Quiz
ON15,16,17 Supportive care
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Perguntas do quiz (47)
1Mucositis = Painful inflammation and [blank_start]ulceration[blank_end] of the mucous membranes lining the digestive tract (especially [blank_start]mouth and throat[blank_end]). [blank_start]40-75[blank_end]% of all CT patients will experience mucositis. It can lead to infections, [blank_start]nutritional[blank_end] disorders, severe pain, compromised airway, tissue necrosis, and significant [blank_start]bleeding[blank_end].
Usually begins to manifest 5-7 days after CT (typically [blank_start]2-3 weeks[blank_end]).
Risk factors include:
- High-dose CT with alkylating agents (eg [blank_start]cyclophosphamide[blank_end]) or topoisomerase II inhibitors (eg [blank_start]doxorubicin[blank_end])
- Pre-existing oral lesions/infections, poor dental [blank_start]hygiene[blank_end]/dentures
- [blank_start]White[blank_end] ethnicity
- [blank_start]Smoking, alcohol consumption,[blank_end] malnutrition- Aulceration
- Bmouth and throat
- C40-75
- Dnutritional
- Ebleeding
- F2-3 weeks
- Gcyclophosphamide
- Hdoxorubicin
- Ihygiene
- JWhite
- KSmoking, alcohol consumption,
2Mucositis prevention:
Remove risk factors (e.g. [blank_start]dental[blank_end] therapy)
Drink adequate [blank_start]water[blank_end]
Cryotherapy ([blank_start]ice chips swishing for 30 min[blank_end] before bolus CT; not oxaliplatin)
[blank_start]Saline and bicarbonate[blank_end] mouth rinse
Treatment
Routine mouth care
Analgesia (topical [blank_start]lidocaine[blank_end], topical morphine, oral morphine if [blank_start]severe[blank_end])
[blank_start]Magic mouth wash [blank_end]
Saliva substitutes - Adental
- Bwater
- Cice chips swishing for 30 min
- DSaline and bicarbonate
- Elidocaine
- Fsevere
- GMagic mouth wash
3Diarrhoea:
Caused by direct toxicity to the [blank_start]epithelial[blank_end] cells leading to inflammation with [blank_start]prostaglandin[blank_end] release .
Most common with [blank_start]5-FU, capecitabine, irinotecan,[blank_end] EGFR inhibitors.
Tx:
[blank_start]Loperamide 4mg[blank_end] orally, then [blank_start]2mg every 2 hours[blank_end] until diarrhoea free
[blank_start]Octreotide[blank_end] – for patients not responding to loperamide
NOTE Anti-diarrhoeals should [blank_start]not[blank_end] be used in patients with suspected [blank_start]C. Diff[blank_end] and do not forget importance of [blank_start]diet and hydration[blank_end]
Constipation:
Affects 50-70% of patients on chemotherapy
Can lead to anorexia, nausea, vomiting, abdominal pain, bowel [blank_start]obstruction and perforation [blank_end]
Risk medications: [blank_start]Vinca alkaloids, opioids, antiemetics[blank_end] (ondansetron)
Treatment: Stool softener, stimulants, fleet enema, manual or surgical evacuation, hydration - Aepithelial
- Bprostaglandin
- C5-FU, capecitabine, irinotecan,
- DLoperamide 4mg
- E2mg every 2 hours
- FOctreotide
- Gnot
- HC. Diff
- Idiet and hydration
- Jobstruction and perforation
- KVinca alkaloids, opioids, antiemetics
4Hypersensitivity reactions can cause acute [blank_start]dyspnoea[blank_end], pruritic [blank_start]rash[blank_end], fever, nausea/vomiting, rigors, flushing, [blank_start]brady[blank_end]cardia, [blank_start]hypo[blank_end]tension, angioedema. These are severe in <[blank_start]5%[blank_end] of patients.
