Cancer Drugs

Skin and Hair cells

• regenerate every second due to their continuous exposure to environmental damage and the need for repair.

• cancer drugs can mess with regeneration of healthy cells like these leading to hair loss and skin reactions during treatment

Hyperplasia

• too much division often leading to cell mutations

Atrophy

• cells decrease in size

Hypertrophy

• cells increased in size often because of chronic HTN

Hyperplasia

• rapid increase in the number of cells being divided caused by meds, irritation

Metaplasia

• one mature cell is replaced by a different mature cell type, often due to chronic irritation or inflammation.

Dysplasia 

• abnormal development or growth of cells, tissues, or organs, often indicating a precancerous condition.

neoplasia

• new, abnormal growth of tissue that may be benign or malignant, often associated with cancer.

What causes cancer

• mutations, inflammation, infections, environmental

Adenoma vs Adenocarcinoma 

• Adenoma is a benign tumor arising from glandular tissue, while adenocarcinoma is a malignant tumor that originates from glandular cells and can invade nearby tissues.

Osteoma vs Osteosarcoma

• Osteoma is a benign bone tumor, whereas osteosarcoma is a malignant bone tumor that can rapidly grow and spread.

Lymphomas

are cancers that originate in the lymphatic system, primarily affecting lymphocytes. They can be classified as Hodgkin or non-Hodgkin lymphoma,

Leukemia

is a type of cancer that affects blood-forming tissues, including the bone marrow and lymphatic system, leading to the production of abnormal blood cells.

Protoncogene

• 1: Normal, healthy genes that regulate cell growth, cell division, and differentiation.

  Think:
  ➡ “GO” genes — they tell cells when it’s okay to grow.

Oncogenes

• A mutated or overactive proto-oncogene that leads to uncontrolled cell growth → cancer.

Think:
➡ “STUCK GAS PEDAL” — cell keeps dividing non-stop.

Tumor suppressor genes ON

• These genes prevent uncontrolled cell growth by:

  • Slowing cell division

  • Repairing damaged DNA

  • Triggering apoptosis (cell suicide) if damage can’t be fixed

tumor suppressor genes OFF

What happens when they’re OFF?

➡ Cell cycle checkpoints fail
➡ DNA damage is not repaired
➡ Abnormal cells survive
➡ Cancer develops

Key Point (NCLEX!):
Tumor suppressor genes must usually have both alleles mutated to be turned OFF
➡ Unlike oncogenes, which need only one mutated allele

Care Taker Genes

• Caretaker = “CARE TAKES of DNA”
  ➡ Fix DNA
  ➡ Maintain stability
  ➡ Prevent cancer-causing mutations

Methylation of DNA

• Gene Type	Cancer Effect	Methylation Pattern
  Oncogenes	Overactive	Hypomethylated (on)
  Tumor suppressor genes (p53, RB)	Turned off	Hypermethylated
  Caretaker genes (BRCA1, MLH1)	DNA repair fails	Hypermethylated

Anticancer Drugs

• systemically kill all cells with similar properties

• often affect all rapidly dividing cells like (GI, skin, hair, bone marrow)

• SE: nausea, vomiting, alopecia, fatigue, osteoporosis, Steven johnsons syndrome

Nursing Considerations for Anticancer Drugs 

• if red rash is rapidly forming stop the infusion and ice the site to slow down medication progression 

• pts will be at higher risk of falls due to osteoporosis 

Types of Anticancer Drugs

1. Antimetabolites: interfere with DNA/RNA synthesis

2. Antitumor antibiotics: disrupt DNA replication/transcription

3. Alkylating: damage the DNA by adding an alkyl group

4. Plant Alkaloids: block cell division during mitosis

Targeted Therapy

• more specific to different types of cancer cells leading to fewer SE

• MOA: interferes with specific molecules involved in tumor growth and spread

• Drawback: not enough targets if early diagnosed, cancer cells mutate fast so not effective for long, research often hard to test on

• end in nib, man, mib

Direct BRM

• directly attack the cancer cells 

indirect BRM

• boost the immune system to help the body fight cancer more effectively.

Functions of the immune system cells

• B and T cells: cells produce antibodies, while T cells directly kill infected or cancerous cells.

• Neutrophils: cells that phagocytize pathogens and dead cells

• Basophils: releasing histamines to promote blood flow and recruit other immune cells.

• Eosinophils: cells that combat multicellular parasites and are involved in allergic responses.

• Monocytes/Macrophages: engulf and digest pathogens, clear dead cells, and help initiate immune responses.

Colony stimulating factors 

• promote production of blood cells for leukemia 

• 1. erythropoietin: RBCs

• 2. granulocytes: WBCs (ex: filgrastin, pegfilgrastin) 

Interleukins

• work with leukocytes to stimulate the immune response and enhance the activity of immune cells against cancer.

• ex: Aldesleuken

Interferons

• proteins that inhibit viral replication and enhance the immune response, by activating an anti-inflammatory response against tumors and viruses.

• They can also increase the activity of natural killer cells and macrophages.

Costicosteroids 

• ex: prednisone has antiinflammatory properties and is used to reduce swelling and pain in cancer treatment.

• NC: can increase risk of infections, have patient rinse mouth after use 

Tamoxifen

• blocks estrogen receptors in breast tissue, slowing growth of estrogen-dependent tumors

• increases risk of blood clotting and bleeding and can increase risk of endometrial cancer

• Teach to report:

  • Leg swelling

  • Chest pain

  • Shortness of breath

  • Sudden headache or weakness

PT teaching for corticosteroids

• wash hands

• disinfect objects

• mask in public

• no crowds

• no flowers or fresh fruit

• no latex