Cancer Flashcards

1
Q

cancer is the second leading cause of death in developed countries, after heart diseases and CVD. true or false

A

False, it is THE leading cause of death

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2
Q

what is the main cause of cancer? through which evidence?

A

environmental factors including diet is a large part of the cause of cancer. this is seen through the differences in cancer prevalence worldwide ad changes in prevalence among population that migrate

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3
Q

which factors interact which can cause cancer development

A

interactions between genetics, endogenous milieu [hormones and oxidation] and exogenous exposures

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4
Q

nutritional factors may contribute to about ____ of tumors

A

30%

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5
Q

what is the most important risk factor for developing cancer

A

age

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6
Q

what is the most prevalent type of cancer in men? and in women?

A
  • prostate cancer

- breast cancer

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7
Q

which is the most deadliest type of cancer in men? and in women?

A

lung cancer for both

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8
Q

cancer definition

A

uncontrolled growth of abnormal cells in the body

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9
Q

characteristics of cancerous cells (7)

A
  • escape normal growth signals
  • can replicate indefinitely, can form tumors
  • can avoid programmed cell death (apoptosis)
  • cal alter energy metabolism
  • can avoid immune surveillance
  • can invade other tissues (metastasis)
  • can develop a blood supply (angiogenesis)
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10
Q

what are benign tumors

A

they are non cancerous, do not invade and metastasize

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11
Q

what are the steps involved in carcinogenesis

A

activation/initiation of cell due to chemical/radiation/virus exposure -> genetic change -> initiated cell -> selective clonal expansion -> preneoplastic lesion -> genetic change-> malignant tumor -> genetic change -> clinical cancer -> genetic change -> cancer metastasis

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12
Q

what are the effect of chemical/radiation/virus exposure on cell nucleus

A
  • activation of potooncogenes
  • inactivation of timor-suppressor genes
  • inactivation of genomic stability genes
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13
Q

what causes selective clonal expansion

A
  • defects in terminal differentiation
  • defects in growth control
  • resistance to cytotoxicity
  • defects in programmed cell death
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14
Q

what is epigenetics and its role in cancer

A

factors happening between genotype and phenotype that will affect gene structure, function and expression [DNA methylation, acetylation of the histones] - they include environmental factors including nutrition [promote or suppress risk of cancer[

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15
Q

the inherited genetic mutation involving BRCA1 gene increases risk of ____ and ____ cancer

A

breast and ovarian cancer

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16
Q

_____ of the promoter region of Timor suppressor genes causes its silencing

A

hypermethylation [epigenetic change]

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17
Q

what is nutritional genomics and proteomics

A

interactions between diet and genes and their products [ie. proteins]

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18
Q

carcinogens found in foods, PUFA, and iron can cause ____

A

oxidative damage to DNA

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19
Q

_______ or ____ can decrease oxidative damage to DNA

A

antioxidant nutrients (vitamin C and E) or cofactors in antioxidant enzymes (selenium, copper)

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20
Q

there is a direct role of ____ in DNA synthesis, repair and methylation

A

folate

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21
Q

____ found in green tea, apples and chocolate and ____ affect gene expression in cell culture

A

catechizes and flavonoids

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22
Q

what are the effects of bioactive food compounds [nutrients, natural components, contaminants] on carcinogenesis

A

DNA repair, cell differentiation, hormone regulation, carcinogen metabolism, inflammatory response, apoptosis, cell growth cycle

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23
Q

___, ___ and ___ account for 30% of all cancers

A

tobacco and diet and obesity

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24
Q

what does “incidence of cancer cases” refer to?

A

number of new cancer cases diagnosed in a given population during a specific period of time, often a year because cancer can be cured treated
-> prevalence is used for T2D, HTN, CVD referring to proportion of individuals because of chronic factor

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25
Q

why has the number of cancer cases diagnosed each year has been increasing?

A

because of the growing and aging population

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26
Q

cancer rates have been increasing over the years. true or false

A

false, when the effect of age and population size are removed, the risk of cancer has been decreasing => not developing more cancers than before

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27
Q

which cancers are seen at higher incidence in developed countries

A

breast, prostate, colon

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28
Q

which cancer is seen at higher incidence in developing countries

A

liver cancer [hepatitis B + aflatoxin]

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29
Q

what is a descriptive type of study addressing diet and cancer and what are its limitations?