Causes:
Taxanes - [blank_start]2nd/3rd[blank_end] exposure, [blank_start]fast[blank_end] onset, premedicate with [blank_start]H1 and H2 antagonists and steroids[blank_end]
[blank_start]L-asparaginase[blank_end] (first dose requires test dose, IM less frequent)
Monocolonal antibodies (pre-medicate with [blank_start]paracetamol, antihistamines and steroids[blank_end]) - If severe, stop or interrupt infusion and give fluids and [blank_start]adrenaline[blank_end].- Adyspnoea
- Brash
- Cbrady
- Dhypo
- E5%
- F2nd/3rd
- Gfast
- HH1 and H2 antagonists and steroids
- IL-asparaginase
- Jparacetamol, antihistamines and steroids
- Kadrenaline
5Photosensitivity is a dermotological toxicity causes by some medicines. Wear sunscreen, cover up, avoid sunbeds. Which medicines can cause this?
- A5-FU, MTX, Vinblastine
- B5-FU, MTX, Vincristine
- CCapecitabine, MTX, Prednisolone
- DCapecitabine, MTX, Paclitaxel
6Alopecia
- occurs 1-2 [blank_start]weeks[blank_end] post-chemotherapy
- reversible (1-2 [blank_start]months[blank_end] after cessation of therapy)
- [blank_start]taxanes[blank_end] cause total body alopecia (axillary and pubic hair, eyebrows and eye lashes)- Aweeks
- Bmonths
- Ctaxanes
7Hand-Foot Syndrome (palmer-plantar/acral erythema):
- Tender erythematous skin on palms of hands and sometimes soles of feet
- Causes: [blank_start]5-FU, capecitabine,[blank_end] liposomal [blank_start]doxorubicin[blank_end], high dose cytarabine
Treatment: drug cessation and symptomatic treatment ([blank_start]10% urea[blank_end] emollient, analgesia, [blank_start]cold[blank_end] compress, topical [blank_start]corticosteroids[blank_end]- A5-FU, capecitabine,
- Bdoxorubicin
- C10% urea
- Dcold
- Ecorticosteroids
8Extravasation
With an irritant drug: [blank_start]Short[blank_end]-term injury. No necrosis. May induce [blank_start]local[blank_end] inflammatory reaction. Blood [blank_start]return[blank_end] remains intact.
With a vesicant drug: Hardening, burning, can lead to tissue [blank_start]necrosis[blank_end]. DNA binding or DNA non-binding. DNA [blank_start]binding[blank_end] may affect underlying ligaments, nerves, and bone.
[blank_start]Anthracyclines[blank_end] (vesicant) cause the most severe extravasation.
Treatment:
Stop [blank_start]infusion[blank_end], Leave [blank_start]venous[blank_end] access, Aspirate, Plan
Anthracyclines: [blank_start]cold[blank_end] compresses
Vinca alkaloids: [blank_start]warm[blank_end] compresses
Antidotes: Dexrazoxane or [blank_start]dimethyl sulfoxide[blank_end] topical solution for anthracycline extravasation; [blank_start]hyalurinodase[blank_end] for vinka alkaloids- AShort
- Blocal
- Creturn
- Dnecrosis
- Ebinding
- FAnthracyclines
- Ginfusion
- Hvenous
- Icold
- Jwarm
- Kdimethyl sulfoxide
- Lhyaluronidase
9Tumour Lysis syndrome: lysis of large numbers of cancer cells.
Metabolic abnormalities: hyperuricaemia, hyperkalaemia, hyperphosphataemia, secondary hypocalcaemia and uraemia (increased [blank_start]uric acid, potassium, phosphate[blank_end], decreased [blank_start]calcium[blank_end])
Symptoms: nausea and [blank_start]vomiting[blank_end], diarrhoea, anorexia, lethargy, oedema, fluid overload, [blank_start]congestive[blank_end] heart failure, haematuria, cardiac [blank_start]dysrrhythmia[blank_end], seizures, muscle cramps, tetany, syncope.
More common on the [blank_start]first[blank_end] cycle of treatment.
