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Clinical Nutrition 1 > Cancer Pathophysiology and Cachexia > Flashcards

Cancer Pathophysiology and Cachexia Flashcards

1
Q

Primary tumor?

A

First tumour identified, then classified according to size and invasion of the surrounding tissues

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2
Q

Secondary tumors ?

A

Other tumors of the SAME histological origin as the primary tumor (primary has escaped, and has generated another tumor)

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3
Q

Regional lymph nodes?

A

Tumors may progress, malignant cells escape their tumors and release in the blood –> Activate lymph nodes which become activated, enlarged and inflamed

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4
Q

Are are regional lymph nodes classified ?

A

According to distance from primary tumor

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5
Q

Mestastasis?

A

Invasion of cancer into distal tissues and organ

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6
Q

(T/F) If there is a primary tumour in the left lung, and a secondary tumour in the right lung, this is NOT considered metastasis

A

FALSE, although within the same organ, still considered metastasis -> cancer has spread.

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7
Q

Effects of CA in digestive tract?

A

Obstruction (dysphagia, N/V, anorexia, malabsorption)and anemia from occult losses

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8
Q

Effects of CA in lung?

A

Obstructive of resp tract, SOB

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9
Q

Effects of CA in bone?

A

Pain

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10
Q

Effect of CA in gynaecological organs?

A

Intestinal obstruction, ascites, fertility

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11
Q

Diagnosis of cancers?

A
  • Biochemical markers
  • Tumour imaging techniques
  • Invasive techniques
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12
Q

Example of biochemical marker?

A

PCA protein in prostate, allow for early detection

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13
Q

Examples of tumor imaging techniques?

A

MRI, CT, PET, Chest-xray, bone scans, mammographs

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14
Q

MRI?

A

Magnetic resonance imaging

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15
Q

CT?

A

Computed tomography, emits localized radiotherapy

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16
Q

PET?

A

Position emission tomography –> Glucose drink will produce fluorescence, and detect tumours as they avidly consume glucose.

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17
Q

Invasive techniques?

A

Biopsy, cytologic aspiration, laparoscopy

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18
Q

Carcinomas?

A

Epithelial tissue

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19
Q

Sarcomas?

A

Connective Tissue

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20
Q

Lymphomas?

A

Lymphatic system

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21
Q

Gliomas?

A

Glial cells of CNS

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22
Q

Adenocarcinomas?

A

Glands

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23
Q

Leukemias?

A

Bone marrow

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24
Q

For solid tumors, how is staging of cancer assessed?

A

TNM (Tumour-Node-Metastases) system

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25
Q

In the TNM system, how is the primary tumour classified?

A

T - from T1-T4 depending on size

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26
Q

In the TNM system, how are the lymph nodes classified?

A

N - from N0-N3 depending on how many lymph nodes are affected

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27
Q

In the TNM system, how is metastases classifies?

A

M - M0 or M1 (All or nothing)

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28
Q

Stage 0?

A

Carcinoma in situ (very early form)

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29
Q

Stage 1?

A

Localized

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30
Q

Stage II?

A

Early locally advanced

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31
Q

Stage III?

A

Late, locally advanced

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32
Q

Stage IV?

A

Metastasized

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33
Q

T2N0M1?

A

Stage 4 cancer, as there is metastases

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34
Q

6 main anti-cancer treatments?

A

1) Surgical removal
2) Radiotherapy
3) Chemotherapy
4) Biological therapies
5) Hematopoietic stem cell transplants
6) Gene therapies

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35
Q

What is the first choice in curative Tx of cancer? What is it appropriate for?

A
  • Surgical removal
  • May be palliative, meaning that in the case of metastases, will remove a certain tumour but not all
  • Mostly for primary, local (stage I) cancers
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36
Q

Nutritional impact of surgery?

A

If within upper an lower GI –> Impact on feeding routes

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37
Q

Radiotherapy? Which cells are most susceptible?

A

An ionizing TARGETED radiation which will alter DNA to control growth/kill malignant cells
-Highly proliferating cells

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38
Q

is radiotherapy curative? When?

A

For smaller tumors, and may be targeted with other treatments, such as after surgical removal.

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39
Q

Advantages of radiotherapy?