A

cancer rates in populations having different diets are compared [first observation students done to generate hypothesis]
however, diet is only one of many variables and nutrient intake data are difficult to collect

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30
Q

what is a case-control type of study addressing diet and cancer and what are its limitations?

A

retrospective study - earlier diets reported by patients with a specific type of cancer are compared with matched controls without cancer
however, possible recall bias and selection bias may occur and proxy respondents with rapidly fatal cancers

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31
Q

what is a prospective cohort type of study addressing diet and cancer and what are its limitations?

A

incidence of cancer is compared in persons whose diets (and other factors) are determined before follow-up begins
however, thousands of people need to be enrolled and health monitored for many years for statistical power + difficult for rare types of cancers

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32
Q

what is an interventional type of study addressing diet and cancer and what are its limitations?

A

incidence of cancer in 2 groups randomized to specific interventions is compared
however, adherence to dietary changes is difficult, blinding is often not possible, optimal dosages need to be ascertained, duration is unknown and may be long

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33
Q

what are some research approaches used for diet and cancer interactions

A
  • dietary data often collected using food frequency questionnaire
  • biochemical indicators may be useful for some nutrients (serum oxidative markers, vitamin D)
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34
Q

what are the main recommendations given by the American cancer society 2012 for cancer prevention

A
  • achieve and maintain a healthy weight throughout life
  • be physically active
  • eat a healthy diet, with an emphasis on plant foods
  • limit processed meat and red meat
  • eat at least 2 1/2 cups of vegetables and fruits each day
  • choose whole grains
  • limit alcohol intake
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35
Q

obesity is highly associated with which types of cancers

A

colon, post-menopausal breast cancer, and kidney cancer

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36
Q

why is there an association between obesity and cancer

A

if initiated cell is put in an environment that contains alot of energy substrates promoting cell division -> more chances to proliferate and cause cancer

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37
Q

what are the mechanisms involved between energy balance, growth rates, obesity and cancer

A
  • levels of metabolism of hormones (insulin, estradiol) and growth factors IGF-1
  • effects on inflammation and immune function
  • increased reflux -> increased risk of esophagus cancer
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38
Q

what is some evidence of healthy weight and prevention of cancer

A
  • intentional weight loss may reduce risk of postmenopausal breast cancer and possibly others
  • modest weight loss improves insulin sensitivity and hormone metabolism
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39
Q

thoughts on correlation between dietary fat/refined sugar and cancer

A

it was thought that high fat der was promoting cancer [breast, colon, prostate] BUT in reality more fat intake has associated with higher energy intake so the effect on cancer is due to excess ENERGY not fat itself or type of fat

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40
Q

what is more important when considering a healthy diet for cancer risk

A

PATTERN

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41
Q

red mean and processed meat associated with ____ cancer

A

colorectal

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42
Q

what is the correlation between processed meat an colorectal cancer? what is the proposed mechanism

A

50% increased risk with 25g increment of processed meat.

  • preservatives (nitrites and salt) -> nitrates -> nitrosamines [linked to Amino residues] which are cancerous
  • cooking at high temperature which generates polycyclic aromatic hydrocarbons PAH and heterocyclic amines
  • heme promotes formation of nitrosamine
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43
Q

what are some specific fruit/vegetable associations with promising protective effects?

A
  • lycopene -> prostate cancer
  • cruciferous vegetables and several cancer sites
  • allium vegetables and stomach cancer
  • folate rich F&V and colon cancer
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44
Q

providing isolated nutrients such as beta-carotene, vitamin C and E, selenium has shown benefits in reducing cancer risk. true or false

A

false - no benefits shown, could possible increase risk => not recommended to take antioxidant supplements

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45
Q

what is the proposed mechanism of fibres and lowering GI cancers

A

they dilute or bind potential carcinogens, limit contact with mucosa by speeding transit, alter colonic flora, reduce pH, serve as substrate to flora producing short-chain fatty acids

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46
Q

dietary fibres probably protects against ____

A

colon cancer

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47
Q

what are the proposed mechanisms between alcohol consumption and increased cancer risk

