Cancer Care Treatment Flashcards
(95 cards)
1
Q
What are the classifications of anticancer drugs?
A
- Alkylating agents
- Antimetabolites
- mitotic inhibitors
- antibiotics
- Nitrosoureas
- antibody
- enzyme
- DNA synthesis inhibitors
- Signal transduction inhibitor
- Differentiation agent:
- Hormones and hormone antagonists:
- Proteasome inhibitors:
- DNA topoisomerase I inhibitors
- Agents that inhibit DNA repair
- Arsenic trioxide
- Inhibitors of DNA methylation
- Chimeric toxic protein:
2
Q
classifications of anticancer drugs: examples of alkylating agents
A
cyclophosphamide
chlorambucil
mechlorethamine
melphalan
3
Q
classifications of anticancer drugs: examples of antimetabolite agents
A
methotrexate
pemetrexed (Alimta), 6-mercaptopurine, 5-fluorouracil, capecitabine, cytosine arabinoside, gemcytabine
4
Q
classifications of anticancer drugs: examples of mitotic inhibitors
A
vinblastine, vincristine, paclitaxel (Taxol), docetaxel (Taxotere)
5
Q
classifications of anticancer drugs: examples of antibiotics
A
actinomycin D, doxorubicin (Adriamycin), daunomycin, bleomycin
6
Q
classifications of anticancer drugs: examples of Nitrosoureas
A
carmustine (BCNU), lomustine (CCNU)
7
Q
classifications of anticancer drugs: examples of antobodies
A
trastazumab (Herceptin), bevacizumab (Avastin),
cetuximab (Erbitux), rituximab (Rituxan)
8
Q
classifications of anticancer drugs: examples of enzymes
A
asparaginase
9
Q
classifications of anticancer drugs: examples of Agents that inhibit DNA synthesis
A
hydroxyurea
10
Q
classifications of anticancer drugs: examples of agents that damage DNA
A
cisplatin, carboplatin, oxaliplatin
11
Q
Chemotherapy: Mechanisms of Drug Resistance
A
- The cell membrane is impermeable
- The drug is actively pumped out of the cell by the Pglycoprotein
- The drug is not metabolized to an active form
- The drug is inactivated
- The drug target is increased e.g. increased level of
enzyme or gene amplification - Mutation in a target protein decreases the affinity for
the drug - Alternative biochemical pathways are increased
- There is a decrease in topoisomerase II and DNA
breaks - DNA damage is repaired
12
Q
Chemotherapy: How do alkylating agents work?
A
The alkylating agents either spontaneously or after metabolism yield an unstable alkyl group, R-CH2+, which reacts with nucleophilic centers on proteins and nucleic acids. In most cases they may be considered to be cell
cycle nonspecific agents. Many are bifunctional and can cross-link two DNA chains.
13
Q
What are the principles of immunotherapy?
A
Immunotherapy is a treatment that uses the body’s own natural defenses to fight cancer. White blood cells (T cells) that make up the immune system can be stimulated in several ways by specially designed drugs that allow them to recognize and kill cancer cells.
Early immunotherapy drugs worked in a general way by boosting the body’s immune system to fight cancer cells. However, recent research has discovered several proteins on the surface of T cells that act like a brake, or checkpoint, preventing them from attacking cancer cells.
14
Q
Immunotherapy: how do checkpoint inhibitors work?
A
- CTLA-4 (1996): Ipilimumab, an immune checkpoint inhibitor that turns off CTLA-4 and allows the T cells to do their work..
- PD-1 (2000) Several drugs have been developed to turn off PD-1 in many types of cancer, allowing existing T cells near the tumor to attack.
15
Q
Targeted immunotherapies principles
A
- Targeted immunotherapies attack specific proteins on the surface of cells that help identify cancer and stimulate an immune response.
- Monoclonal antibodies are designed to identify specific abnormalities on the surface of cancer cells.
