Pharm week 4 w/ study guide

What is growth fraction?

Ratio of dividing cells → resting cells in a tumor.

Which cancers respond best to chemotherapy?

High-growth-fraction cancers (leukemias + lymphomas) because many cells are dividing.

Why are solid tumors less sensitive to chemotherapy?

Low growth fraction → fewer cells dividing.

Why does chemotherapy damage hair follicles, bone marrow, and GI tissue?

These normal tissues divide rapidly, so chemotherapy cannot fully distinguish them from rapidly dividing cancer cells.

What occurs in G₀?

Resting phase.

What occurs in G₁?

Cell prepares to copy DNA.

What occurs in S phase?

DNA synthesis/duplication.

What occurs in G₂?

Cell prepares for mitosis.

What occurs in M phase?

Mitosis (cell division).

Why are chemotherapy drugs combined?

Attack different cell-cycle phases + mechanisms → ↑ cell death + ↓ resistance.

What is chemotherapy?

Drugs that kill rapidly dividing cells (cancer cells + some healthy cells).
cyclophosphamide, cisplatin, doxorubicin.

What is targeted therapy?

Drugs that attack a specific cancer receptor or molecule (imatinib, trastuzumab)

What is hormonal cancer therapy?

Blocks hormones that stimulate certain cancers (tamoxifen, letrozole.)

What is immunotherapy?

Helps the immune system recognize + attack cancer (pembrolizumab, nivolumab)

Why can chemotherapy cause hyperuricemia?

Rapid cancer-cell death → DNA breakdown → ↑ uric acid.

How is chemotherapy-related hyperuricemia prevented?

IV fluids + allopurinol.

How does allopurinol protect the kidneys?

It decreases uric-acid formation and prevents crystal buildup.

What is tumor lysis syndrome?

Rapid cancer-cell destruction → intracellular contents enter blood → metabolic abnormalities + kidney injury.

What is the tumor-lysis mnemonic?

“Cells crash → uric acid climbs → kidneys clog.”

What does chemotherapy-related bone marrow suppression cause?

↓ RBCs + WBCs + platelets.

What does anemia cause?

↓ RBCs → fatigue, pallor, weakness + dyspnea.

What does neutropenia cause?

↓ Neutrophils → infection risk.

What does thrombocytopenia cause?

↓ Platelets → bleeding risk.

Which chemotherapy finding requires immediate reporting?

Fever or infection signs (possible neutropenia).

What should be checked before chemotherapy?

CBC + kidney/liver function + infection

What toxicities should be monitored during chemotherapy?

Infection + bleeding + stomatitis + kidney

What is the chemotherapy exam pattern?

Drug → major toxicity → assessment → priority action.

What class is methotrexate (MTX)?

Antimetabolite-antifolate + DMARD.

How does methotrexate work?

Blocks folic-acid activity → disrupts DNA synthesis during S phase.

What is methotrexate used for?

Several cancers + rheumatoid arthritis.

What is a DMARD?

Drug that slows rheumatoid arthritis progression + joint destruction.

How do DMARDs differ from NSAIDs?

DMARDs slow disease; NSAIDs relieve pain + inflammation.

What is methotrexate’s major adverse effect?

Bone marrow suppression (anemia + leukopenia + thrombocytopenia).

Which findings suggest methotrexate bone marrow suppression?

Fever, sore throat, bruising or bleeding.

Which labs are monitored with methotrexate?

CBC + kidney function + liver function.

Why monitor kidney function with methotrexate?

Kidney impairment → drug accumulation + toxicity.

Why avoid alcohol with methotrexate?

Alcohol + methotrexate → ↑ liver injury risk.

Can methotrexate be used during pregnancy?

No. It is teratogenic and can cause fetal harm.

What pregnancy teaching applies to methotrexate?

Avoid pregnancy during treatment + for at least 6 months after

What is the methotrexate mnemonic?

MTX = Monitor blood, kidneys + liver.”

What class is doxorubicin (Adriamycin/Doxil)?

Anthracycline antitumor antibiotic.

How does doxorubicin work?

Damages cancer cells → stops growth + triggers apoptosis.

What is doxorubicin’s major toxicity?

Cardiotoxicity → cardiomyopathy + heart failure.

What must be monitored with doxorubicin?

Cardiac function, including left ventricular ejection fraction (LVEF) before/during therapy

Which history requires caution with doxorubicin?

Heart failure or cardiomyopathy.

Which findings suggest doxorubicin cardiotoxicity?

Dyspnea, edema, crackles, fatigue + decreased LVEF.

Which labs are monitored with doxorubicin?

CBC + electrolytes + kidney/liver function + uric acid.

Why monitor uric acid with doxorubicin?

Cancer-cell destruction → hyperuricemia + kidney injury.

What expected discoloration occurs with doxorubicin?

Red or reddish-orange urine, sweat + tears.

What is the doxorubicin mnemonic?

“DOXO damages the heart + dyes fluids red.”