Risk factors: high tumour cell proliferation [blank_start]rate[blank_end], bulky disease (greater than [blank_start]10[blank_end] cm), chemosensitive malignancies*, high intensity or highly [blank_start]potent[blank_end] therapy, novel or targeted therapy.
*Malignancies associated with a higher risk: [blank_start]Non-Hodgkin's[blank_end] lymphoma, Burkitt's lymphoma, [blank_start]acute[blank_end] lymphoblastic leukaemia and acute myeloid [blank_start]leukaemia[blank_end], and occasionally those with solid tumours.
Additional risk factors: [blank_start]renal[blank_end] insufficiency or renal failure, dehydration, decreased [blank_start]urinary[blank_end] flow, pre-existing uraemia or hyperuricaemia, pre-existing hyperphosphataemia.
Prophylaxis in intermediate or high risk: Vigorous [blank_start]IV[blank_end] hydration, [blank_start]allopurinol[blank_end], [blank_start]rasburicase[blank_end] (n those who do not adequately respond to hydration and allopurinol)- Auric acid, potassium, phosphate
- Bcalcium
- Cvomiting
- Dcongestive
- Edysrrhythmia
- Ffirst
- Grate
- H10
- Ipotent
- JNon-Hodgkin's
- Kacute
- Lleukaemia
- Mrenal
- Nurinary
- OIV
- Prasburicase
- Qallopurinol
10Ocular toxicity
- with [blank_start]Cytarabine[blank_end]-HiDAC
- excessive tearing, pain, photophobia, presence of foreign body,
- prevention: [blank_start]artificial[blank_end] tears, [blank_start]topical[blank_end] corticosteroids
Treatment: [blank_start]D/C[blank_end] cytarabine and administer topical corticosteroids
Otological toxicity
- w/ [blank_start]Cisplatin[blank_end]
- Damage to [blank_start]inner ear[blank_end]
- [blank_start]Cumulative and irreversible[blank_end] side effect
- When detected, replace with [blank_start]carboplatin[blank_end] if appropriate
- [blank_start]Monitor[blank_end] auditory function- ACytarabine
- Bartificial
- Ctopical
- DStop
- ECisplatin
- Finner ear
- GCumulative and irreversible
- Hcarboplatin
- IMonitor
11Nephrotoxicity
- w/ [blank_start]Cisplatin[blank_end]
- Dose [blank_start]limiting[blank_end]
- Risk with [blank_start]higher[blank_end] doses, [blank_start]previous[blank_end] exposure, pre-existing [blank_start]kidney[blank_end] damage, use of other nephrotoxic agents
- [blank_start]25-40[blank_end]% incidence
- Manifests as increases in [blank_start]serum creatinine[blank_end], decreased [blank_start]urine[blank_end] output, [blank_start]hypo[blank_end]kalemia, hypomagnesemia, hyponatremia
- Prevention: [blank_start]lower[blank_end] doses, sub with [blank_start]carboplatin[blank_end], aggressive [blank_start]hydration[blank_end], magnesium, ?mannitol
- Monitor: [blank_start]fluid[blank_end] balance, weight, assess for signs/symptoms of fluid overload
- Treatment: [blank_start]Stop[blank_end] cisplatin, replenish electrolytes – revising ARF in 310- ACisplatin
- Blimiting
- Chigher
- Dprevious
- Ekidney
- F25-40
- Gserum creatinine
- Hurine
- Ihypo
- Jlower
- Kcarboplatin
- Lhydration
- Mfluid
- NStop
12Which of these is NOT a risk factor for chemo induced nausea and vomiting?