16
Q
The 3 “E”s of immuno-editing of cancer
A
• Elimination • Equilibrium • Escape
17
Q
Describe Equilibrium in immuno-editing of cancer
A
- Escaping tumor cells persist in a delicate balance of growth and immune suppression.
- Immune system is able to keep tumor cells from growing out of control, but unable to eliminate them completely.
- During this phase tumors develop new adaptations to evade the immune system
18
Q
Describe Escape in immuno-editing of cancer
A
- Tumors adaptations to disrupt equilibrium and suppress the immune system.
- A common method is to manipulate checkpoint pathways, which act as natural “brakes” for an immune response.
19
Q
What mechanisms are used by tumours to evade the immune system?
A
• Hypoxia in tumors induces HIF-1SDF-1, a chemokine to attract MDSCs and TAM to the tumor microenvironment through the receptor CXCR4.
• Down regulate MHC-I
• Myeloid-derived suppressor cells (MDSCs ) and tumor-associated macrophages (TAMs), they can
• induce Tregs, and directly inhibit CTLs.
• secrete cytokines such as IL-10 that promote a regulator phenotype among intratumoral DC
• express PD-L1 and PD-L2, which inhibit CTL function through the PD-1 receptor
• TGF-b
• reactive oxygen species (ROS)
• reactive nitrogen intermediates (RNI)
• arginase and nitricoxide synthase (NOS),
deplete l-arginine, an important metabolite for CTL function.
20
Q
Current immunotherapies used for lung cancer
A
- monoclonalantibodies • therapeuticvaccines
- adoptivecelltherapy
- checkpoint inhibitors
21
Q
Summarise chemotherapy
A
• Normally, cells live, grow and die in a predictable way.
• Cancer occurs when certain cells in the body keep dividing and
• •
forming more cells without the ability to stop this process.
Chemotherapy involve destroying cancer cells by keeping the cells from further multiplying.
Chemotherapy is toxic to all cells–including those that are perfectly healthy. While relatively effective, this can lead to unpleasant side-effects
22
Q
Side effects of chemotherapy
A
Alopecia
Pulmonary fibrosis Cardiotoxicity Local reaction Renal failure Myelosuppression Phlebitis
Mucositis
Nausea/vomiting
Diarrhea/Constipation Cystitis Infertility/dysfunction Myalgia
Neuropathy
23
Q
Grading of toxicity in chemotherapy
A
- Grade 1: minimal symptoms
* Grade 2: Requires medication • Grade 3: Needs hospitalisation • Grade 4: Life threatening
24
Q
Immune related adverse reactions
A
- Based on the severity of the adverse reaction, pembrolizumab should be withheld and corticosteroids administered
- Upon improvement to Grade ≤ 1, corticosteroid taper should be initiated and continued over at least 1 month
- Pembrolizumab may be restarted within 12 weeks after last dose of pembrolizumab if the adverse reaction remains at Grade ≤ 1 and corticosteroid dose has been reduced to ≤ 10 mg prednisone or equivalent per day
- Based on limited data from clinical studies in patients whose immune-related adverse reactions could not be controlled with corticosteroid use, administration of other systemic immunosuppressants can be considered
25
Monitoring and management of Immune- related pneumonitis
Immune-related pneumonitis
• For signs and symptoms of pneumonitis
• Suspected pneumonitis should be confirmed with
radiographic imaging and other causes excluded
• • •
Administer corticosteroids for Grade ≥2 events
(initial dose of 1–2 mg/kg/day prednisone or equivalent followed by a taper)
Withhold pembrolizumab for Grade 2 pneumonitis until adverse reactions recover to Grade 0-1
Permanently discontinue pembrolizumab for Grade 3, Grade 4, or recurrent Grade 2 pneumonitis
26
What is Parenteral Nutrition (PN)?
PN involves the delivery of a volumetrically
controlled infusion through a venous catheter an
effective means of providing nutritional support.
