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Malnutrition and cachexia Flashcards

1
Q

The pathway of cysteine synthesis

A

The only part that goes from methionine to cysteine is sulphur group, carbons are totally different

serine gives the carbon skeleton

At first, from methionine we take off the methyl group

then, we add serine, resulting in homocysteine

Serine comes from glucose

Then cysteine can be converted to taurine

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2
Q

Cysteine can be converted to what ( apart beign utilized for protein synthesis)

A

Can be converted to glutathione, tripeptide, taurine

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3
Q

Functions of taurine

A

Beta- amino acid

Essential AA for cats

Involved in the development of retina for premature babies

Invovled in muscle metabolism

Not in DNA

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4
Q

Draw the cycle for cysteine synthesis

A
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5
Q

Critical control point here

A

Homocysteine- powerful prooxidant

Because the moment it is produced it should be converted back to methionine or converted to cysteine

If higher than very low, can cause oxidative stress

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6
Q

What compound is homocysteine

A

Technically an AAs , but it is not used in the protein

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7
Q

Enzyme involved in AA metabolism and thus in methione-cysteine circle is

A

B6-pyrodoxine

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8
Q

Enzymes invovled in transferring methyl groups

A

Folate and B12

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9
Q

If there is high homocysteine, does it mean that we have problems with high protein intake, because it is their intermediate?

A

No, problem is in coenzymes

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10
Q

Regulation of methione-cysteine pathway happens in

A

The liver

If you have not healthy liver-> no breaking down of methionine-> no synthesis of taurine and cysteine

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11
Q

When cysteine can be a conditional essential AAs

A

Premature infants ( not enough enzymes)

ill liver

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12
Q

Composition of glutathione

A

gamma-glutamate-cysteine-glycine

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13
Q

What happens with cysteine in solution

A

It is oxidized to cystine, which is 2 cysteine molecules together and it precipitates

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14
Q

Role of glutathione

A

Important intracellular redox agent

A substrate for another enzyme that conjugates with electrophiles (toxins, xenobiotics, drugs) and removal of reactive oxygen species

Protection of protein, lipid membranes and DNA (glutathione provides NADH)

Important for immune system function

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15
Q

Another name for tylenol and its metabolisma nd why you should be careful with dosage

A

acetaminophen or paracetomol

Painkiller and fever reducer

It is conjugated with glutathione to create an intermediate that can be excreted

If too much taken, potentially toxic to the liver, because uses all of glutathione, so no redox status control of liver cells

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16
Q

what drug is given in the case of paracetomol overdose

A

N-acetylcysteine-> by putting nitrogen cysteine becomes more stable and can be given in liquid form as a drug, so glutathione is saved for redox status

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17
Q

When glutathione status is decreased

A

During short term and long term fasting

Protein deficiency ->lower synthesis rate

Higher consumption is increased in inflamamtion/infection (burns, AIDS)

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18
Q

How creatine can be an exampel of inter organ colloboration for metabolism

A

In liver SAM to SAH, so methyl groups is added (can be conjugated with methione to cysteine pathway, because they have this step)

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19
Q

Synthesis of creatinine occurs how

A

Non-enzymatically from creatine and phosphocreatine

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20
Q

Creatinine levels in urine can be roughly estimated as

A

As an indicator of muscle mass

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21
Q

Should you consider taking glutathione and creatine

A

Glutathione-tripeptide-> will not survive in HCl

Increasing creatine pool is probably for power but not for endurance (here you are more limited in oxygen-myoglobin pool)

Increased creatine in muscles-> hydrophilic-> attraction of water-> increased lean body mass, but does not increase power

Can be useful for upregulating myosin synthesis, cytoskeleton, protein and glycogen-> so may be a little anabolic

But a reasonable ergogenic aid for atheletics

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22
Q

What is starvation

A

The physiological condition created in the body as a consequence of chronic insufficient food intake

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23
Q

2 types of starvation

A

Can be physiological (coordianted adaptation to reduce nutrient supply-> goal is to prolonging survival)

and pathological (metabolic scenario, where two many compromised functions has occured and now it is a pathology-> disease) will lead to protein-energy malnutrition

