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HUNT 243 exam > Adulthood/ older adults > Flashcards

Adulthood/ older adults Flashcards

1
Q

What are the 4 segments of adulthood & their characteristics?

A

early adulthood 20- 39 years
Becoming independent/ leaving parental home
Planning, buying & preppring food
Renewed interest in nutrion “for the kids”

Midlife 40s:
Active family responsibilities
managing schedules & meals becomes a challenge
Reviewing life’s accomplishment
Recognition of one’s mortality (interest for non-communicable diseases)

Sandwich: 50s:
Multigenerational caregivers (caring for children + aging parents + maintaining carrere)
High prevalence of chronic disease

Later adulthood: 60+:
Transition to retirement
More leisure time
Greater attention to PA & nutrition
Added significance for food choices & lifestyle factors (esp for chronic disease)
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2
Q

What are
Coronary Heart Disease (CHD)
Coronary Artery Disease (CAD)
Ischemic Heart Disease (IHD)?

A

damage that occurs when blood vessel become narrow & blocked

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3
Q

What is a myocardial infarction/ heart attack?

A

death of heart muscle due to interruption of blood supply

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4
Q

What is Atherosclerosis?

A

narrowing of heart vessel due to fatty plaque that intrudes into the lumen, blocking blood flow

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5
Q

What are statins.

A

MEDICATIONS THAT LOWER BLOOD CHOLESTEROL

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6
Q

How is Atherosclerosis initiated?

A
  1. Endothelial cells damaged
  2. Initiates the expression of cellular adhesion molecules
  3. Capture circulating monocytes U translate into intima
  4. Become macrophages (collect more fat) -> form foam cells (causes enlargement of plaque)
  5. foam cells accumulate & causes toxic lipid cause
  6. Plaque ruptures
  7. platelets come to repair damage (cause thrombus formation: blood clot)
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7
Q

Why does Atherosclerosis have the potential to cause angina?

A

blood has to pump harder & faster ->

Heart attack occurs when greater portion is blocked

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8
Q

What are some heart attack symptoms in men & women?

A

Men:
Nausea & vomiting
Jaw, neck, back pain, chest pressure, shortness of breath

Women: nausea/ vomiting, jaw, neck & upper back pain, sometimes chest pain, pain in lower chest & upper abdomen
Shortness of breath, fainting, indigestion, extreme fatigue

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9
Q

What is a coronary artery bypass graft?

A

Attach another vein to heart; open up heart; stop heart

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10
Q

What is an antioplasty?

A

insert a capita into the femoral or radial artery

Inflate ballon which breaks up fatty plaques & stent is left behind to leave the artery open

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11
Q

Why do women fare worse with CHD?

A
  1. Women develop CHD 10years later than men as estrogen increases HDL & decreases LDL
  2. During menopause lose protective risk (same risk as men)
  3. more likely to have hyperlipidaemia, DM & HT
  4. Less likely to undergo tertiary care interventions to participate in cardiac rehabilitation
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12
Q

What are risk factors for CVD?

A
  1. Nutrition: dietary modification: most effective reduction of risk
  2. Glucose
  3. BP
  4. Cholesterol
  5. Smoking,
  6. weight
  7. sedentary
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13
Q

What are other modifiable risk factors of CVD?

A
  1. Low SES
  2. Mental ill-health
  3. Psychosocial stress
  4. Alcohol use
  5. Use of certain medications
  6. Left ventricular hypertrophy
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14
Q

What are non- modifiable risk factors of CVD?

A

advancing age
Hereditary/ family history
Gender
Race/ ethnicity

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15
Q

What is the relationship between blood cholesterol & heart disease?

A
  1. Risk of CHD decreases with 1 mmol/L lower serum cholesterol concentration
  2. Reduction in mortality for each 1 mmol/L decrease In LDL cholesterol
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16
Q

How does fat become lDL?

A
  1. Fat is packaged into chylomicrons
  2. fatty acids cleaved off
  3. Travel to liver
  4. Packaged into lipoproteins
  5. Fat is delivered to cells, as it loses flat becomes denser
    LDL -> disadvantageous to heart health
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17
Q

How is HDL protective?

A

picks up cholesterol form tissues & brings back to liver

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18
Q

What are the clinical guidelines for cholesterol?