The term TPN, although frequently used, is misleading and outdated. It implies the solution is nutritionally complete. In practice, not all PN solutions contain the full spectrum of macro and micronutrients, or will meet an individual’s nutritional requirements, and unless someone is nil by mouth they will be taking some nutrients orally.
27
When to consider Parenteral Nutrition (PN)
Consider PN if the patient has:
• Inaccessible small bowel
• Non-functioning or functioning insufficiently small bowel e.g.
short bowel
• Post operative patients on bowel ‘rest’
• Patients who are likely to be nil by mouth for 5 days or more e.g. prolonged ileus
• Severe inflammatory bowel disease
• Severe pancreatitis in whom naso jejunal feeding is not possible
• Unsuccessful enteral feeding e.g. continuous vomiting
28
Typical contents of PN
* PN bags used in MKUH are pre-compounded ‘standard’ bags by a pharmaceutical company
* Protein is referred to in grams of nitrogen
* Carbohydrate is provided as glucose
* Fat is provided in the form of lipid
* Fluid and electrolytes can be adjusted daily depending on the patients’ blood biochemistry and any abnormalities corrected prior to commencing PN
* Vitamins and minerals chemical stability can be affected by light and temperature, and destabilisation can be harmful, and must be stored at the correct temperature and protected from light
29
Who can administer PN
* Due to the risk of sepsis and metabolic complications associated with its delivery, staff are required to attend Parenteral Nutrition (PN) training and achieve a level of competency in order to be able to administer parenteral nutrition (PN)
* This is supported by the British Association of Parenteral and Enteral Nutrition (BAPEN), who recommend that continuing education programmes exist for all staff involved in the clinical care of patients receiving this therapy (Pennington 1996)
* Nurses must have completed the IV drug administration assessment training prior to completing PN training.
30
Administration of PN
• Initially PN is initiated as a continuous infusion (i.e., each bag over 24 hours)
• Cyclical PN (usually overnight), thought to be less harmful to the liver, and allows the patient to
be free from the infusion during the day (Thorell & Nordenstrom 2001).
• Long-term PN fed patients who are not fluid dependent do not need to receive PN every day.
Maximum hang times/changing the giving set
• Lipid containing solutions are hung for a maximum of 24 hours
• Giving-sets changed every 24 hours (DoH 2001, CDC 2002)
• There are no specific recommendations for other PN regimens but as glucose solutions enhance
microbial growth, applying these guidelines to all PN regimens seems appropriate.
Needle-less devices
Needle free access devices reduce the risks of needle-stick injury and transmission of blood borne pathogens, and can be left insitu for up to 7 days.
31
What Intravenous Access for PN. Advantages of central
Considered good IV practice to select smallest size catheter necessary for chosen therapy so as to have maximum blood flow around device
```
Central
• Rapid dilution of irritant drugs
• Stable access, ↓ tissue damage
• Simultaneous infusion of incompatible drugs
• Avoids repeated cannulations
• Risk of line sepsis
```
```
Peripheral
• Can start immediately
• Requirements compromised with peripheral PN
• Only Kabiven 7 goes peripherally
(can be given centrally)
• Increased risk of thrombophlebitis
```
32
Venous access considerations for PN
Short / long term use
• Elective or emergency
• Flow rate of intended therapies
– Continuous or cyclical? • Need for other IV therapies
Multi or single lumen
• Who will be inserting the device and how?
• Where? - Ultrasound/Radiology • Is the patient is self caring?
Cuffed or un-cuffed / Gauge of catheter
• Any known allergies to catheter materials
• Who will be caring for the device?
Multi-lumen CVC
• Have lumens of differing size entering the bloodstream at different points along the superior vena cava
Once a lumen has been selected for PN it should be used exclusively so as to reduce the risk of line infection
33
Identifying lines, midline vs PICC line
A PICC line is a catheter usually iinserted into the basilic vein in the upper arm, with the tip in the Superior Vena Cava.
A Midline is peripherally inserted into the basilic vein via the veins of the antecubital fossa or upper arm with the tip terminating in the axillary vein.