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24
Q

The most common aspect of starvation

A

Protein-energy malnutrition

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25
Q

What was diet of study for starvation

A

1500 kcal

50 g protein per day (close to RDA, but RDA for adequet energy intake), but if not enough kcal, some AAs are going to be used for energy

for 6 months

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26
Q

Due to what loss the adaptation to starvation occured

A

loss of a lot of fat (in the end only 1%), lean tissue mass, increased extracellular fluid mass ( because changes in protein metabolism and regulation of water)

Rate of weight change in the end was zero (no fat and muscle less in the end)

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27
Q

What is successul adaptation to starvation

A

No loss of body substance despite continued food deprivation

Stable body composition must mean cessation of fat loss and cessation of lean tissue loss

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28
Q

What happened to metabolism to reduce the energy expenditure

A

Reduced resting energy expenditure (reduced mass of metabolically active tissue (basal metabolic rate), reduced energy expenditure per unit active tissue (per kilo of muscle mass), reduced heart rate and muscle tone

Reduced non-resting energy expenditure (reduced work of moving and reduction of voluntary movements)

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29
Q

Why there is a reduced of protein requirement in starvation and what is nitrogen balance

A

Diminished lean tissue mass

More efficient retention of dietary protein

Lean tissue mass stabalizes despite continued low protein intake

Nitrogen balance at first is going to be negative and then after 6 month it is going to be zero

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30
Q

Benefit and cost of successful adaptation

A

Benefit: survival

Cost: lean tissue loss, fatigue and inactivity, immunodeficiency, reduced tolerance to stress

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31
Q

Clinical features of PEM

A

Reduced body weight

Muscle wasting and decreased strength

Reduced respiratory and cardiac muscular capacity

Skin thinning

Decreased metabolic rate

Hypothermia

Apathy

Edema

Immunodeficiency

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32
Q

Draw the scheme how the body is going to adapt to decreased protein and energy intake and how it can be successful and how it can fail

A

Hypoalbunemia- problems with electrolyte and fluid balance

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33
Q

What is unsuccessful adaptation to malnutrition

A

Add micronutrient deficient (iron, B1)

Stress (trauma,cancer, inflammation/infection)

And all adaptations before become catastrophic

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34
Q

What happens with resting metabolic rate with starvation and different diseases

A
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35
Q

what happens with nitrogen excretion starvation vs injury

A
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36
Q

the 6 causes of muscle atrophy

A
  1. Cachexia-cancer, systemic inflammation
  2. Hormone excess or deficiency
  3. Old age-sarcopenia
  4. Protein-energy malnutrition-starvation
  5. Inactivity-disuse atrophy
  6. Neuromuscular disease
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37
Q

What can we learn from famine in netherlands

A

Epigenetics of everyone was affected

But especially pregnant women

Intrauterine growth restricted (IUGR)

This infants had increased chronic disease and even their own babies were affected->Barker hypothesis

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38
Q

What is statistics of child mortality because of femine and how many children are undernourished

A

5,5 million children under five are dying in 2017

90 million under five are undernourished and underweight

39
Q

What is 1000 days of opportunity and what can be done

A

The key time ( from conception to 1000 day of the child)

Support breatfeeding, support women (nutrition and health) and children at the community level, better diets for babies and toddlers, Increased Investment in Children and Families (Paid time off for working parents to care for their newborns), The right foods introduced to babies at the right times, The right knowledge and skills for parents and caregivers to properly nourish young children, Societal investments in the wellbeing of every baby and toddler

40
Q

What is wasting and what is stunting

A

Wasting - low weight for height

Stunting-low height for age

41
Q

What is the disease in children that can be considered as successful and its characteristics (when, onset, what happens, what is weight-for-age, appetite)

A

Marasmus

Infancy (6 to 18 months of age)

Severe deprivation or impaired absorption of protein, energy, vitamins and minerals