- AFemale
- B<50
- CHaving morning sickness in pregnancy
- DEver having motion sickness
- ENon-drinker or light drinker
- FPrevious chemo
- G>50
13Types of Nausea/Vomiting
Acute (up to 24h after CT; peak [blank_start]5-6[blank_end] hours)
Delayed (starts [blank_start]>24h[blank_end] after CT to [blank_start]7[blank_end] days)
Anticipatory (begins as next [blank_start]dose/cycle[blank_end] becomes closer)
Breakthrough (happens despite [blank_start]treatment/prevention[blank_end])
Refractory (prevention/treatment does [blank_start]not[blank_end] work)
If not managed appropriately:
Serious [blank_start]metabolic[blank_end] imbalance, de[blank_start]hydration[blank_end], anorexia
Deterioration in physical and mental status, [blank_start]treatment[blank_end] withdrawal- A5-6
- B>24h
- C7
- Ddose/cycle
- Etreatment/prevention
- Fnot
- Gmetabolic
- Htreatment
- Ihydration
14Classiciation of treatment emetogenic risk:
Minimal (<10%)
Low (10-30%) [[blank_start]5-FU, capecitabine[blank_end]]
Moderate (30-90%) [[blank_start]taxanes, doxorubicin[blank_end]]
High (>90%) [[blank_start]cisplatin[blank_end]]
Optimal emetic control in the [blank_start]acute[blank_end] phase (the first 24 hours) is essential to [blank_start]prevent[blank_end] nausea and vomiting in the [blank_start]delayed[blank_end] phase (24 to 72 hours post chemotherapy).- A5-FU, capecitabine
- Btaxanes, doxorubicin
- Ccisplatin
- Dacute
- Eprevent
- Fdelayed
15Drug: Aprepitant
Class: [blank_start]Neurokinin[blank_end] receptor [blank_start]antagonist[blank_end]
Indicated for prevention of N/V in [blank_start]high and moderate[blank_end] emetogenic chemotherapy. [blank_start]CYP3A4[blank_end] inhibitor. Always used in [blank_start]combination[blank_end].- ANeurokinin
- Bantagonist
- Chigh and moderate
- DCYP3A4
- Ecombination
16Prophylaxis and Treatment:
- High emetogenic potential: use [blank_start]Ondansetron (q8h)[blank_end] + [blank_start]Dexamethasone[blank_end] (q12h) + [blank_start]Aprepitant[blank_end]
- Moderate emetogenic potential: [blank_start]Ondansetron (q12h)[blank_end] + Dexamethasone [blank_start](q12h) [blank_end]
- Low emetogenic potential: [blank_start]Ondansetron stat[blank_end] dose or [blank_start]metoclopramide before[blank_end]
- Minimal emetogenic potential: None but can use as needed (dexamethasone or metoclopramide or prochlorperazine)- AOndansetron (q8h)
- BAprepitant
- COndansetron (q12h)
- DDexamethasone
- E(q12h)
- FOndansetron stat
- Gmetoclopramide before
17Anaemia is a lack of red blood cells/haemoglobin.
- AVerdadeiro
- BFalso
18Which of these is NOT a cause of anaemia?
- ABlood loss
- BMissing vitamins or minerals, eg iron
- CMajor organ problems
- DChronic kidney disease
- ERed blood cells destroyed faster than they can be made (haemolytic)
- FCancer and cancer treatment
- GChronic liver disease
19Anaemia in cancer can be caused by a number of different mechanisms:
The cancer:
- Cancer [blank_start]competes[blank_end] with the marrow’s function and interferes with normal red blood cell production (e.g. leukaemia)
- Cancers of the gastrointestinal system (colon and stomach cancers) or fast growing tumours may cause frequent [blank_start]bleeding[blank_end]
- Triggered immune response with the release of various [blank_start]cytokines[blank_end] that interfere with bone marrow function and [blank_start]shorten[blank_end] red cell survival
- Cancer cells release cytokines that can lead to iron [blank_start]sequestration[blank_end], reducing the production of red blood cells (RBCs)
The treatment
- Chemotherapy agents target rapidly dividing cells- Acompetes
- Bbleeding
- Ccytokines
- Dshorten
- Esequestration
20Which of these is NOT a cancer-specific risk factor for anaemia?