- Kabiven 7 ONLY peripheral use
CHECK the medical notes – Both line may look very similar
34
Risks of Central Venous Access: Air embolus clinical features.
Chest pain, dyspnoea, tachycardia, hypotension, hypoxia
35
Risks of Central Venous Access: Pneumothorax clinical features.
Pain on inspiration/expiration, dyspnoea
36
Risks of Central Venous Access: Pneumothorax clinical features.
Dyspnoea, tachycardia
37
Risks of Central Venous Access: Catheter malposition clinical features.
Back flow of blood, coughing, ear/neck pain, palpitations/arrhythmia’s, aspiration
38
Risks of Central Venous Access: Cardia arrhythmias clinical features.
If the catheter extends beyond the SVC and touches the cardiac wall
39
Risks of Central Venous Access: Thrombosis clinical features.
Swelling of neck/chest/arm/leg, skin discolouration, skin temperature changes, infusion difficulties, aspiration
40
Risks of Central Venous Access: Arterial puncture clinical features.
Arterial puncture
| Accidental puncture can lead to hematoma formation and swelling in the surrounding area
41
Post insertion line care
Surgical Aseptic technique at all times
Dedicated ‘labelled’ lumen – use only for feeding
Never use line for sampling except in extremis
Minimal handling, Vigilance and standardised practice
Observations & check exit site
Documentation confirming correct tip position Positive Flush Technique, preventing blood Reflux
into the catheter lumen, achieved by maintaining a forward motion on the syringe plunger while simultaneously injecting the last 0.2ml of flush solution using 10ml syringe or above
Flush with saline between infusions using a turbulent flow technique, i.e. the line is cleared effectively using a “push-pause” technique and complete with positive pressure lock
42
What to do when Suspect a line related sepsis
- Paired cultures soon after admission
- If clinically unstable, stop PN and do not use the line at all but leave insitu whilst
awaiting results and peripheral fluids etc.
- If clinically stable the line can be used for crystalloid fluids if access is poor, but not
PN whilst awaiting results, and cover with broad spectrum abx.
- Peripheral fluids if possible
- Liaise with tertiary centre ASAP following admission and follow their guidelines
(even if they differ from our local guidelines)
- Transfer pt to tertiary centre if appropriate
- Exclude other causes of sepsis e.g. sputum, urine, wound swab etc.
- Consider line lock antibiotics following micro advice
- Pull line if micro state line can not be salvaged (do not routinely pull the line
without BC review)
- Paired cultures after course abx has finished
- Give at least one cycle of HPN through line after -ve BC have come back before d/c
43
What to monitor with patients having PN
* Line placement: dedicated lumen
* Baseline bloods – daily until on full regime then 2-3 times/week (inc. Phosphate, Potassium, Calcium, Glucose, Magnesium)
* Baseline lipids
* +/- IV fluids
* Pabrinex OD for at least 3/7 up to 10 /7
* BM’s (6 hourly for first 24-48hrs, BD/random) • Weekly weight
44
Causes of death in Children Cancer Survivor Study (CCSS)
* Cancer recurrence/ second neoplasm SMR =19.4
* Pulmotoxicity SMR = 9.2
* Cardiotoxicity SMR = 8.2
* infections
45
Risk factors for late effects of cancer treatment
• Primary neoplasm (retinoblastoma, HL, STS)
• Younger age at the time of therapy
• Female sex
• Radiotherapy
• Chemotherapy (alkylating
agents, topoizomerase inhibitors)
• Genetic predisposition ( Li-Fraumeni syndrome, NF t.1, Fanconi anemia, gene polimorphisme)
• environment
• Hodgkin lymphoma >ALL, ANLL, CML, bone
tumors, thyroid cancer, breast/ skin cancer
• Retinoblastoma > osteosarcoma
• Nephroblastoma (genetic form) >osteochondroma,
adenocarcinoma
• T-ALL > ANLL
• Radiotherapy > osteosarcoma, STS, skin cancer
• Radiotherapy of neck > thyroid cancer
46
Late effects of cancer treatment: Management
```
• Patient education
• Detailed history, including family history
• Careful clinical examination
• Advice on reduction risk behaviours,
