspirin/salicylates?

GI irritation + bleeding.

Which patients should avoid or use caution with salicylates?

Bleeding disorder

Is gastric acid a barrier defense?

Yes → stomach acid destroys many swallowed/ingested pathogens.

What is chemotaxis?

Chemical attraction that brings neutrophils + macrophages to injury/infection and makes them more aggressive.

What do B cells do?

Become plasma cells → produce antibodies (humoral immunity).

What do cytotoxic T cells do?

Directly destroy or mark infected

What do helper T cells do?

Activate other immune cells

What do suppressor T cells do?

Slow the immune response → prevent continued inflammation and cell damage.

What is the easiest way to remember B cells vs. T cells?

B = antibodies in Body fluids; T = Target abnormal cells.

Which immune cells destroy cancer or virus-infected cells without prior exposure?

Natural killer (NK) cells.

What do complement proteins do?

Damage the antigen’s membrane → fluid enters → antigen bursts.

Which antibody appears first during the first exposure to an antigen?

IgM (“M = first Made”).

What do interferons naturally do?

Prevent viral replication + suppress malignant-cell growth.

What do interleukins do?

Allow leukocytes to communicate and activate immune responses.

Besides activating T and B cells

what does IL-1 cause?

What does tumor necrosis factor (TNF) do?

Promotes inflammation and may inhibit tumor growth.

How do corticosteroids reduce inflammation?

Suppress the inflammatory + immune responses.

Which corticosteroids may be used systemically?

Prednisone + dexamethasone.

Which corticosteroids may be used topically?

Hydrocortisone + betamethasone → local anti-inflammatory effect.

How do antihistamines reduce inflammation?

Block histamine’s actions during the inflammatory response.

Which antihistamine is first generation and sedating?

Diphenhydramine (Benadryl).

Which antihistamine is second generation and only mildly sedating?

Cetirizine (Zyrtec).

How do salicylates work?

Inhibit prostaglandin synthesis → decrease pain, fever, and inflammation.

What is aspirin used for?

Pain + fever + inflammatory conditions.

Which blue-highlighted salicylates treat ulcerative colitis/IBD?

Balsalazide + mesalamine + olsalazine.

What are the major risks of salicylates?

GI irritation + bleeding + salicylate toxicity.

When should salicylates be avoided or used cautiously?

Bleeding disorder, renal impairment, pregnancy/lactation, or surgery within 1 week.

A patient taking aspirin is scheduled for surgery next week. What is the concern?

Aspirin increases bleeding risk → notify the provider.

Can a patient who does not respond to one salicylate respond to another?

→ salicylates differ in absorption, metabolism, potency, and tolerance.

How do NSAIDs work?

Block COX-1/COX-2 → ↓ prostaglandins → ↓ pain, fever, and inflammation.

What therapeutic effects do NSAIDs provide?

Analgesic + antipyretic + anti-inflammatory.

What does COX-1 normally protect?

Stomach lining + platelet function + kidney blood flow.

What does COX-2 mainly produce?

Prostaglandins responsible for pain, fever, and inflammation.

Why can nonselective NSAIDs cause ulcers and bleeding?

COX-1 inhibition → ↓ stomach protection + altered platelet function.

Why may COX-2 inhibitors increase cardiovascular risk?

They may increase the risk for MI + stroke.

When are NSAIDs contraindicated?

Allergy to an NSAID or salicylate.

Which additional allergy contraindicates celecoxib?

Sulfonamide allergy.

Which blue-highlighted NSAIDs should be recognized?

Ibuprofen + naproxen + diclofenac + indomethacin + ketorolac + celecoxib.

Which NSAIDs are propionic acids?

Ibuprofen (Motrin/Advil) + naproxen (Naprosyn).

Which NSAIDs are acetic acids?

Diclofenac + indomethacin + ketorolac.

Which NSAID is a selective COX-2 inhibitor?

Celecoxib (Celebrex).

What is the high-yield NSAID safety mnemonic?

“GI

Is acetaminophen (Tylenol) an NSAID?