Develops slowly Severe weight loss and muscle wasting, including the heart

Lower than 60% weight-for-age

Anziety and apathy

Good appetite is possible

Skin and bone appearance

42
Q

Is it easier to treat marasmus or kwashiorkor

A

Marasmus

43
Q

What is kwashiorkor (when, what is the prevalence, onset, signs and what happens), weight- for -age , appetite

A

Unsuccessful adaptation

Older infants and younf children 18 months to 2 years of age ( weaning period vulnerable) , usually the first child when the second is born

5% prevalence in some countries

Inadequate protein and energy intake

Rapid onset

Some muscle wasting, some fat retention

Weight for age (60-80%)

Appetite

Edema and fatty liver

44
Q

How should you treat kwashiorkor and marasmus

A

Kwashiorkor - might have infection (respiratory or digestive) or other metabolic stress, electrolyte imbalance. Need to restore electrolyte balance and all other urgence situations, then infection and then nutrition

Marasmus -just gradually refeed

45
Q

Long term consequences of PEU for children

A

Decreased development (physical, social, cognitive)

Adult productivity

Reproduction

Potential of the society as a whole

46
Q

Infections that can occur to PEU children and why they can occur

A

Lack of antibodies

Nb no longer synthesized-> anemia

Fever

Fluid imbalance (heart failure, possible death)

Infections:

Dysentery

Diarrhea

Pheumonia and other respiratory infections

Urinary tract infections

Measles

Tuberculosis

Parasitic infections

Parasitic infections due to Fe and vitamin A deficiencies

47
Q

Rehabilitation of PEU children should include

A

Nutrition must be cautios, slowly increasing protein

Programs should involve the local people

48
Q
A
49
Q

What is edema

A

Plasma proteins leave leaky blood vessels and move into tissues

Proteins attract water,causing swelling

When pressure is applied to the swollen tissue, it leaves an indentation

50
Q

Impact of cancer on nutritional status

A

Presence of tumor (substances secreted by the tumor, demand of the tumor), the host repsonse to those tumor substances and anti-cancer treatment response

All of these influence nutrition status

51
Q

Consequences of compromised nutrition status in cancer

A

Reduced intake, altered metabolism-> malnutrition and weight loss-> decreased quality of life, decreased response to treatment, decreased survival

52
Q

What is cachexia

A

weakness and wasting of the body due to severe chronic illness

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

More muscle mass

Secondary effect

53
Q

What is canadian task force and what is their benefits

A

Early identification of patients at risk, or experiencing,
malnutrition allows for early intervention
 Helps design appropriate nutrition support
 Improves patient wellbeing, survival, immune function
and reduced morbidity
 Improves response to treatment

54
Q

what are defficiences particularly common in elderly people

A

Vitamin D, vitamin C

55
Q

Draw the scheme how different chronic illnesses increase weight loss and weakness

A

Insulin resistance because of cortisol

Hypogonadism means diminished functional activity of the gonads—the testes or the ovaries—that may result in diminished production of sex hormones.

56
Q

Why muscle wasting predicts poor cancer-associated outcomes

A

↑ fatigue
 ↑ treatment‐induced toxicity
 ↓ host response to tumor
 ↓ performance status
 ↓ survival

57
Q

What is sarcopenic-obesity and what outcomes it has

A

obesity with depleted muscle mass
 ≈15% of patients with lung or gastro‐intestinal tumors
 worse outcomes than obese or sarcopenic patients

Lung or GI tumors that experience cachexia

58
Q

In what cancers cachexia is more prevalent

A

Overall prevalence: 50‐80%

 Upper gastro‐intestinal cancer

 Lung cancer

59
Q

The key aspect in cachexia is

A

Weight loss

60
Q

What is undernutrion, malnutrition, starvation, sarcopenia

A

Undernutrition: insufficient food intake
 Malnutrition: insufficient intake in one or more
nutrients (can also refer to over‐ or undernutrition)-> you cna be overweight and malnourished
 Starvation: food deprivation (all nutrients)
 Sarcopenia: decreased muscle mass (even in the
absence of weight loss)

61
Q

What is the dual contribution of metabolic change and reduced food intake in cachexia