especially smoking and sunbathing
```
47
Late effects of cancer treatment: Thoracic radiation therapy >15Gy
• Delayed pericarditis
• Pancarditis, which includes pericardial and myocardial fibrosis,
with or without endocardial fibroelastosis
• Myopathy
• Coronary artery disease (CAD)
• Functional valve injury
• Conduction defects
48
Signs and symptoms of Cardiomyopathy (after chemotherapy)
fatigue, cough,dyspnea on exertion, peripheral edema, hypertension,
tachypnea/rales, tachycardia, cardiomegaly, syncope, palpitations,
arrhytmias
49
Signs and symptoms of Valvular damage (after radiation therapy >40Gy)
weakness,cough, dyspnea on exertion, new murmur
50
Signs and symptoms of Pericardial damage (after radiation therapy >35 Gy)
fatigue, dyspnea on exertion, chest pain, cyanosis, ascites, peripheral
edema, hypotension, friction rub, muffled heart sounds, venous distension,
pulsus paradoxus
51
Signs and symptoms of Coronary artery disease (after radiation therapy > 30Gy):
chest pain on exertion, dyspnea, diaphoresis, pallor, arrhytmias
52
Effects of radiation therapy on Respitatory system
• Pneumonitis acute (>40 Gy alone - or lower dose + dactynomycin/ anthracyclines )
• 12 – 14 Gy – reduced total lung capacity and vital capacity
to about 70%
• Pulmonary fibrotic disease with permanent restrictive
disease
53
Late effects of cancer treatment: Urinary system
```
Renal failure due to:
•Disease: nephroblastoma, NHL, leukemia >
> renal infiltration
> blood vessels compression
> hypertension
```
Chemotherapy can cause glomerular dysfunction, tubular dysfunction, toxicity with renal acidosis and Fanconi's syndrome, hemorrhagic cystitis
Radiotherapy can cause renal failure, renal arteriosclerosis, nephrotic syndrome, bladder fibrosis or hypoplasia, bladder tenderness
54
Late effects of cancer treatment: Gastrointestinal tract
Enteritis due to:
•Chemotherapy (actinomycin D, doxorubicin)
•Radiation >40Gy
•Surgery (abdominal surgery enchance RT effect) - abdominal pain - diarrhea, decreased stool bulk - emesis - weigth loss, poor linear growth
Can cause adhesions, fibrosis esopahgueal strictures, fibrosis of small or large intestine,
55
Late effects of cancer treatment: presentation of small intestine fibrosis
```
Fibrosis small intestine due to:
• Radiation > 40 Gy
• Abdominal surgery -
diarrhea -
weight loss
- obstruction
- abdominal pain -
constipation
```
Indications:
* high –fiber diet
* decompression, resection, balloon dilatation
56
Late effects of cancer treatment: presentation of largeintestine fibrosis
```
Large intestine/ colon fibrosis due to:
• Radiation >40 Gy
• Abdominal surgery
Signs:
- abdominal colic
- rectal pain
- constipation
- melena
- weight loss
- obstruction
```
Indications:
*stool softeners, high-fiber diet
57
Late effects of cancer treatment on hepatic system
```
Fibrosis/ cirrhosis due to:
• Chemotherapy ( mtx, act D, 6-MP, 6-TG)
• Radiation >30 Gy
• Surgery
• Hepatitis B/C infection
```
58
Late effects of cancer treatment on endocrine system
Overt hypothyroidism
- radiation >20 Gy to the neck, cervical spine
- TBI
- partial or total thyroidectomy
can also cause:
Compensated hypothyroidism-Hyperthyroidism
Thyroid nodules
59
Late effects of cancer treatment:
Symptoms of overt hypothyroidism
hoarseness, fatigue, weight gain, cold intolerance, dry brittle hairs, alopecia, constipation, lethargy, pubertal delay,
bradycardia, hypotension
60
Late effects of cancer treatment:
Symptoms of hyperthyroidism
nervousness, tremor, heat intolerance,
weight loss,increased apppetite, insomnia, diarrhea, moist
skin, goiter
61
Neuroendocrine Late effects of cancer treatment
GH deficiency
- Radiation >24 Gy
- Surgery (tumor in region of H-P axis)
Adrenocorticotropic hormone deficiency
- Radiation >40 Gy/ surgery
Thyrotropin-releasing hormone deficiency
- Radiation > 40 Gy
Precocious puberty
- Radiation >20 Gy
Gonadotropin deficiency
- Radiation >40 Gy/ surgery
Hyperprolactinemia
- Radiation >40 Gy/surgery
62
Late effects of cancer treatment: what can cause metabolic syndrome?