A

Targeted, therefore relatively little damage to the surrounding tumors

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40
Q

Explain the dose/fractionation of radiotherapy

A

We will split up the amount of radiotherapy needed into separate treatments, meaning the side effects will follow the treatment schedule (less chronic)

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41
Q

Discuss the nutritional implications of radiotherapy treatment to head and neck

A
  • Mucositis (inflammation of epithelia of mouth, larynx, esophagus)
  • Dysgeusia
  • Xerostomia (ry mouth)
  • Dysphagia
  • Odynophagia (disturbed smell)
  • Severe esophagitis
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42
Q

Possible nutritional therapy for undergoing radiotherapy treatment to head and neck?

A

High risk of malnutrition, enteral feeding likely

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43
Q

Discuss the nutritional implications of radiotherapy treatment to abdomen and pelvis?

A
  • Severe diarrhea
  • malabsorption
  • Radiation enteritis
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44
Q

Which kind of cells are highly effected in radiotherapy and chemotherapy ?

A

Highly proliferative cells which often cause nutritional consequences (Taste buds, epithelial cells)

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45
Q

What is chemotherapy? is it specific?

A

Cytotoxic drugs, which block DNA and RNA synthesis/cell division at different stages, but NOT specific and will target healthy cells as well

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46
Q

When is chemotherapy often used?

A

Stage 4, metastases

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47
Q

How is chemotherapy usually administered?

A

Orally, IV infusion or intra-muscular injection

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48
Q

Similar to radiotherapy, chemotherapy is administered on a dose/fractionation schedule. Discuss the nutritional implications

A

Patients will experience bouts of side effects, therefore we want to implement nutritional intervention between cycles - preventing malnutrition.Adopt to their chemotherapy schedules

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49
Q

Side effects of chemotherapy?

A

Systemic

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50
Q

What are biological therapies?

A

Will be used to treat the cancer itself, the progression OR side effects

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51
Q

Examples of biological therapies? (3)

A

1) Immunotherapy
2) Biological response modifiers
3) Targeted therapy

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52
Q

Immunotherapy?

A

-Use’s bodies own immune system to eradicate cancer cells –> May also administer cytokines, interferons and interleukins

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53
Q

Biological response modifiers?

A

Will induce apoptosis, growth factor inhibitors, block angiogenesis

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54
Q

Targeted therapy?

A

Monoclonal antibodies that will deliver toxic molecules to the cancer cells (type o immunotherapy)

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55
Q

When is hematopoietic stem cell transplantation used?

A

For blood cancers, uses the transplant of bone marrow from patient or someone else

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56
Q

Risks of hematopoietic stem cell transplantation

A

Rejection of the graft (graft vs. host disease)

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57
Q

What kind of gene therapy is undergoing testing in clinical trials?

A

If we know the genes that the tumours are expressing, we could develop and agent against it –> More customized, less systemic side effects

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58
Q

Examples of chemotherapy drugs (A I-TAA)

A
  • Alkylating agents
  • Indirect DNA agents
  • Topoisomerase inhibitors
  • Anti-tumour antibiotics
  • Antimitotics
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59
Q

Common, systemic side effects of all chemotherapy drugs?

A
  • Bone marrow suppression (less synthesis of WBC and RBC –> Anemia)
  • Alopecia, Anorexia
  • Renal, Cardiac and Hepatic toxicity
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60
Q

Biological and targeted therapy agents side effects?

A

Specific to the agent - but usually more tolerable than chemotherapy, but can still be severe.

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61
Q

Biological and targeted therapy agent examples (CHASMS)?

A
  • Cytokines
  • Hematopoietic growth factors
  • Angiogenesis inhibitors
  • Signal transduction inhibitors
  • Monoclonal AB
  • Selective estrogen receptor modulators
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62
Q

Cytokine, Monoclonal AB and Hematopoietic SE?

A

Flu-like symptoms, allergic rxn, low blood counts, organ damage

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63
Q

Angiogenesis inhibitor SE?

A

Dysgeusia, anorexia, diarrhea, weakness

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64
Q

Signal transduction inhibitor SE?

A

Anorexia, weight-loss, swelling

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65
Q

Selective estrogen receptor modulator SE?

A

Hot flashes, sweats

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66
Q

Effect of upper resp/digestive tract tumour?

A

Obstruction, dysphagia

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67
Q

Surgery effects of upper resp/digestive tract tumour?

A

Mastication and deglutition (swallowing) problems

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68
Q

Radiotherapy effect of upper resp/digestive tract tumour?

A

Dysgeusia, xerostomia, pain

69
Q

What can exacerbate side effects of treatment of upper resp/digestive tract tumour?

A

Combination of tobacco, alcohol abuse and poor nutritional status w/ chemo Tx.

70
Q

Nutritional intervention in upper resp/digestive tract tumour?