- APlatinum-based chemotherapy
- BPre-existing low haemoglobin level before cancer diagnosis
- CCancers that involve the marrow space (leukaemia or lymphoma)
- DRisk of tumour bleeding
- ECertain types of tumors (e.g. ovary)
- FAlkylating agent chemotherapy
21Select ALL the signs of anaemia.
- AChest pain
- BPale skin, nail beds, mouth, gums
- CSwelling in hands/feet
- DFatigue
- ETachycardia
- FShortness of breath
- GDizziness
- HGroin pain
- IBradycardia
- JSwelling of nodes
22Terminologies:
Ferritin – amount of iron [blank_start]stored[blank_end] in body (iron storage [blank_start]protein[blank_end] that keeps iron in a soluble and non-toxic form)
Transferrin or total iron [blank_start]binding[blank_end] capacity - a measure of the [blank_start]maximum[blank_end] amount of iron the blood can carry
Haemoglobin – oxygen carrying structures
Haematocrit – volume % of [blank_start]red blood[blank_end] cells in blood
Mean Corpuscular Volume/Mean Cell Volume (MCV) – ‘[blank_start]size[blank_end]’ of red blood cells
Reticulocyte count - measure the level of reticulocytes in your blood- Astored
- Bprotein
- Cbinding
- Dmaximum
- Ered blood
- Fsize
23The MCV is used to categorise anaemia.
Microcytic anaemia – MCV < [blank_start]80 fL[blank_end]
Normocytic anaemia – MCV [blank_start]80 – 95 fL[blank_end]
Macrocytic anaemia – MCV > [blank_start]95 – 100 fL[blank_end]
(Some references define macrocytic anaemia as > 100 fL.)
- A80 fL
- B80 – 95 fL
- C95 – 100 fL
24High MCV – Macrocytic Anaemia / Megaloblastic anaemia.
- Vitamin [blank_start]B12[blank_end] (dietary or pernicious anaemia) or [blank_start]Folate[blank_end] deficiency
- Both are required for [blank_start]DNA[blank_end] synthesis and so deficiency results in symptoms occurring in rapidly dividing tissues ([blank_start]bone marrow, GI[blank_end])
- Usually deficiency from [blank_start]dietary[blank_end] sources (vegetarians, poor nutrition)
- Treatment: supplementation (oral or injections if poor absorption):
[blank_start]IM[blank_end] injection of vitamin B12 (hydroxocobalamin) – 1mg [blank_start]three[blank_end] times weekly x 2 weeks, then 1mg every 3 [blank_start]months[blank_end]
Oral folic acid – [blank_start]5mg daily[blank_end] for 4 months (may then use as prophylaxis)- AB12
- BFolate
- CDNA
- Dbone marrow, GI
- Edietary
- FIM
- Gthree
- Hmonths
- I5mg daily
25Normal MCV – Normocytic anaemia:
High reticulocyte count suggests [blank_start]ongoing[blank_end] blood loss – acute blood loss, haemolysis. Low reticulocyte count suggests body is unable to [blank_start]produce[blank_end] RBCs at a healthy rate.