- steroids
| - radiation ? >18 Gy
63
Late effects of cancer treatment:
Radiation therapy> 20 Gy :
> soft tissue hypoplasia > asymmetry of muscle mass when compared with the untreated area, decreased range of motion, stiffness, and pain in affected
area > spinal abnormalities: scoliosis, kyphosis, lordosis, decreased sitting height > back pain, hip pain, uneven shoulder height, rib humps or flares, deviation from the vertical curve, gait abnormalities
diminution of bone growth
64
Late effects of cancer treatment: Risk factors for obesity
* Female survivors
* ALL
* CNS radiation
* Steroids
* Cranial irradiation
* Genetic predisposition
* Polimorphism in the leptin receptor gene
* Brain tumors (hypothalamic dysfunction)
65
Late effects of cancer treatment: How might Leuko-encephalopathy present?
History of treatment with MTX, Ara-C, radiation >18 Gy
seizures, neurologic impairment
66
Late effects of cancer treatment: How might CNS focal necrosis present?
History of treatment with MTX,cisplatin, carmustine, radiation >50 Gy
headaches, seizures, papilledema, hemiparesis, speech/learning/memory deficits
67
Late effects of cancer treatment: How might large vessel stroke present?
History of treatment with radiation >50 Gy
headache, seizures, hemiparesis, aphasia, focal neurologic findings
68
Late effects of cancer treatment: How might ototoxicity present?
History of treatment with cisplatin, carboplatin, radiation >35 Gy, surgery
abnormal speech development, hearning
69
Late effects of cancer treatment: How might myelitis present?
History of treatment with radiation >45 Gy, surgery
paresis, spasticity, altered sensation, loss of sphincter control
70
Late effects of cancer treatment on the ears
* Chronic otitis (radiation >35 Gy)
* Sensorineural hearing loss (cisplatin, carboplatin, radiation >40 Gy)
* Decreased production of cerumen (radiation >30 Gy)
* Chondritis ( radiation 50 Gy)
* Chondronecrosis (radiation 60 Gy)
71
Late effects of cancer treatment on the eyes
```
Radiation >50 Gy:
•Decreased tear production
•Lacrimal duct fibrosis
•Ulceration of eyelids
•Conjunctiva: necrosis, scarring
•Thinning of aclera
•Cornea ulceration
•Neovascularization
•keratinization
•Cataract
•Secondary glaucoma
•Iris neovascularization
•Retina: infarction, exudates, hemorrhage, teleangiectasia, neovascularization, macular edema, optic neuropathy
```
72
Late effects of cancer treatment on the dental health
* Xerostomia (decreased salivary gland function) due to radiation >40 gy
* Abnormal tooth and root development due to radiation >10 Gy and chemotherapy
73
Which two veins join to form the right brachiocephalic vein?