A

Enteral nutrition, sometimes permanent

71
Q

Effect of esophagus tumour?

A

Obstruction, dysphagia, anorexia, anemia from occult losses

72
Q

Surgery effect of esophagus tumour?

A

Early satiety, regurgitation, gastricstasis

73
Q

Radiotherapy effect of esophagus tumour?

A

Esophagitis –> makes it hard to eat, dysphagia, odynophagia, fibrosis

74
Q

Nutritional intervention of esophagus tumour?

A

Enteral nutrition

75
Q

Effect of stomach tumour?

A

Obstruction, anorexia, anemia, water and electrolyte imbalances

76
Q

Surgery effect of stomach tumour?

A

Early satiety, achlorydia, dumping syndrome, loss of intrinsic factor

77
Q

Aclorydia?

A

When stomach surgery removes certain parts of the stomach, could affect pH, digestion an promote bacterial growth

78
Q

Dumping syndrome?

A

Surgery to stomach- rapid passage of food into SI, creates acute hyperG, weakness, hot flashes and diarrhea

79
Q

Radiotherapy effect of stomach tumour?

A

Fibrosis, ulcers

80
Q

Nutritional intervention of stomach tumour?

A

Enteral nutrition by jujunostomia after Tx (bypassing the mouth)

81
Q

Effect of pancreas, biliary tract tumour?

A

Weight loss, abdominal pain, anorexia, malabsorption, secondary diabetes

82
Q

Surgery effect of pancreas, biliary tract tumour?

A

Pancreaticoduodenectomy, pancreatic insufficiency (Depending on location of cancer in pancreas, may have to remove large amounts, difficult surgery)

83
Q

Effect of liver tumour?

A

Weight loss is frequency, anorexia

84
Q

Surgery effect of liver tumour?

A

Usually partial hepatectomy with no specific effect

85
Q

Radiotherapy effect of liver tumour?

A

Anorexia, nausea, risk of heptomegaly, risk of hepatitis if high does

86
Q

Why is post-op nutritional support important in liver cancer?

A

As it has the capacity to regenerate itself

87
Q

What is notable about liver cancer?

A

Primary liver Ca is rare, but metastases to liver is very common (especially from colorectal cancer)

88
Q

Effect of SI, colon, rectum tumour?

A

Obstruction anemia from occult losses, malabsorption, steatorrhea

89
Q

Surgery effect of SI, colon, rectum tumour –> Illeac resectons ?

A

Decr.B12, Ca, Mg, lipoprotiens, bile salt absorption

90
Q

Surgery effect of SI, colon, rectum tumour –> Colectomy ?

A

Water and electrolyte losses

91
Q

Radiation effect of SI, colon, rectum tumour?

A

Cramps, diarrhea, malabsorption, steatorrhea, fistula

92
Q

What is fistula?

A

Perforation, where there is joining with another tissue but only in most severe cases

93
Q

Effect of lung tumour?

A

Weight loss, cachexia

94
Q

Radiotherapy effect of lung tumour?

A

Possible impact on esophagus

95
Q

Effect of breast tumour?

A

Increased weight is considered with some breast cancers

96
Q

Radiotherapy effect of breast tumour?

A

Possible impact on intestinal mucosa

97
Q

Effect of gynaecological organ tumours?

A

Intestinal obstruction, enteropathy, ascites

98
Q

radiotherapy effect of gynaecological organ tumours?

A

Possible impact on intestinal mucosa

99
Q

Nutritional intervention of gynaecological organ tumours?

A

Diuretic or sodium restriction is NOT relevant

100
Q

Effect of bone metastases?

A

Pain, anorexia

101
Q

What is a common effect of drugs to control pain in bone metastases?

A

Slow down GI motility, leading to constipation

102
Q

Define cachexia

A

A complex metabolic syndrome associated with underlying illness and characterized by loss of muscle, with or without the loss of fat mass

103
Q

Prominent feature of cachexia?

A

Weight loss

104
Q

What drives most complications of cachexia?

A

Muscle loss

105
Q

Cancer is a ___ while cachexia is a _____

A

disease

syndrome

106
Q

Ultimately, what does muscle wasting lead to?

A

Weakness, weight-loss, reduced strength, functionality, VO2 which will affect quality of life

107
Q

What contributes to muscle wasting?

A
  • Anorexia
  • Inflammation
  • Insulin Resistance
  • Hypogonadism
  • Anemia
108
Q

What does muscle wasting predict?

A

Poor cancer-associated outcomes

109
Q

Poor cancer associated outcomes with muscle wasting?