A
  • production of acetaldehyde -> DNA damage

- for breast cancer, alcohol may increase estrogen levels

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48
Q

dairy products and dairy consumption is associated with decreased risk of ____

A

colon cancer

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49
Q

proposed mechanism of calcium intake and reduced risk of colon cancer

A

binding toxic secondary bile acids and ionized fatty acids to form soaps in the lumen, or reducing proliferation and inducing apoptosis in the mucosal cells

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50
Q

what is the threshold for beneficial effects of calcium intake on colon cancer

A

700-800mg/day

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51
Q

which factor has convincing level of evidence on decreasing risk of cancer? [with associated cancer]

A

physical activity - colon cancer

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52
Q

which factors have convincing level of evidence on increasing risk of cancer? (4) [with associated cancer]

A
  • overweight and obesity (many cancers)
  • alcohol (oral cavity, pharynx, larynx, esophagus, liver, breast)
  • processed meat (colorectal)
  • high-dose beta-carotene supplements (lung)
  • aflatoxins (liver)
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53
Q

which factors have probable level of evidence on decreasing risk of cancer? (4) [with associated cancer]

A
  • physical activity (breast)
  • dairy products and calcium (colorectal)
  • whole grains and fibre (colon)
  • coffee (liver and uterus)
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54
Q

which factors have probable level of evidence on increasing risk of cancer? (2) [with associated cancer]

A
  • red meat (colorectal)

- salt preserved foods (stomach)

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55
Q

which factors have limited-suggestive level of evidence on decreasing risk of cancer? (2) [with associated cancer]

A
  • food containing carotenoids, vitamin C [fruits and veg] (oral cavity, oesophagus, stomach, colorectal)
  • fish, vitamin D
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56
Q

which factor has limited-suggestive level of evidence on increasing risk of cancer? [with associated cancer]

A
  • grilled + barbecued meat and fish (heterocyclic amines, PAH) nitrosamines
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57
Q

which factors have limited-no conclusion level of evidence on decreasing risk of cancer? [with associated cancer]

A

omega-3 FA, carotenoids, vitamins B6,B12, folate, C, D, E, Se, non-nutrient plant constituents, garlic, soy, sugar, tea

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58
Q

primary tumor

A

first tutor identified, classified according to size and invasion of surrounding tissues

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59
Q

secondary tumor

A

other tumors of the same histological origin as the primary, located nearby

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60
Q

metastasis

A

invasion of distal tissue and organs

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61
Q

how are tumors diagnoses

A
  • biochemically through biomarkers
  • imaging techniques (MRI, CT, PET, chest X-ray, ultrasound, mammogram, bone scans
  • biopsy, laparoscopy
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62
Q

carcinomas

A

epithelial tissue

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63
Q

sarcomas

A

connective tissue

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64
Q

lymphomas

A

lymphatic system

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65
Q

gliomas

A

glial cells of CNS

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66
Q

adenocarcinomas

A

glands

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67
Q

leukemias

A

bone marrow

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68
Q

why is it important to stage the cancer

A

staging the progression of the cancer is the driving point of approach to treat cancer [treatment options and prognostication]

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69
Q

what is the TNM system for staging cancer

A
  • primary Tumor [T: T1 to T4]
  • lymph Nodes [N: N0 to N3]
  • Metastasis [M: M0 or M1]
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70
Q

what are the different stages of cancer

A
  • stage 0: carcinoma in situ (early form)
  • stage 1: localized
  • stage 2: early locally advanced
  • stage 3: late locally advanced
  • stage 4: metastasized
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71
Q

what are the 5 anti-cancer treatments

A
  • surgical removal
  • radiotherapy
  • chemotherapy
  • biological therapies
  • hematopoietic stem cell transplantation
  • gene therapy
72
Q

what is the first choice for curative treatment for cancer

A

surgical removal

73
Q

what is the principle/mechanism of action of radiotherapy

A

it aims at killing cancerous cells using ionizing ration altering DNA to control the growth/kill malignant cells

74
Q

when is radiotherapy treatment used

A

for curative treatment or adjacent with other treatment regimen (surgery) and it is targeted for tumors with relatively limited damage to surrounding tissues

75
Q

what are the side effects go radiotherapy

A
  • head and neck [most side effects]: mucositis, dyspepsia, dysphagia, esophagitis => high risk of malnutrition
  • abdomen and pelvis: diarrhea, malabsorption, radiation enteritis
76
Q

what is the mechanism of action of chemotherapy

A

cytotoxic drugs that block DNA and RNA synthesis or cell division at different stages