Which two veins join to form the left brachiocephalic vein?
right subclavian vein and right internal jugular
§
left internal jugular and left subclavian
74
Indications for non-tunnelled catheter
```
Fluid Therapy,
CVP
Monitoring,
Antibiotics,
Vasoactive
Drugs
```
dwelling time 7 days
75
pros and cons of non-tunnelled catheter
advantages: multiple lumens, easy to insert
disadvantages: short term use
76
pros and cons of skin tunnelled catheter
advantages: Long term Use, Lower infection rates
disadvantages: Surgical Insertion and removal
77
Indications for skin tunneled catheter
Chemotherapy,
Parenteral
Nutrition
dwelling time 6 weeks to years
78
Indications for port as vascular access
long term antibiotics, access in children
dwelling time 3 months to years
79
pros and cons of port as vascular access
Advantages: Cosmetic benefit, Low maintenance
Low infection rates
Disadvantages: Surgical incision and
removal; less suitable for frequent continous access
80
pros and cons of apheresis (non-tunneled) as vascular access
Advantages: Permits high blood flow rates for
extracorporeal circuits
Disadvantages: Large bore, requires flushing with
higher strength Heparin, Surgical incision and removal
81
pros and cons of PICC line for vascular access
Advantages: Easy to insert and remove and gen ward
Disadvantages: Higher thrombosis
rate particularly in poly urethrane catheter
82
pros and cons of midline for vascular access
Advantages: Easy to insert and remove in gen ward
Disadvantages: Higher thrombosis rate
83
Indication for apheresis (non-tunneled) as vascular access
Dialysis, apheresis, rapid volume transfusion
10- 20 days to months - years
84
Indication for PICC line
Medium term access for drugs, IV fluids and chemotherapy
Up to 12 months
85
Indication for midline vascular access
Antibiotics, Analgesia, Fluid Therapy
4 weeks
86
Common Complications of vascular lines
Catheter-Related Sepsis
Catheter-Related Thrombosis
Mechanical Phlebitis
Extravasation Injury
87
What is Radiotherapy ?
Radiotherapy uses high-energy rays to treat diseases Photons (x-rays)
Electrons
Particle therapy eg protons
88
Name three broad types of radiotherapy
External Beam Radiotherapy
Brachytherapy
Radioisotope Therapy
89
How does radiotherapy work?
DNA damage Single strand breaks Double strand breaks Free radicals
External Beam Radiotherapy
Patients do not become radioactive
90
Whats are the aims of radiotherapy?
Radical Radiotherapy: Cure Radical Radiotherapy
Radical Chemoradiotheapry Combined with molecular treatments
Adjuvant / Neoadjuvant Radiotherapy: Part of a curative treatment Adjuvant Radiothearpy: eg Breast cancer
Neo-Adjuvant Radiotherapy: eg Rectal Cancer
Palliative: Aiming to control symptoms
eg. pain, haemoptysis, emergency treatment of spinal cord compression
91
Which cancers can be cured with radiotherapy?
```
Radical Radiotherapy
Head and Neck Cancers
Lung
Oesophageal
Skin
Prostate
Anal Cancers
```
Adjuvant / Neoadjuvant
Breast
Rectum
92
What does GTV stand for regarding radiotherapy?
Gross Tumour Volume
| Visible, palpable or demonstrable extent of tumour
93
What does CTV stand for regarding radiotherapy?
CTV: Clinical Target Volume GTV + margin for sub-clinical spread
94
What does ITV stand for regarding radiotherapy?
ITV: Internal Target Volume
| Takes variation of CTV in position, shape and size.
95
Side Effects of radiotherapy (divide into acute and late)
```
Acute
Tiredness
Skin changes
Site specific
eg. Lung: cough, breathlessness
eg. Prostate: bladder irritation, discomfort on defecation eg. Breast: breast oedema, skin redness, cough
Late
Site specific
Scarring of surrounding tissues
eg Lung: lung fibrosis / breathlessness
eg. Skin/breast: skin changes / telangectasia eg. Children / young adults: second malignancies
Side Effects
```