A
  • Increase fatigue
  • Increased treatment induced toxicity
  • Decreased host response to tumour (much of the immune system lies in the muscle)
  • Decreased performance, functionaliyty
110
Q

Define sarcopenic obesity

A

Obesity with depleted muscle mass

111
Q

Why are outcomes worse with obese/sarcopenia individuals?

A

Less responsive oto treatment

112
Q

Which CA has more prevalence of SO?

A

Lung or GI tumours

113
Q

Prevalence of cachexia in CA?

A

5-80%

114
Q

Which cancers have a greater prevalence of cachexia?

A

Upper GI, Head/neck, lung (altered metabolism)

115
Q

What are the two main components of the onset of cachexia?

A
  • Metabolic changes

- Reduced Food intake

116
Q

Metabolic changes?

A
  • Hyper-catabolism (increased protein degradation)

- Hypo-anabolism (less response to anabolic stimuli)

117
Q

What are metabolic changes driven by?

A

Systemic inflammation

118
Q

What can systemic inflammation lead to?

A

Primary Anorexia (reduced food intake)

119
Q

Primary anorexia?

A

Driven by the systemic inflammation (i.e. consequence by the physiological change of the illness itself)

120
Q

Secondary anorexia?

A

Caused by the treatment of the disease, or complications of the disease (i.e. dysphagia in pharyngeal cancer)

121
Q

Together, what do metabolic changes and reduced food intake lea to?

A

Negative energy and protein balance - and ultimately poor outcomes

122
Q

What is the MAIN difference between starvation and cachexia?

A

Increase in REE and protein degradation (more active metabolism)

123
Q

Which hormones change in cachexia vs starvation?

A

Serum insulin may increase or remain the same, cortisol increases

124
Q

Precachexia?

A
  • Weight loss <5%

- Anorexia and metabolic changes

125
Q

Cachexia?

A
  • Weight loss >5%
  • BMI <20 and weight loss >2%
  • Sarcopenia and weight loss >2%
  • Often reduced food intake, systemic inflammation
126
Q

Refractory cachexia?

A

-variable degree of cachexia, where cancer is pro-catabolic and not responsive to treatment
< 3 months expected survival

127
Q

Why is it important to intervene early in cachexia?

A

Nutritional support in refractory cachexia is not effective

128
Q

A the refractory stage of cachexia approaches, what are changes in body composition?

A

Muscle and adipose tissue rapidly drops off (even in overweight/obesity)

129
Q

Inflammation leads to an ____

A

acute phase response

130
Q

What is an acute phase response?

A

Coordinated adaptation of body to limit and clear tissue damage caused by hydrolyses released from inflammatory, injured, malignant cells

131
Q

Where are acute-phase proteins synthesized?

A

In the liver

132
Q

In acute-phase, positive acute-phase proteins (increase/decrease) by over 25% and negative-phase proteins (increase/decrease) by over 25%

A
  • Increase

- Decrease

133
Q

Does the synthesis of negative-acute phase proteins decrease during inflammation?

A

NO

134
Q

Explain why albumin (NAP) is low during inflammation

A

Synthesis may increase, however inflammation promotes the permeability of vascular walls - albumin escapes to tissues and low albumin in blood

135
Q

NAP examples?

A
  • Albumin
  • Transferine
  • Transthyretin
  • TBP
  • IGF-1
  • Alpha-fetoprtoeint
136
Q

PAP examples?

A
  • Complement system
  • CRP
  • Coagulation, fibrinolytic system
  • Antiproteases
137
Q

What is the acute-phase response modulated by? Where are they produced by?

A
  • Cytokine

- Produces by tumour or host

138
Q

Which inflammatory cytokine are often seen in cancer?

A
  • TNF-alpha
  • IL-1 and IL-6
  • IFN-gamma
  • Leukaemia inhibitory factor
139
Q

Besides inflamation, what are other side effect of cytokines?

A
  • Decrease in appetite (primary anorexia)
  • Decrease GI function (early satiety, N/V)
  • Inhibit LPL (less storage of dietary fat)
  • Inhibit GH and IGF-1 signalling
140
Q

Which cytokine may induce insulin resistance?

A

IL-6

141
Q

Describe the host-tumour interactions between cytokines, protein degradation and nutritional status

A
  • Cytokines directly or indirectly (by impacting appetite) will increase muscle protein breakdown
  • Increase AAs in circulations are taken up by liver
  • Liver synthesize glucose, APP an excess AA lost as nitrogen in urine
142
Q

Cachexia is often accompanied by hyper-metabolism, which increases REE, but what happens to other component of energy expenditure? How is total energy expenditure compared to healthy individuals?