77
Q

what is the limitation of chemotherapy

A

not very specific so it acts on other healthy cells that are replicating rapidly -> epithelial cells are the most affected => side effects

78
Q

what is the most commonly used biological therapy for cancer and how does it work

A

immunotherapy: use body’s own immune system to eradicate cancer cells

79
Q

what are biological therapies used for

A

to treat cancer itself, progression or side effects

80
Q

what is the typical first line treatment given for chemotherapy

A

alkylating agents - cisplatin and carboplatin

81
Q

what are some common side effects to chemotherapy agents

A
  • bone marrow suppression
  • N/V, stomatitis, diarrhea
  • alopecia
  • anorexia
  • renal toxicity (cisplatin)
  • hepatotoxicity (5-fluorouraci)
  • cardiotoxicity (doxorubicin)
82
Q

what are drug classes used in biological and targeted therapy

A
  • selective estrogen receptor modulators [tamoxifen - treat breast cancer]
  • signal transduction inhibitors [mTOR inhibitors]
  • angiogenesis inhibitors
  • monoclonal Ab delivering radioisotopes or toxins
  • cytokines (∞, IL-2)
  • hematopoietic growth factors
83
Q

definition of cachexia

A

complex metabolic syndrome associated with underlying illness and characterized by loss of muscle with to without loss of fat mass. The prominent clinical feature is weight loss

84
Q

low muscle mass can occur at all BMIs. true or false

A

true:

  • underweight with low MM
  • normal wt w/ low MM
  • obese with low MM
  • morbid obese with low MM
85
Q

what do we call low muscle mass with excess fat

A

sarcopenic-obesity

86
Q

what does muscle wasting predict in terms of cancer

A

predicts poor cancer-associated outcomes

87
Q

what are the consequences of low muscle mass

A

increased: fatigue, disease progression, treatment-induced toxicity, less cues completed
decreased: host response to tutor, performance status, survival

88
Q

what is the overall prevalence of cachexia in cancer patients

A

50% [almost half of cancer patients will develop cachexia]

89
Q

dual contribution of ______ and ______ to cachexia

A

metabolic change and reduced food intake

90
Q

what are the metabolic changes that contribute to cachexia development

A

hypercatabolism and hypoanabolism due to systemic inflammation and catabolic factors

91
Q

what are the consequences of metabolic changes and reduced food intake leading to cachexia

A

negative energy and protein balance

92
Q

what is the difference between primary and secondary anorexia

A

primary - from systemic inflammation affecting hypothalamus and regulation of appetite and satiety
secondary - comes from anti-cancer treatment with all the side effects

93
Q

what are the major differences between starvation and cachexia

A
  • cachexia: accelerated loss of lean mass in cachexia, increase in REE, increase in protein degradation [increased protein turnover], insulin resistance
  • long-term starvation: severely affects body fat, reduced caloric intake, treated decrease in TEE, decrease in REE
94
Q

what are there 3 stages of cachexia

A
  • precachexia [weight loss <5%, anorexia and metabolic change]
  • cachexia
  • refractory cachexia [<3 months expected survival ]
95
Q

what are the 5 markers of cachexia

A
  1. weight loss and changes in body composition [loss of fat and fat-free mass]
  2. inflammation and acute phase response
  3. hypermetabolism
  4. metabolic alterations
  5. anorexia
96
Q

what is the obesity paradox in terms of cancer survival

A

obesity will increase the risk of cancer but if you have cancer with higher BMI, you will survive longer, independent of degree of weight loss => stores of energy that can used by host has a protective effect

97
Q

which factors result in a poor prognostic for survival

A

muscle of low quality (inter muscular adipose tissue) + high degree of weight loss + low BMI

98
Q

what is the acute-phase response

A

coordinated adaptations of the body to limit and clear the tissue damage caused by hydrolyses released from inflammatory, injured or malignant cells

99
Q

acute-phase proteins are synthesized by _____ and can either be _____ or ____

A

hypatocytes

positive (increased []) or negative (decreased [])