No → it provides analgesic + antipyretic effects but little anti-inflammatory action.

What is known about acetaminophen’s mechanism of action?

Exact MOA is not well understood; it acts in the CNS/hypothalamus to reduce pain and fever.

What is acetaminophen used for?

Mild–moderate pain + fever.

What is acetaminophen’s most important adverse effect?

Hepatotoxicity.

What increases acetaminophen hepatotoxicity?

Overdose + chronic use + alcohol consumption.

Which patient should avoid acetaminophen?

A patient with significant liver disease or chronic alcohol use disorder.

How does acetaminophen interact with warfarin?

May increase bleeding risk.

Which drugs increase acetaminophen liver toxicity?

Carbamazepine, phenytoin, barbiturates, and rifampin.

A patient takes acetaminophen daily and drinks alcohol heavily. What is the priority concern?

Severe liver damage.

What should patients check before taking acetaminophen?

Combination-drug labels → prevent an accidental overdose.

How are DMARDs different from NSAIDs?

DMARDs slow joint damage; NSAIDs only relieve symptoms.

What is the goal of DMARD therapy?

Control inflammation + preserve joint function + prevent permanent damage.

Which major DMARD treatments should you recognize?

Methotrexate + biologic medications.

How do TNF blockers treat rheumatoid arthritis?

Block TNF → ↓ inflammation + slow joint destruction.

Which blue-highlighted TNF blockers should be recognized?

Infliximab + adalimumab (Humira) + etanercept (Enbrel).

How are TNF blockers administered?

Most are subcutaneous; infliximab is IV.

What must be screened before starting a TNF blocker?

Active infection/sepsis + TB + hepatitis B.

Why should TNF blockers be avoided during an active infection?

Immune suppression may cause the infection to become severe.

What serious boxed warning is associated with TNF blockers?

Increased risk for lymphoma and other malignancies.

Which neurologic condition is a major concern with TNF blockers?

Demyelinating disease (multiple sclerosis).

Which cardiovascular problems can TNF blockers cause?,

Heart failure + MI + hypotension.

What vaccines should patients avoid during TNF-blocker therapy?

Live vaccines.

A patient receiving adalimumab develops fever and cough. What should the nurse do?

Hold the medication and notify the provider → possible serious infection.

A patient with multiple sclerosis is prescribed a TNF blocker. What should the nurse do?

Question the prescription because TNF blockers may worsen demyelinating disease.

A patient with severe heart failure is prescribed a TNF blocker. What should the nurse do?

Question the prescription because TNF blockers may worsen heart failure.

What is the treatment goal during an acute gout attack?

Rapidly decrease inflammation + pain.

Which medications treat an acute gout attack?

NSAIDs + colchicine + corticosteroids.

When is colchicine most effective?

When started early during the acute gout attack.

What is the treatment goal for chronic gout?

Lower uric acid → prevent future attacks and joint damage.

How does allopurinol work?

Inhibits xanthine oxidase → decreases uric acid production.

Is allopurinol used to provide immediate pain relief during an acute attack?

No → it provides long-term uric acid control.

What is an easy way to remember acute vs. chronic gout drugs?

Colchicine = calm current attack; allopurinol = avoid another attack.

What do immune stimulants do?

Strengthen immune activity to help fight infection or cancer.

What do immune suppressants do?

Decreases immune activity for transplant, autoimmune disease, or some cancers.

What are the main immune stimulants?

Interferons + interleukins + colony-stimulating factors.

How do interferon drugs work?

Block viral replication + make antiviral proteins + slow tumor growth.

What are interferons used to treat?

Selected viral infections + cancers.

What are interferons’ high-yield adverse effects?

Flu-like symptoms + bone-marrow suppression + depression/suicidal thoughts.

Why do interferons cause flu-like symptoms?

Immune stimulation triggers an inflammatory response.

What is the priority monitoring during interferon therapy?

CBC + liver function + mood/suicidal thoughts + infection.

Which condition requires caution with interferons?

Cardiac disease.

Which drugs increase interferon-related bone-marrow suppression?

Zidovudine + other myelosuppressive drugs.