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NUTR 424 Cancer > Nutritional Complications of Anti-cancer Therapy (Week 6 Lecture 2) > Flashcards

Nutritional Complications of Anti-cancer Therapy (Week 6 Lecture 2) Flashcards

1
Q

How is nutritional compromise commonly observed in cancer patients?

A
  • weight loss
  • anorexia
  • malabsorption
  • maldistribution of fat and lean body masses, including liver and muscles
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2
Q

What results in nutritional compromise?

A
  • cancer
  • malabsorption
  • surgery
  • radiation
  • systemic therapy
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3
Q

How does cancer result in nutritional compromise?

A
  • Production of inflammatory mediators leading to catabolism of muscles and fat.
  • Decrease in intake due to dysphagia and early satiety.
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4
Q

How does systemic therapy result in nutritional compromise?

A

Classical cytotoxic chemotherapy

Targeted agents to
* Extracellular domain of receptor
* Intracellular kinases
* Other parts of the intracellular domain- allosteric

Immunotherapy:
* Cytokines
* Immune cell: Activator and Anti-suppressors.

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5
Q

What is indirect nutritional complications?

A

Nutritional derangement arising from non-specific side effects of anti-cancer therapy, including:
* Dysgeusia
* Anorexia or early satiety
* Nausea and vomiting
* Mucositis and esophagitis
* Diarrhea
* Malabsorption.
* hyperlipidemia
* hyperglycemia
* hypothyroidism

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6
Q

Grading of toxicity

A

The NCI-CTCAE criteria is a standardized language for grading of toxicity or symptoms from cancer and therapy (universal language). From grade 1-5 i.e. mild to fatal.
* Not all toxicity or symptoms or laboratory finding have all 5 grades.
* If the term is not found, then use grade 1-5 or mild, moderate, severe or fatal.
* Currently, we are using version 5.1.

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7
Q

Describe the complication of dysgeusia?

A

Change in taste, often described by patients as metallic taste Leading to change in what type(s) of food that they will eat.
* A result of decrease in the number of taste buds
* Common side effects of many chemotherapeutic agents.
* Recently, NTRK inhibitors interfere with NTRK2 in central nervous system

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8
Q

Grading for dysgeusia

A
  • 1: altered taste and no change in diet
  • 2: altered taste with change in diet, including oral supplement; noxious or unpleasant taste or loss of taste
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9
Q

Describe the nutritional complications of nausea and vomiting

A
  • Decrease in intake
  • Avoidance to eat.
  • Is a combination of change in smell perception, change in taste perception, activation of the vomiting centre in the brainstem.
  • drugs cause most nausea and vomiting of anything
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10
Q

Grading for nausea

A
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11
Q

Grading for vomiting

A
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12
Q

Nutritional complications of anorexia/ early satiety

A

Feeling full in the stomach earlier than expected, leading to total reduction of food intake or preferential food intake.

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13
Q

Causes of anorexia/ early satiety other than chemotherapy

A
  • Obstruction of gastric outlet or duodenum
  • Inflammatory mediators of cancer
  • Delay in gastric emptying.
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14
Q

Grading for anorexia

A
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15
Q

What is mucositis?

A

Inflammation of the mucous membrane (sores)

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16
Q

Where is mucositis observed?

A

Chemotherapy: up to 40%
* Breast cancer
* Colorectal cancer
* Head and neck cancer

Bone marrow transplantation: up to 75%.

Radiation therapy in
* Head and neck (especially back of mouth)
* Upper esophagus.

Fungal overgrowth by Candidia spp. due to steroids (goes into blood stream)

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17
Q

grading for oral mucositis

A
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18
Q

Describe esophagitis

A

inflammation of esophagus

19
Q

What results in esophagitis?

A
  • Chemotherapy and radiation: direct damage of the mucosa (Esophagus, Lung, Larynx)
  • Fungal infection by Candida spp.
  • Viral infection by CMV, HSV.
  • Reflux due to steroid.
20
Q

Grading for esophagitis

A
21
Q

What results in malabsorption?

A
  • Resection of part of bowels
  • Radiation
  • Chemotherapy
22
Q

resection of bowel parts causing malabsorption

A
  • Gastric resection: decrease in food transit time into small bowel, leading to dumping syndrome, malabsorption and osmotic diarrhea.
  • Small bowel: usually after a large portion resection or damage of the epithelial cells/crypts of Langerhan, leading to malabsorption and osmotic diarrhea. (60-80% substantial problem)
  • Pancreas: Loss of pancreatic enzyme for digestion, thus malabsorption and osmotic diarrhea.
23
Q

Radiation causing malabsorption

A

Mucosal damage leading to a combination of malabsorption and secretory diarrhea.

24
Q

Chemotherapy causing malabsorption

A

Agent dependent; commonly observed in:
* Chemotherapy for colorectal cancer: Irinotecan, oxaliplatin, capecitabine and 5-FU. Leading to inflammation and/ulceration of mucus membrane and secretory diarrhea.
* Novel anti-cancer agents: epidermal growth factor targeting agents and anti-cytotoxic T-lymphocyte antigen antibody (anti- CTLA-4). Secretory diarrhea versus inflammation/ulceration.
* Notch inhibitor: globet cell hypertrophy, leading to secretory diarrhea.