100
Q

which are the negative acute phase proteins

A
albumin
transferrin
tranthyretin
thyroxine-binding globulin
IGF-1
alpha-fetoprotein
101
Q

acute phase response is modulated by ____

A

cytokines

102
Q

which pro-inflammatory cytokines have been found in high levels in some cancer

A
  • TNF-alpha
  • IL-1 and IL-6
  • IFN-gamma
  • LIF
103
Q

what are the effects of cytokines

A
  • decreases appetite and food intake (reduces substrate supply to muscle), GI functions [decreased gastric emptying], blood flow
  • inhibit lipoprotein lipase, growth hormone and IGF-1 signalling
  • induces insulin resistance (IL-6)
  • catabolic effect
  • increases proteolysis (skeletal muscle wasting)
104
Q

in cachectic individuals, we see an increase in ____ and decrease in _____ in regards to metabolism

A

increase in REE and decrease in TEE

105
Q

how do cachectic individuals lose weight if they have overall decreased TEE

A

the energy intake is more decreased than reduction of TEE -> weight loss

106
Q

what are the metabolic alterations in regards to lipids during cachexia

A
  • increased turnover of fatty acids
  • increased lipolysis, FFA
  • decreases LDL activity
  • increased VLDL, hypertriglyceridemia
107
Q

what are the metabolic alterations in regards to glucose during cachexia

A
  • glucose is the preferred fuel for tumors
  • tumors produce lactate -> cori cycle (uses ATP)
  • increased gluconeogenesis -> increased proteolysis in the muscle
  • insulin resistance
108
Q

what are the metabolic alterations in regards to proteins during cachexia

A
  • negative nitrogen balance
  • increased protein turnover and muscle proteolysis (provides AA for gluconeogenesis, acute-phase protein synthesis and tumor growth)
  • decreased muscle protein synthesis
  • increased hepatic protein synthesis for acute phase proteins
109
Q

most of the skeletal muscle degradation in cancer cachexia and many wasting conditions is done through which pathway?

A

ATP-dependent ubiquitin-proteasome pathway

110
Q

during cachexia, there is a decrease in ___ factors and an increase in ____ factors

A

decrease in anabolic

increase in catabolic

111
Q

which anabolic factors are decreased during cachexia

A
  • insulin
  • IGF-1
  • growth hormone
  • thyroid hormone
  • testosterone
112
Q

which catabolic factors are increased during cachexia

A
  • glucagon
  • cortisol
  • pro-inflammatory cytokines
  • prostaglandins
  • tumor-derived factors
113
Q

tumors increase _____, _____, _____ and in turn _____ which are all energy demanding explaining the elevated _____

A

lipolysis, cori cycle, proteolysis and in turn gluconeogenesis
-> energy demanding -> elevated REE

114
Q

normally, repletion suppresses ______ and in turn inhibits feeding where as depletion activates these stimulating feeding

A

hypothalamic orexigenic signals (NPY)

115
Q

normally, repletion activates ______ and in turn inhibits feeding and increase energy expenditure where as depletion suppresses these stimulating feeding

A

anorexigenic signals (POMC)

116
Q

in cachexia, there is dysregulation of homeostasis in regulation of appetite and food intake due to persistent activation of ______ neurons

A

POMC => anorexigenic signals that inhibit feeding and increase energy expenditure

117
Q

what could cause early satiety in cancer patients

A
  • reduce GI motility
  • increased gastric emptying time
  • autonomic dysfunction and opioid analgesics
118
Q

what are the cutoffs of diagnosing cachexia

A
  • weight loss >5% OR
  • BMI <20 and weight loss >2%, reduced food intake/systemic inflammation]
  • appendicular muscle mass consistent with sarcopenia and any degree of weight loss >2%
119
Q

cachexia can be treated. true or false

A

false, it can only be MANAGED

120
Q

which are some therapeutics agents in cancer cachexia that could increase appetite

A
  • pro gestational agents
  • corticosteroids
  • cannabicoids
121
Q

which are some therapeutics agents in cancer cachexia used for symptom management

A
  • antiemetics
  • antidepressants
  • corticosteroids
  • anti GI motility agents
  • narcotics and other analgesics
122
Q

what are the 4 targets for cachexia therapy making it a multi-modal approach

A
  • energy intake
  • activity
  • inflammation
  • mental health/anxiety
123
Q

which factors of cancer affect nutritional status

A
  • presence of tumor
  • host response
  • anti-cancer treatment
124
Q

what are the consequences of a compromised nutritional status during cancer

A
  • decreased quality of life
  • decreased réponse to treatment
  • decreased survival
125
Q

what is nutritional screening

A

process of identifying characteristics known to be associated with nutritional problems