A

On the one hand it is systemic inflammation and catabolic factors(cytokines) - (leading to hyoercatabolism and hypoanabolism) and also primary or secondary anorexia( leading to reduced food intake)

Overall, negative energy and protein balance

62
Q

What are cytokines

A

Hormone like substances, secreted by immune cells (lymphocytes,macrophages) or tumor that cause catabolic and proinflammatory effects

They in part are in charge of causing anorexia, acting on the brain-> decreased interest in food, decreased appetite

They also signal muscle cells to increase protein breakdown to increase break down of glucogenic amino acids to make insulin, even when there is no need for extra insulin, but they have insulin resistant stae, so they continue to synthesize insulin

They act locally (paracrine and autocrine) and systemically (endocrine)

63
Q

In cachexia there hypermetabolism because

A

As a response to tumor or treatment

64
Q

What is pyrexia

A

fever

65
Q

Compare nutritioal alterations in starvation and cachexia (bodyweight, body cell mass, body fat, caloric intake,TEE,REE,protein synthesis, protein degradation, serum insulin, serum cortisol

A

Body cell mass (lean mass)

66
Q

What are stages of cachexia and what are defining features

A
67
Q

At what stage should we intervene

A

precachexia

68
Q

In cachexia stage what we can measure

A

cytokines

69
Q

How the traditional weight loss differs from weight loss in cachexia

A

Traditional: roughly equal proportions of fat mass and fat-free mass (mainly from skeletal muscle, although we also lose from visclerall tissues like liver and gut)

Cachexia (more muscle break down rather than fat)

70
Q

Acute phase response in cachexia is a response to

A

inflammation, infection, injury (surgery)

71
Q

What are acute-phase proteins

A

Fibrinogen (increase-> psoitive acute proteins)

And decrease in albumin (negative acute-phase proteins)

72
Q

Albumins: function

A

Transport of nutrients around the body, trasnport toxins to the liver

73
Q

Examples of big three proinflammtory cytokinesTumor

A

Tumor-necrosis factor alpha (TNF-alpha)

Interleukins 1 and 6 (IL-1, IL-6)

not the big three, but better to know

Interferon gamma (IFN-gamma)

Leukemia inhibitory factor (LIF)

74
Q

functions of cytokines

A

decreased appetite and food intake, resulting from both
central and peripheral elements
 decreased GI functions: decreased gastric emptying , intestine mobility
 decreased blood flow
 Inhibit lipoprotein lipase (LPL)
 Inhibit growth hormone and IGF‐1 signaling
 Induce insulin resistance (IL‐6)

75
Q

draw a scheme: interaction between inflammation, liver, brain , muscle

A

What happens to energy expenditure

76
Q

What happens to energy expenditure in patients with cachexia

A

Decreased overall expenditure, because of all inflammatory processes

But TEF- 5%, which is the lower bound of normal metabolism

Increased resting metabolic rate (85-90%)

And decreased PAL (physical activity energy ) from 15-30% to 5-10%

77
Q

What are circulating anabolic and catabolic factors in cachexia

A

Glucagon and cortsiol promote net catabolism and insulin resistance

Increased mobolization of lipids and increased turnover of fatty acids, Increased lipolysis, FFA, VLDL

Decreased LPL , so overall hypertriglyceridemia (VLDL)

78
Q

Main fuel for tumors and the outcome from it

A

Glucose is a fuel for tumors

Tumors produce lactate-> cori cycle (uses more ATP)

Increased gluconeogenesis->increased proteolysis (muscle)

Promotion of insulin resistance

79
Q

WHat happens with nitrogen balance in cachexia

A

Negative

Increased basal protein turnover

Increased or no change in muscle proteolysis: provides AA for GNG,
acute‐phase protein synthesis and tumour growth
 ↓ or ↔ in muscle protein synthesis
 ↑ hepatic protein synthesis (APPs)

Comparing to starvation, where protein turnover is decreased

80
Q

intracellular protein degradation pathway that is important

A

ATP‐dependent ubiquitin‐proteasome pathway
 The most important in skeletal muscle proteolysis in
many wasting conditions, including cancer cachexia

