Malnutrition & Older Adults Flashcards

1
Q

what are some risk factors for malnutrition in older adults?

A
  • decrease in bodily functions (GI, renal, liver)
  • chronic diseases
  • multiple medications
  • need of physical assistance for self-care
  • tooth loss/oral pain
  • poor diet (socioeconomic, social, changed tolerance)
  • reduce social contact
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2
Q

what elements are involved with the reduced appetite of elderly?

A
  • decrease in taste buds/receptors
  • decreased smell

in institutionalized settings, it is being more looked into to give more attention to the visual appeal of the food to increase appetite

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3
Q

factors for malnutrition in elderly?

A
  • sensory impairment
  • altered energy need
  • decreased physical activity
  • muscle loss
  • psychosocial
  • environmental
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4
Q

what is senescence?

A

condition or process of deterioration with age

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5
Q

why does aging happen?

A

prolonged exposure to stresses (drugs, uv light, mutagens, radiation) leads to gradual cellular mutations leading to errors in DNA and compromised protein synth (decreased cell functions)

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6
Q

talk about DNA repair

A

DNA repair enzymes are responsible. diet has influence on their health. There is evidence that folate deficiency leads to decreased capacity to repair DNA.

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7
Q

talk about the interactions between aging and hormone secretions

A
  • decreased GH. increases adipose tissue and decreases lean body mass
  • decreased testosterone/estrogen
  • decreased insulin
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8
Q

talk about GH and aging

A

there are parallels between individuals with GH disorders and aging with the same results to body composition, meaning treatment may be same. That said, the administration of these treatments led to side effects like carpel tunnel, headaches, tinnitus, and Alzheimer’s. Despite the seen improvement in LBM, there was no indication of its functional capacity for exercise/physical/cognitive

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9
Q

talk about Dehydroepiandrosterone-Sulfate (DHEA)

A

precursor to androgens/estrogens in peripheral tissues. generate 50% of androgens. drop with age for maintaining muscle strength, bone density, anti-inflammation, and psychological well-being.

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10
Q

talk about insulin resistance

A

seems to be due to increase in visceral and body fat. important bc increase in BG levels can increase risk of hyperglycemia, which can then lead to adverse effects from advanced glycosylation end products (AGEs). There is also indication that it leads to cognitive impairments like Alzheimer’s disease.

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11
Q

what is glycation?

A

non-enzymatic reaction between glucose and proteins that results in the cross-linking of proteins (advanced glycosylation end products)

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12
Q

what’s special about AGEs?

A

they’r hard to break down and they impact extracellular proteins
- scaffolding (maintaining integrity of blood vessel walls)
more prominent AGEs can lead to stiffening of blood vessel walls –> hypertension, increased risk of atherosclerosis

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13
Q

talk about free radicals

A
  • important function in stimulation of cell proliferation (e.g. increasing muscle mass w/exercise)
  • at high levels, they can damage macromolecules that can result in accumulated damage leading to disruptions in organ and tissue functions
  • caloric restriction (30-50%) appears to limit free radical damage –> increases lifespan especially with smaller animals, though quality of life seems compromised (less sex drive)
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14
Q

what’s the hormetic effect?

A

adaptation to demands

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15
Q

what is the mitochondrial free radical theory?

A

mitochondria are likely to be damaged by free radicals, which affects oxidative phosphorylation. This results in decreased capacity for the mitochondria to improve/duplicate. Damaged mitochondria tend to be cleared by autophagy, however if the damaged mitochondria continue on, when they replicate the produce mitochondria that don’t do oxidative phosphorylation, leading to compromised energy levels (not enough NAD+ generated).

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16
Q

what is immunosenescence?

A

diminishment in immune competence with age where T and B cells lose function (adaptive immune response). We have a limited reserve of naive T cells diminishes over time and so the ability to mitigate pathogenic infections declines

17
Q

talk about cytomegalovirus

A

it’s linked with teratogenicity when with active exposures. it’s usually a passive infection tho, and constant exposure to it can deplete naive T cell reserve.

Also associated with increased susceptibility to chronic inflammatory diseases, esp in the elderly who are more susceptible to microbial infections.

18
Q

what is inflammaging?

A

there is chronic inflammation associated with the weakened immune system. increases risk of autoimmune disorders

19
Q

talk about age-associated dysbiosis

A

the bacteria in the gut are less prevalent/diverse, and the ones that remain are the pathogenic ones that participate in systemic inflammation. intestinal epithelium becomes more damaged, releasing proinflammatory factors into circulation. e.g. Clostridium difficile. Probiotics seem to be efficacious in limiting pathogenic activity.

Doing a fecal transplant from younger to older individuals seems to reverse age related changes in the gut microbiota. Animal models have seen increased lifespan as well.

20
Q

talk about the telomere theory

A

there’s a biological clock due to damage to telomeres (at tip of chromosomes). telomerases are there to keep them spic and span, but when this goes away, the “death gene” (P53) halts DNA replication. Damaged cells usually go through apoptosis which limits their proliferation, limiting the damage of functionality of any organ or tissue. With senescence comes the enabling of mTOR. Rapamycin and other mTOR inhibitors have been investigated to limit immunosenescence. Clinical trials have been using metformin to target this too.

21
Q

what kinds of physiological changes occur to elderly?

A
  • decrease in functional taste buds
  • decreased salivary secretion (xerostomia)
  • decreased esophageal function –> dysphagia
  • decreased gastric function/emptying
  • decreased liver/biliary function
  • decreased pancreatic secretion
  • change in intestinal morphology
  • change in intestinal morphology
22
Q

why is dysphagia bad?

A

causes choking and death

23
Q

what does the decline in gastric function/emptying lead to?

A
  • less gastric acid production (B12 bioavailability)
  • decreased parietal cell mass
  • decreased maintenance of commensal flora
  • increased risk of ulcers from dyspepsia
24
Q

decreased biliary function leads to what?

A

bile is involved in the emulsification of lipids, making fatty foods more difficult to take in and poor digestibility of cruciferous vegetables.

25
Q

what kinds of things happens as a result of changed intestinal morphology?

A
  • constipation
  • lactose intolerance which leads to
  • increased risk of vit A, D, B2, and protein deficiencies