126
Q

what is nutritional assessment

A

process of assessment of body compartments and analysis of structure and function of organ systems and their effects in metabolism

127
Q

how to calculate (unintentional) weight loss

A

% weight loss = (initial weight - current weight)/initial weight *100

128
Q

_______ is the most powerful independent variable that predicts mortality in cancer

A

unintentional weight loss

129
Q

classification of severity of weight loss

A
1 week: 1-2% (sig), >2% (sev)
1 month: 5% (sig), >5% (sev)
3 months: 7.5% (sig), >7.5% (sev)
6 months: 10% (sig), >10% (sev)
unlimited: 10-20% (sig), >20 (sev)
130
Q

what are the 2 most important factors of the dietary assessment in cancer patients

A

ENERGY and PROTEIN intake

-> sufficient energy required to use dietary protein correctly and avoid nitrogen losses

131
Q

what is the major component of prognostic of development of cachexia

A

loss of muscle mass

132
Q

which tools are used to asses loss of muscle mass

A
  • anthropometry: mid-upper arm muscle area MAMA
  • urinary creatinine
  • 3-methyl-histidine excretion
  • Bioelectrical impedance BIA
  • DXA: appendicular muscle mass index
  • CT sci or MRI
133
Q

how is mid-upper arm muscle area calculated

A

calculated from mid-arm circumference and triceps skinfold

134
Q

what is considered a low mid-upper arm muscle area

A

<15th percentile for age and sex

135
Q

why is urinary creatinine a tool used for assessing loss of muscle mass

A

urinary creatinine is a metabolite of creatine phosphate, mainly found in skeletal muscle => index of muscle mass

136
Q

why is 3-methylhistidine a tool used for assessing loss of muscle mass

A

3-methylhistidine is released from actin and myosin degradation -> marker of myofibrillar protein degradation

137
Q

about bioelectrical impedance

A
  • estimates fat-free mass [body fat by difference]
  • based on body water
    => 2 compartment model
138
Q

how does DXA assess loss of muscle mass

A

imaging technique based on different tissue density - measures bone, lean soft and fat tissues resulting in total lean body mass and appendicular muscle mass

139
Q

____ correlates with muscle mass

A

muscle strength

140
Q

what are some functional tests that can be done to assess loss of muscle mass

A
  • gait speed (4m walking test)
  • chair rise (test leg strength and power - time for 5 chair rises)
  • 6min walking tee (endurance test)
  • balance test
141
Q

with inflammation, which could occur during cachexia albumin levels tend to be ____

A

lower

142
Q

what are some biochemical tests that can be abnormal due to cancer

A
  • vitamin B12 (high with leukaemia, liver mets and low with gastrectomy)
  • calcium (high with mets, lymphomas, parathyroid tumor)
  • folate (low with some drugs)
  • glucose (high with corticosteroids, pancreatic cancer)
  • hemoglobin (low with radio and chemotherapy, leukaemia, lymphoma)
  • potassium (high in treatment with cisplatin)
  • lymphocyte count (low with radio/chemotherapy, leukaemia, corticosteroids)
143
Q

what are the consequences/treatments for low hemoglobin due to radio/chemo therapy, leukaemia, lymphoma

A
  • hypochromic anemia: respond to iron supplement
  • megaloblastic anemia: folat for b12 supplement
  • normochromic anemia: blood transfusion
144
Q

what are some indications of dehydrations

A
  • high blood concentrations of: blood electrolytes, blood urea nitrogen, creatinine, hematocrit
  • urine specific gravity
  • clinical signs: low BP, thirst, rapid heart rate, skin dryness
145
Q

many inflammation/catabolic markers may be present during cancer but usually measured as ____ and ____

A

C-reactive protein and albumin

146
Q

which tool is used to categorize the degree of inflammation in cancer patients

A

the Glasgow prognostic score

147
Q

what is the Glasgow prognostic score based on

A

CRP: low <10mg/L or high >10mg/L
Albumin: low <35g/L or normal >35g/L

148
Q

what does LOW CRP and NORMAL albumin reveal according to the Glasgow prognostic score