Low WBCs and platelets – [blank_start]leukemia, aplastic anaemia[blank_end]
Normal or high WBCs/platelets – [blank_start]chronic[blank_end] conditions (progress to microcytic as disease progresses), [blank_start]malignancy[blank_end]
- Treatment: Transfusion, [blank_start]erythropoiesis[blank_end]-stimulating agents - Aongoing
- Bproduce
- Cleukemia, aplastic anaemia
- Dchronic
- Emalignancy
- Ferythropoiesis
26Blood transfusions:
- Raises [blank_start]haemoglobin[blank_end] quickly to improve symptoms and ensure adequate oxygen delivery
- Most commonly administered if haemoglobin is <[blank_start]80 g/L[blank_end]
- Need to match blood type
- Risks:
Transfusion related [blank_start]lung[blank_end] injury
Very low risk of viral contamination (Hep B, C, HIV)- Ahaemoglobin
- B80 g/L
- Clung
27Erythropoiesis-stimulating agents:
1. Epoetin alfa (recombinant [blank_start]human[blank_end] erythropoietin)
- Stimulate erythropoiesis by binding to [blank_start]erythroid precursor cell receptors[blank_end], stimulating differentiation and proliferation
- Stimulate release of [blank_start]reticulocytes[blank_end] from bone marrow
- Increase synthesis of cellular [blank_start]haemoglobin[blank_end] – need adequate iron stores
- Contraindicated: uncontrolled [blank_start]hypertension[blank_end], unable to receive thromboprophylaxis
- Adverse effects: hypertension, GI [blank_start]intolerance[blank_end], headache, influenza symptoms, very rarely cause [blank_start]red cell aplasia, skin reactions [blank_end]- Ahuman
- Berythroid precursor cell receptors
- Creticulocytes
- Dhaemoglobin
- Ehypertension
- Fintolerance
- Gred cell aplasia, skin reactions
28Low MCV - Microcytic Anaemia:
Cell size is decreased due to reduced [blank_start]haemoglobin[blank_end]; either less haem (i.e. iron) or an imbalance in [blank_start]globin chain[blank_end] synthesis (in genetic disorders which alter globin production)
The main causes:
- Low ferritin = [blank_start]Iron[blank_end] deficiency (blood loss, dietary deficiency, occasionally malabsorption)
- Normal or high ferritin =
TIBC low: Anaemia of [blank_start]chronic[blank_end] disease (also associated with normocytic anaemia)
OR TIBC normal or high: [blank_start]Haemoglobinopathies[blank_end] (e.g. thalassaemia), lead intoxication, sideroblastic anaemias (rare [blank_start]genetic[blank_end] or acquired disorders)
- In a primary care setting in New Zealand, [blank_start]iron deficiency and chronic disease[blank_end] will be the most likely causes of microcytic anaemia.- Ahaemoglobin
- Bglobin chain
- CIron
- Dchronic
- EHaemoglobinopathies
- Fgenetic
- Giron deficiency and chronic disease
29In cancer patients, iron deficiency is usually due to nutritional deficiencies - poor oral intake, chemotherapy-induced nausea/vomiting.
- AVerdadeiro
- BFalso
30Which of these is NOT an iron rich food?
- AMeat and fish
- BSweet potatoes
- CDark green, leafy vegetables
- DYogurt
31What dose of elemental iron should deficient patients receive daily?
- A100-200mg
- B50-100mg
- C200-400mg
32Patient education points for iron salts:
More effective if taken on [blank_start]empty[blank_end] stomach
Can take with food if causes stomach upset
May discolor stools ([blank_start]dark/black[blank_end])
Do not take with [blank_start]antacids or calcium[blank_end]
May need to space from certain medications
Vitamin C (orange juice) may increase iron absorption (myth?)
[blank_start]Constipation[blank_end] common- Aempty
- Bdark/black
- Cantacids or calcium
- DConstipation
33Aplastic anaemia:
- Non-[blank_start]malignant[blank_end] condition where the bone marrow fails to produce enough blood cells
- Exposes patients to [blank_start]anaemia[blank_end] (RBC), [blank_start]infections[blank_end] (WBC), [blank_start]bleeding[blank_end] (platelets)
- Can occur at any time but usually associated with [blank_start]bone marrow[blank_end] damage
- From:
Chemotherapy, antibiotics, [blank_start]propylthiouracil, phenytoin, quinine[blank_end]
Exposure to certain chemicals such as benzene
Radiation exposure
Viruses- Amalignant
- Banaemia
- Cinfections
- Dbleeding
- Ebone marrow
- Fpropylthiouracil, phenytoin, quinine
34Which of these is not an appropriate treatment for aplastic anaemia?