A

Tot cholesterol <4 mmol
LDL cholesterol <2 mmol
HDL cholesterol > 1 mmol?L
Total: HDL: <4

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19
Q

What is an Atherogenic diet?

A
  1. promote deposit of plaque 2. characterised by high sat/trans fat
  2. low in V & F
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20
Q

Effect of different fats on cholesterol?

A
  1. Sat fat: increase all types (have neglible effect of steriac fatty acid)
  2. Trans-unsat: decrease HDl & increase LDL

3/ PUFA: decrease LDL & VLDL (sig reduces risk)

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21
Q

Why does stroke occur?

A

Occurs when the bloody supply is interrupted/ reduced. Preventing brain tissue from getting oxygen & nutrients (brain cells die in minutes)

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22
Q

What are the complications of stroke?

A
  1. Paralysis or loss of muscle movement
  2. Difficulty talking/ swallowing
  3. Memory loss/ thinking difficulties
  4. Cognitive dysfunction
    emotion problems
  5. Pain/Changes in self-care ability & behaviour
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23
Q

What are the 3 types of stroke?

A
  1. Ischemic: blood flow obstructed
  2. Transient ischemia attack: temporary ministroke
  3. Haemorrhagic stroke: weakened blood vessels ruptures spilling blood into brain
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24
Q

What is strokes modifiable risk factors?

A

Obesity, PA, heavy/ binge drinking, Hypertension, high cholesterol, diabetes, obstructive sleep apnea, CVD, family history

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25
Q

What is strokes non-modifiable risk factors?

A

age, ethnicity, sex (males more at risk), hormones

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26
Q

What is DASH (Dietary approaches to stop hypertension)?

A

A diet high in veges, fruits, low fat dairy products, wholegrains, poultry, fish & nuts
Less sat fat, more CHO, more protein, fibre & less cholesterol

designed to reduce BP

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27
Q

What is the composition of the dash diet?

A 
8,300 Kj
max sodium: 2,300 mg/day (1500 recommended)
6-8 sevrings grains
6or less servings meat, poultry/ fish
Fruit & veges: 4-5
Low fat dairy: 2-3
Fats & oils 2-3
weekly:
Nuts, seeds, dry beans & peas: 4-5
Less than 5 sweets
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28
Q

Why does visceral adiposity increase stroke risk

A
  1. Release cytokines (IL-6, TNF-a) which adversely affects cells, sensitivity to insulin, BP & blood clotting
  2. Releases free fatty acids: enter portal vein & travels to liver; Increases LDL & lowers HDL
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29
Q

What waist measurements are associated with an increased risk of CVD?

A

men&raquo_space; 101cm; women >88cm

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30
Q

What age related changes in energy expenditure occur in adults?

A

ecline in early adulthood (2.9%, 2% / per decade for men & women respectively)

31
Q

Why is high Triacylglycerides:

associated with increased risk CVD & diabetes

A

hyper triglycerides interfere with LDL & HDL metabolism (more small dense LDL & dysfunctional HDL)

32
Q

What is metabolic syndrome?

A

3+ of the following symptoms = metabolic syndrome

  1. Waist circumference (M: >102; W: >88)
  2. Fasting glucose: >100
  3. HDL (M: <40; W: <50)
  4. BP: >130/85
  5. Fasting triglycerides: >150
33
Q

What is metabolic syndrome a stronger risk factor for?

A

CVD, type 2 diabetes, stroke, fatty liver disease, chronic kidney disease etc..

34
Q

What are the 3 types of diabetes?

A

Type 1: minimal/ no production of insulin
Type 2: Defective production of insulin/ insulin resistance
Prediabetes: blood glucose marginally elevates & vascular changes occur

35
Q

What is the prevalence of diabetes?

A

Over 6% adults in NZ have diabetes

Ethnic differences: 15% pacific island (expected to increase to 40%)

36
Q

What are the complications of diabetes?

A

CVD, nerve damage, kidney damage, eye damage, foot damage, skin conditions, hearing impairment, Alzheimer’s disease, depression

37
Q

What is the ethology of diabetes?

A

Type 1: progressive autoimmune disease

Type 2: insulin resistance develops over time

38
Q

What are the physiological effects of diabetes?