81
Q

describe ubiquitin-proteosome system

A

Series of three enzymes caleed ligases, its tying several ubiquitin molecules to the protein that is targetted to be degraded and then the protein that is targeted it gets in the proteasome and then ubiquitin recycled again

This pathway is promoted by cortsiol,glucagon and cytokines

82
Q

Draw the scheme how tumor dusrupt homeostasis in the body with muscle, liver and fat tissue

A

Liver:Increased urea sythesis, increased lipogenesis because excess of glucose, increased in lypolysis in adipose tissue that will promote hypertriglyceridemia

83
Q

Cachexia is associated witn mor ethan 50% of ____

A

Anorexia

An done of the treatmetns of cachexia is to recognize why we have anorexia (cytokines, treatment, lack of appetite, etc.)

84
Q

What is early satiety

A

In anorexia, they are full after a few drops

Maybe a result from reduced GI motility, increased gastric emptying time, nervous system dysfunction, morphin related lack of appetite, or metabolic signals of satiety dysregulation

85
Q

Why there can be nausea and chemosensory abnormalities during cancer

A

Nausea may occur as:
 Side effect of drugs
 Abdominal disease, intracranial metastases, metabolic derangements,
GI stasis

Distorsion of taste and smell:
 Includes: hypersensitivity to odors and flavors, persistent bad tastes,
phantom smells, food aversions
 Apart from treatment, may result from chronic nutritional deficiencies

86
Q

Clinical diagnosis of cancer cachexia

A

Weight loss >5% over past 6 months
(in absence of simple starvation)
OR
BMI <20 kg/m2 and any degree of weight loss >2%
OR
Appendicular muscle mass consistent with sarcopenia
(<7.26 kg/m2 in men; <5.45 kg/m2 in women)
and any degree of weight loss >2%

87
Q

Additional assessment to diagnosis of cachexia

A

Anorexia or reduced food intake
 Questionnaires or <70% of usual food intake

 Catabolic drive
serum CRP levels

 Muscle mass and strength
DXA, BIA, MAMA, handgrip strength

 Functional and psychosocial effects
questionnaires

88
Q

What are the goals of cachexia treatment

A

 increased Lean body mass (weight stabilisation ?)
Predispose to a better response to radio‐ or
chemo‐therapy
 increased Immunocompetence
 Symptom management
 increased Perception of well‐being

89
Q

What nutritional counseling should be in case of cachexia

A

 Should be individual
 Provide adequate energy and protein (usually 25‐30
kcal/kg/d, 1.2‐1.5 g pro/kg/d) but best to increase usual
intake.
 Multi vitamins and minerals, omega‐3 fatty acids (anti-inflammatory)
 Adapt dietary strategy according to:
Appetite
Rounds of therapy
Symptoms
Accessible route of feeding (oral, enteral, parenteral)
 Encourage physical exercise

90
Q

For whom enteral nutriton should be applied and to whom parenteral

A

Enteral

for patients with obstructions, gastric atony or limited
absorptive capacity
 Preserves GI architecture, barrier, immune functions and gut permeability

Parental

When enteral route not accessible, but not recommended in advanced
cancer patients receiving chemotherapy
 Difficulty of predicting survival is the main challenge for choosing the
right patients for TPN

91
Q

What are specific AAs that can be given

A

Leucine stmulates protein synthesis and insulin secretion → may have
anabolic properties

Glutamine & arginine ↑ immune competence, help wound healing :
could be beneficial pre and post‐operatively

92
Q

Omega 3 should not be given to patients with

A

Anti-coagulant therapy

93
Q

What chemical agenst can be given to patients to increase appetite

A

Progestational agents (megestrol acetate): ↑ appe􀆟te and
weight gain but not lean mass. Serious side effects: oedema,
thromboembolism.
 Corticosteroids: transient increase in appetite and well‐being. Only
for restricted periods (1‐3 weeks). Side effects: insulin resistance,
muscle wasting, osteopenia.
 Cannabicoids: dronabinol may have potential but inconsistent
evidence

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