What class is vincristine (Oncovin)?

Vinca alkaloid + mitotic inhibitor.

How does vincristine work?

Disrupts microtubules during M phase → stops mitosis.

What is vincristine’s major toxicity?

Neurotoxicity → peripheral neuropathy.

Which findings suggest vincristine neurotoxicity?

Tingling, numbness, burning pain, weakness + ↓ reflexes.

What should be assessed before vincristine?

Neurologic status + muscle strength.

How do vincristine and vinblastine differ?

Vincristine → nerves; vinblastine → bone marrow suppression.

What IV access is preferred for vincristine?

A central line because vincristine can severely damage tissue if extravasation occurs.

What is the vincristine mnemonic?

“VINCRISTINE = nerve crisis.”

What class is filgrastim?

Granulocyte colony-stimulating factor (G-CSF).

How does filgrastim work?

Stimulates bone marrow → ↑ neutrophil production.

Why is filgrastim given after chemotherapy?

Shortens neutropenia → ↓ infection risk.

Which value shows filgrastim is effective?

↑ Absolute neutrophil count (ANC).

What is filgrastim’s common adverse effect?

Bone pain from increased bone-marrow activity.

What should be monitored with filgrastim?

CBC + ANC + infection signs.

Does filgrastim treat an active infection?

No; it raises neutrophils but does not replace antibiotics.

Which clients require caution with colony-stimulating factors?

Clients with sickle cell disease, bone-marrow cancers, pregnancy or significant renal/hepatic impairment.

What is the filgrastim mnemonic?

“FILGrastim FILls granulocytes.”

What class is cyclosporine (Sandimmune/Neoral)?

Calcineurin inhibitor + T-cell suppressant.

How does cyclosporine work?

Inhibits calcineurin → ↓ IL-2 → ↓ T-cell activation.

What is cyclosporine used for?

Prevent transplant rejection + treat severe RA, psoriasis + autoimmune disorders.

What is cyclosporine’s priority toxicity?

Nephrotoxicity.

What other adverse effects occur with cyclosporine?

Hypertension + hepatotoxicity + tremor + infection + malignancy risk.

What should be monitored with cyclosporine?

BUN/creatinine + urine output + BP + liver function + drug level.

Which drugs increase cyclosporine nephrotoxicity?

Aminoglycosides, NSAIDs + other nephrotoxic drugs.

A client takes cyclosporine + gentamicin. What is the priority concern?

Kidney injury → monitor BUN, creatinine + urine output.

Why should clients taking cyclosporine avoid sick contacts?

Immunosuppression → ↑ serious infection risk.

Should clients taking cyclosporine receive live vaccines?

No; live organisms may cause infection.

What is the cyclosporine mnemonic?

“Cyclosporine suppresses T cells but stresses kidneys.”

What class is tacrolimus?

Calcineurin inhibitor + immunosuppressant.

How does tacrolimus work?

Inhibits calcineurin → ↓ IL-2 + T-cell activation.

What is tacrolimus mainly used for?

Prevention of organ-transplant rejection.

What are tacrolimus’s major adverse effects?

Nephrotoxicity + neurotoxicity + hypertension + hyperglycemia + infection.

What should be monitored with tacrolimus?

Trough level + BUN/creatinine + urine output + BP + glucose + potassium.

Which tacrolimus finding requires priority action?

↑ Creatinine or ↓ urine output → possible nephrotoxicity.

Why avoid grapefruit with tacrolimus?

Grapefruit can ↑ tacrolimus level → toxicity.

What is the tacrolimus mnemonic?

“TAC blocks T-cell attack but can attack kidneys.”

What class is azathioprine?

Antimetabolite immunosuppressant.

How does azathioprine work?

Blocks purine synthesis → ↓ T-cell + B-cell production.

What is azathioprine used for?

Prevent transplant rejection + treat autoimmune disorders.

What is azathioprine’s major adverse effect?

Bone marrow suppression → infection + anemia + bleeding risk.

What should be monitored with azathioprine?

CBC + liver function + infection/bleeding signs.

Which findings require priority action with azathioprine?

Fever, sore throat, unusual bruising or bleeding.

What long-term risk occurs with azathioprine?

Increased malignancy risk from immunosuppression.

What is the azathioprine mnemonic?

“AZA lowers immune cells → assess CBC.”

What class is glatiramer acetate?

Immune modulator for relapsing multiple sclerosis.

How does glatiramer help multiple sclerosis?

Alters immunity → ↓ immune attack on myelin → fewer relapses.

Does glatiramer cure multiple sclerosis?

No; it reduces relapses but does not reverse existing damage.

What is glatiramer’s common adverse effect?

Injection-site pain, redness, swelling or itching.

What immediate reaction can follow glatiramer injection?

Flushing + chest pain + palpitations + anxiety + dyspnea.

What should the client do during a glatiramer reaction?

Stop activity + seek emergency help if severe, prolonged or unusual.