A
  • TEF and PAL decrease
  • Overall energy expenditure decreases
  • Their overall caloric intake also tends to decrease
143
Q

What are the two MAIN metabolic alterations in cachexia?

A
  • Decreased concentration or responsiveness in anabolic factors
  • Increased concentration of catabolic factors
144
Q

What are anabolic factors?

A

-Insulin, IGF-1, GH, thyroid hormones, testosterone

145
Q

What are catabolic factors?

A

-Glucagon, cortisol, pro-inflammatory cytokine, tumour-derived factors

146
Q

Alterations in lipid metabolism in cachexia?

A
  • Mobilization of lipids from adipose
  • Increased lipolysis
  • Decrease LPL (decreased storage of fat)
  • HyperTG, but endogenous source
147
Q

Alterations in glucose metabolism in cachexia?

A
  • Glucose is preferred fuel of tumours, and tumours will produce lactate.
  • Lactate can contribute to gluconeogenesis
  • Gluconeogenesis is increased, as proteolysis increases
  • Insulin resistance leads to more proteolysis
148
Q

Alterations in protein metabolism in cachexia?

A
  • Negative nitrogen balance (net protein catabolism)
  • Increased basal protein turnover
  • Increased hepatic protein synthesis of APP
149
Q

What does the increase in muscle proteolysis allow for?

A
  • AA for gluconeogenesis
  • APP synthesis
  • Tumour growth
150
Q

What are the 3 pathways of intracellular protein defredation

A
  • Lysosomal (caspases)
  • Calcium-dependant (calpains
  • Ubiquintin-proteosome pathway
151
Q

What is the MOST important pathway in skeletal muscle proteolysis in cancer cachexia?

A

Ubiquintin proteosome

152
Q

Describe the Ubiquintin proteosome pathways

A

Ubq-E3 ligase will link Ubq to a protein fragments, and will be destines for degradation with a proteosome

153
Q

Which genes encode UbqE3 ligase? What are they associated with?

A
  • Atrgenes: MAFbx and MuRF-1

- Greater muscles proteolysis

154
Q

What may increase the expression of atrogenes?

A

-Inflammatory cytosines TNF-alpha, IL-1 and IFN-gamma

155
Q

Why does the cori cycle increase in cancer?

A

The tumour feeds on glucose, produces lactate which participates in the cori cycle

156
Q

Why does proteloysis increase in cancer?

A

Tumour secreted TNF-alpha and PIF (proteolysis inducing factor)

157
Q

Why does gluconeogenesis increase in cancer?

A

Greater quantity of amino acids and lactate in circulation

158
Q

Why does lipolysis increase in cancer?

A

Tumours secreting cytokines or catabolic factors –> Increase FFA, packages into VLDL and endogenous HyperTG

159
Q

What does early satiety arise from?

A
  • Reduced GI motility, Increase in GI emptying

- Dysregulation of metabolic signals of satiety

160
Q

What are direct consequences of antineoplastic therapies?

A
  • Diarrhea, Nausea

- Chemosensory abnormalities

161
Q

What are some pharmacological agents to increase appetite?

A
  • Pro-gestational agents
  • Corticosteroids
  • Cannabinoids
162
Q

Pro-gestational agents?

A

-Birth control progesterone pills, increase appetite, weight gain but NOT lean mass

163
Q

Nutritional implications of pro-gestational agents and corticiosteroids?

A

-Insulin resistance, muscle wasting and osteopenia

164
Q

Corticosteroids?

A

Transient increase in appetite, but only for RESTRICTED periods (1-3 weeks)

165
Q

Common drugs prescribed for symptom management in cancer?

A
  • Antiemetics
  • Antidepressants
  • Corticosteroids
  • Anti GI motility agents
  • Narcotics, analgesic
166
Q

What does thalidomide inhibit?

A

TNF-a, may attenuate weight-loss

167
Q

What does pentoxifylline inhibit?

A

TNF-alpha, but no proven benefits

168
Q

What are potential agents to treat cachexia?

A
  • SARMS (incr. LBM and muscle function in elderly)

- Ghrelin receptor agonist (incr, appetite, weight gain, but NOT handgrip strength)

169
Q

Conclusion surrounding cancer and cachexia?

A

A multi-modal approach, combining dietary, PA and pharmacological agents that must include individual nutritional counselling and early intervention has the best chances of success to treat cachexia

Clinical Nutrition 1 (30 decks)

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