- ABlood transfusions
- BStem cell transplant
- CImmunosuppressants (cyclosporine, anti-thymocyte globulin)
- DBone marrow stimulants eg Epoetin alfa
- EIron salts
35Cancer pain epidemiology:
- Up to [blank_start]70-80[blank_end]% of patients with advanced cancer in NZ have pain
- Patients managed by oncologists (during active treatment), [blank_start]palliative[blank_end] services, [blank_start]hospices[blank_end], and GPs (advanced cancer)
- Commonly the [blank_start]most[blank_end] troublesome symptom of cancer that negatively influences quality of life
- Major [blank_start]economic[blank_end] impact by loss of productivity and caregiver burdens
- One of the most [blank_start]difficult[blank_end] conditions to treat - A70-80
- Bpalliative
- Chospices
- Dmost
- Eeconomic
- Fdifficult
36Types of cancer pain:
- Acute vs. chronic pain
- Nerve pain – [blank_start]pressure[blank_end] on nerves or spinal cord (i.e. neuropathic)
- Bone pain – [blank_start]damage[blank_end] to bone tissue (e.g. metastases)
- Soft tissue or visceral pain – [blank_start]body organ or muscle[blank_end] (e.g. back pain due to kidney)
Phantom pain – pain in a body part/area that has been removed
Referred pain – pain from an organ in the body in a [blank_start]different place [blank_end]- Apressure
- Bdamage
- Cbody organ or muscle
- Ddifferent place
37Which of thesensigns/symptoms could you observe in a sedated patient unable to communicate, that would NOT indicate pain?
- ADiaphoresis (sweating)
- BGrimacing on movement
- CTachycardia
- DPupil dilation
38WHO Cancer Pain Ladder:
Step 1 = [blank_start]Non-opioid[blank_end] +/- adjuvant
Step 2 = Opioid for [blank_start]mild-mod pain[blank_end] +/- non-opioid +/- adjuvant
Step 3 = Opioid for [blank_start]severe pain[blank_end] +/- non-opioid +/- adjuvant
[blank_start]Codeine, Dihydrocodeine[blank_end] - mild, mod
[blank_start]Morphine, Fentanyl[blank_end] - mod, strong
Adjuvants:
[blank_start]Anxiety[blank_end] medications
[blank_start]Antidepressants[blank_end]
Topical medications- ANon-opioid
- Bmild-mod pain
- Csevere pain
- DCodeine, Dihydrocodeine
- EMorphine, Fentanyl
- FAnxiety
- GAntidepressants
39Treating neuropathic pain:
- Antidepressants, anticonvulsants
- Start at [blank_start]low[blank_end] doses and increase as necessary to usual or maximum recommended doses
- Requires at least [blank_start]2 week[blank_end] trial at an adequate target [blank_start]dose[blank_end]
- Requires continual reassessment and monitoring
- Patient should be educated about [blank_start]INDICATION[blank_end], as may be concerned about stigma with antidepressants or anticonvulsants
- If pain not controlled, [blank_start]opioids[blank_end] may be trialed- Alow
- B2 week
- Cdose
- Dindication
- Eopioids
40People with cancer in the bone have abnormally high levels of [blank_start]osteoclasts[blank_end], causing fractures, bone pain, osteoporosis, and hypercalcaemia.
[blank_start]Bisphosphonates[blank_end] (zoledronate or pamidronate) reduce [blank_start]activity[blank_end] of osteoclasts – strengthen bone, reduce pain, treat hypercalcaemia.
Side effects include [blank_start]headaches, nausea, and flu-like[blank_end] symptoms, which usually subside within [blank_start]48[blank_end] hours of the infusion (treat with paracetamol).
Nephrotoxicity risk: adequate [blank_start]hydration[blank_end] can enhance renal protection., may be contraindicated in [blank_start]renal[blank_end] failure.- Aosteoclasts
- BBisphosphonates
- Cactivity
- D48
- Eheadaches, nausea, and flu-like
- Fhydration
- Grenal
41Severe pain may require rapid escalation of parenteral opioid therapy until pain is partially relieved.