A

GPS = 0 -> no cachexia

149
Q

what does LOW CRP and LOW albumin reveal according to the Glasgow prognostic score

A

undernourished

150
Q

what does HIGH CRP and NORMAL albumin reveal according to the Glasgow prognostic score

A

pre-cachexia

151
Q

what does HIGH CRP and LOW albumin reveal according to the Glasgow prognostic score

A

refractory cachexia

152
Q

what is the patient-generated subjective global assessment

A
  • adaptation to SGA because it involves symptoms of oncology patients
  • screening/assessment tool
  • 2 sections: 1 filled by patient one by health-care professional
  • numerical score: useful for triage to initiate intervention
153
Q

what are the 4 sections of the patient form of the PG-SGA

A
  1. weight loss
  2. food intake
  3. symptoms related to cancer/treatment
  4. activities and function
154
Q

what are the 3 possible nutrition diagnoses following nutritional assessment of cancer patients

A
  • involuntary weight loss
  • malnutrition
  • dehydration
155
Q

what is the intent of a preventative nutritional intervention

A

in prevision of treatment that will affect nutritional status (or pre-cachexia)

156
Q

what is the intent of an adjuvant nutritional intervention

A

to improve nutritional status to initiate and support anti-cancer treatments (or in cachexia)

157
Q

what is the intent of an palliative nutritional intervention

A

to improve or maintain quality of life when anti-cancer treatments have stopped (refractory cachexia)

158
Q

what are the goals of nutrition therapy in cancer patients

A
  • increased lean body mass (or weight stabilization if active weight loss)
  • predispose to a better response to radio or chemotherapy
  • increase immunocompetence
  • symptom management
  • improve perception of well-being
159
Q

what is the recommendation regarding energy requirements for cancer patients

A
  • 25-30kcal/kg/day [adjusted to ideal body weight if obese]
  • determine current intakes and recommend increased intakes when severe weight loss
  • patients with obesity may not need more energy but do need more protein
160
Q

what are the recommendations regarding protein intake for cancer patients

A
  • 1.0-1.5g/kg/d
  • 1.2-2.0 g/kg/d id inactivity and systemic inflammation are present
  • 1.0-1.2 g/kg/d with kidney disease
161
Q

multivitamin/mineral supplements may be recommended in amounts close to ____

A

DRIs

162
Q

which diets may be harmful for cancer patients?

A

> diets that restrict energy intake in patients with or at risk pf malnutrition
keto diets: can cause weight loss -> lean muscle mass loss

163
Q

what is the best route of nutritional administration?

A

oral route

164
Q

what are the different rote sos nutritional administration

A
  • oral
  • enteral
  • parenteral (last resort)
165
Q

what is the treatment for hematological cancers

A

hematopoietic stem cell transplantation

166
Q

what has to be done for hematopoietic stem cell transplantation

A

total body irradiation as a conditioning regimen

167
Q

what is the outcome of total body irradiation for hematopoietic stem cell transplantation

A
  • eradicate malignant cells

- immunosuppression

168
Q

what is the nutrition approach for hematopoietic cell transplantation

A
  • avoid foods t risk of causing infections
  • adopt safe food handling during period of neutropenia
  • provide enteral nutrition when GI tract is intact and oral intake is inadequate
  • parental nutrition for patients unable to ingest or absorb adequate nutrients for a prolonged period
169
Q

what are some promising nutrition therapies for cachexia

A
  • omega-3 fatty acids [may have protective effects on chemo-induced toxicities, neuroprotective effects]
  • amino acids [anabolic response]
170
Q

what could be recommended for omega-3 FA intake for most cancer patients

A

<5g/day

171
Q

which specific amino acids have shown positive effects in cachexic patients

A
  • leucine (stimulates protein synthesis and insulin secretion -> anabolic properties
  • glutamine and arginine (increase immune competence, help wound healing)
172
Q

inactivity induces _____

A

muscle loss

173
Q

___ + ___ = lean body mass and strength in elderly and in bed-ridden patients

A

resistance exercise + nutritional supplements

174
Q

exercise is ____ and potentiates the ____ effect of nutrition

A

anabolic

anabolic

175
Q

a multimodal intervention, combining ____, _____ and ______ approaches, that must include individual nutritional counselling and bleary intervention has the best chances of success

A

dietary, physical exercise, and pharmacological