25
Q

Grading for malabsorption

A
26
Q

What results in diarrhea?

A
  • Chemotherapy (irinotecan, 5-FU): Damage of the crypts in the small bowels, leading to secretory diarrhea and decrease in absorption of the electrolytes
  • Immunotherapy and radiation: direct damage to both the crypts and the mucous membrane
  • Targeted agents (EGFR TKI; VEGFR TKI): drug induced dysfunction of the Na/K ATPase of the ion channels, leading to reduction of sodium uptake
27
Q

Grading for diarrhea

A
28
Q

What may result in hyperlipidemia?

A
  • Aromatase inhibitor for treatment of breast cancer: Aromatase is the enzyme for the conversion of androgen to estrodial and estrone in either the ovaries or peripheral fat (2 classes: steroidal and non-steroidal)
  • Bexarotene: a retinoic acid derivative for the treatment of cutaneous T-cell lymphoma leading to rapid and high elevation of TG, VLDL, LDL and total cholesterol by depositing fat in liver so it does not mobilize in blood and other tissue.
  • Alectinib and lorlatinib: ALK inhibitors for NSCLC (non-smoker lung cancer): Mechanism unknown.
  • mTOR inhibitors for RCC causing decrease in LPL leading to hypertriglyceridemia and decrease in LDLr so increase in LDL.
29
Q

Grading for hyperlipidemia

A
30
Q

What results in hypothyroidism?

A
  • Hypothyroidism associated with anti-angiogenic therapy observed as primary hypothyroidism with elevation of TSH and normal to low T3 or T4.
  • Thyroid dysfunction with formation of auto-antibody to thyroid producing cells, leading
    to thyroiditis (more common to be hypo than hyper)and can lead to destruction of the pituitary gland (multiple endocrine organ dysfunction)
31
Q

Grading for hypothyroidism

A
32
Q

What results in hyperglycemia?

A
  • Hyperglycemia due to autoimmune mechanism: destruction of the Islet cells by auto-antibody
  • Altered glucose metabolism
33
Q

What might cause altered glucose metabolism?

A
  • Exaggerated glucose response after glucose administration
  • Decrease in insulin sensitivity via decrease in number and size of Islet cells
  • Decrease in insulin clearance by liver
  • Increase in gluconeogenesis via increase in gluconeogenic gene expressions.
34
Q

Grading for hyperglycemia

A
35
Q

What results in fatty liver?

A

Most common cause of cirrhosis in N. America/W Europe. Observed in 5-FU and irinotecan treated colorectal cancer patients.
* 5-FU: Mitochondrial collapse leading to impairment of oxidation of fatty acids. The reactive oxygen species (ROS) from fatty acid accumulate in hepatocytes.
* irinotecan: Possibly through inhibition of mitochondrial membrane and mitochondrial oxidation and electron transfer along the respiratory chain, resulting in production of ROS.

36
Q

general medical management of nutritional complications

A

Education:
* Patients and family
* Nursing and dietitians
* OURSELVES.

Monitoring:
* General dietary questions
* Physical examination
* Laboratory investigations: Ca, glucose, TSH, albumin
* Scans for sarcopenia.

37
Q

Management of dysgeusia

A
  • No direct medications have been proven useful, but use of lemon juice, zinc supplementation is commonly used.
  • Change of food strategies: Use of blend food, frequent small meals, high protein diet.
38
Q

Management of nausea/ vomiting

A
  • medication for moderate/high
  • medication for low day 1 pre-chemo
39
Q

Management of mucositis & esophagitis

A

Early recognition and intervention with
* Topical anesthetics
* Anti-fungal for suspicious of fungal infection
* keratinocyte growth factor (stimulates skin growth) in bone marrow transplant patients

40
Q

Management of anorexia

A
  • nutritional supplementation: protein intake, EN vs. PN
  • Appetite stimulants: steroid, cannabinoid, anti-depressant
41
Q

Management for hyperlipidemia

A
  • Diet modification as advised by the Canadian Heart Association.
  • Pharmacological intervention: HMG co-A inhibitors
  • Exercise.
42
Q

Management of diarrhea

A

Chemotherapy, radiation or targeted agents:
* Fluid intake
* Diet modification: BRAT diet- banana, rice, apple sauce and bread and avoid greasy and spicy food.
* Pharmaceutical

Immunotherapy related diarrhea/colitis:
* Anti-diarrheal
* Corticosteroid
* if not resolved, GI consult for endoscopy to prove the presence of colitis, then
infliximab

43
Q

Management of hyperthyroidism

A
  • Hypothyroidism by anti-angiogenic therapy
  • Hyperthyroidism: Antithyroid meds, radioactive iodine ablation or surgery.
44
Q

Management of hyperglycemia

A
  • Dietary modification: Avoidance of high glycemic index food
  • Pharmacological intervention: First-Line is metformin, second line other diabetic drugs

NUTR 424 Cancer (19 decks)

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