Moderate pain: total daily dose (TTD) increased [blank_start]25-50[blank_end]% OR add the amount taken [blank_start]as needed[blank_end] the previous day
Reducing by 25-50% in patients who have pain control but experiencing [blank_start]adverse effects[blank_end] is also an option.
Patients with cancer pain will likely need medication long-term or indefinitely. Long-acting products are more convenient; switch after at least [blank_start]48 hours[blank_end] of short-acting opioid so pain is well controlled. First dose of the modified-release preparation is given [blank_start]with, or within 4 hours of[blank_end] the last dose of the immediate-release preparation, to allow time to be effective.- A25-50
- Bas needed
- Cadverse effects
- D48 hours
- Ewith, or within 4 hours of
42To switch from regular acting to long acting:
1. Add up [blank_start]total daily dose[blank_end] of morphine equivalents
2. Decrease by [blank_start]25% [blank_end]
3. Split into required [blank_start]number[blank_end] of long-acting doses
Example: TTD = 130mg morphine x [blank_start]0.75[blank_end] = 97.5mg
/ 2 doses = 50mg every 12 hours long-acting product - Atotal daily dose
- B25%
- Cnumber
- D0.75
43Fentanyl patches:
- Less [blank_start]constipation[blank_end] compared to morphine. It is favourable in the presence of [blank_start]renal[blank_end] impairment
- Starting doses of [blank_start]12.5-25 mcg/h[blank_end] first option for moderate to severe pain
- Usually dosed every [blank_start]72[blank_end] hours but can be increased to every 48 hours
- Start low and go slow (increase dose every 48-72 hours)
- Patient should be on regular morphine prior to patch initiation
When initiating, put on at [blank_start]same[blank_end] time you give last dose of regular morphine
Example: Patient receiving 60mg morphing SR – give last dose of 60mg at same time you put first patch on- Aconstipation
- Brenal
- C12.5-25 mcg/h
- D72
- Esame
44Oxycodone:
- Bi-phasic modified-release tablets for [blank_start]12-hourly[blank_end] administration
- Release [blank_start]40[blank_end]% of drug within 1 hour for most patients and the remaining [blank_start]60[blank_end]% of drug by controlled-release
- The immediate-release and modified-release formulations have [blank_start]similar sounding names[blank_end]! care.
- Usually reserved for patients in whom [blank_start]morphine[blank_end] is not effective at optimal doses, not tolerated, or if morphine is contra-indicated- A12-hourly
- B40
- C60
- Dsimilar sounding names
- Emorphine
45Methadone
- Well tolerated in [blank_start]severe[blank_end] renal impairment. May be effective when there is [blank_start]neuropathic[blank_end] pain because of its [blank_start]NMDA[blank_end] receptor activity.
- Long and widely variable [blank_start]half-life[blank_end]
- Less associated [blank_start]drowsiness, nausea, and constipation.[blank_end]
- Oral dosing is usually [blank_start]2.5-5 mg twice daily[blank_end] initially with [blank_start]weekly[blank_end] dose increases (due to its long half-life and risk of accumulation)
Drowsiness and [blank_start]respiratory[blank_end] depression may develop after several days/weeks on a steady dose.
Has place in palliative care but must be prescribed by experienced practitioner.- Asevere
- Bneuropathic
- CNMDA
- Dhalf-life
- Edrowsiness, nausea, and constipation.
- F2.5-5 mg twice daily
- Gweekly
- Hrespiratory
46Breakthrough dosing:
- [blank_start]10-15%[blank_end] of total daily dose (TTD)
- can be given [blank_start]30 minutes before[blank_end] an activity that causes [blank_start]predictable[blank_end] break-through pain such as a wound dressing
- subcut or IV if swallowing is an issue- A10-15%
- B30 minutes before
- Cpredictable
47Oral oxycodone is approximately 1.5–2 times more potent than oral morphine.
- AVerdadeiro
- BFalso
Informações
- Descrição
- O usuário eliminou as informações de disciplina Quiz sobre ON15,16,17 Supportive care, criado por Usuário eliminado em 09-10-2019.
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