A

frequent urination, increased thirst & hunger, fatigue, weight loss, blurred vision etc.
Micro & macrovascular complications

39
Q

How do we screen for diabetes?

A 
Family history (genetic)
History of gestational diabetes
Elevated HbA1c
racial/ ethnic background
sedentary lifestyle
Hypertension
Low HDL, high triglycerides, CVD 
PCOS
40
Q

What is glycated haemoglobin & what concentrationsof glaciated haemoglobin & fasting glucose are associated with diabetes?

A

Glucose binds to haemoglobin

  1. 50 mmol/mol = diabtetes
    - > fasting glucose >7
  2. 41-49 = prediabetes -> fasting glucose >6.1 – 6.9
  3. <40 diabetes unlikely -> <6
41
Q

What is medical nutrition therapy for diabetes?

A
  1. Diet flexibility & individualisation
  2. Enable to achieve glycemic, weight, lipid & BP goals
  3. Responsive to cultural preferences & maintain eating pleasure
  4. Teach how to use a glucometer
  5. Help increase PA
  6. May require pharmacotherapy (metformin)
42
Q

What did we look at during a CVD risk assessment?

A
  1. Age
  2. gender
  3. ethnicity
  4. NZ index of deprivation
  5. Family history: Premature ischaemic CVD; Type 2 diabetes
43
Q

What past factors are associated with CVD?

A 
angina
myocardial infarction
PCI
CABG
Ischemic stroke
TIA
peripheral vascular disease
Family hypercholesterolaemia
Artial filtriation
Duration of diabetes
Urinary
Smoking
Fasting glucose or glycated haemoglobin
BP
Lipid profile
Serum creatine
BMI
44
Q

When do we screen people with no risk factors for CVD compared to people with risk factors?

A

no risk factors:
M = 45; w = 55
High risk:
M = 30-35; W = 40-45

45
Q

What characterises a Mediterranean diet?

A
  1. High in plant foods, fruit, veges & wholegrains (focus on local & fresh foods)
  2. Sugar & honey assumed occasionally
  3. Low red meat; high fish
  4. Olive oil main fat
  5. Social interactions while eating
46
Q

What % does a Mediterranean diet reduce CVD events?

A

28%

47
Q

What are three theories of aging?

A
  1. Programmed aging:
    Hayflick’s theory of limited cell replication:
    + genetic cells divide according to programmed limit then divide (cell replication limit of 40-60 with no reason to stop replicating)
    + max life: 110-120 years
  2. Molecular clock theory:
    telemores act as protective caps on end of chromosomes (made up of 100os of TTAGGG)
    + tells us when one chromosome ends & another begins
    + end replication problem (telemoress replicate instead; shorten with every cell replication)
    + telemore attrition  with age (shorten with age0
    + loss of telemores stop chromosomes ability to replicate
  3. Free radical oxidative stress theory:
    Free radical: oxygen with unpaired electron (attacks because want to pair up with someyhing)
    + oxidative stress:
    Build up of reactive oxygen species from metabolic processes & environment
    + natural by-product of metabolism
    + essential to keep us safe from pathogens (used by immune system)
    + exposed to free radical from UB light, smoking & air pollution
    + ROS prolonged attacking is associated with long-term attack on tissues
    + associated with CVD, Alzheimer’s
    + can be neutralised by antioxidants
48
Q

Is it possible to slow ageing though nutrition?

A

food restriction to 50% voluntary consumption in lab animals as reduces metabolic rate, reduces H202 & superoxide production

49
Q

What are the benefits of energy rest in monkeys?

A

less diabetes, neoplasia, decrease CVD, scarponia & brain atrophy (age-related mortality also decreased; but more vulnerable to stressors)

50
Q

What are the adverse effects of severe food restriction?

A

Comprised ability to withstand stress; growth, fertility, osteoporosis, muscle mass loss

51
Q

What is functional age?

A

+ reflects the decline in function that occurs with time

+ heterogeneous

52
Q

What is the ‘Third Age”?

A

+ golden years
+ between retirement & age-related physical, emotional & cognitive limitations
+ Retired but healthy & active
+ Have the time to increase PA & give more attention to diet & healthy lifestyles

53
Q

What is The “Fourth age”

A

+ decline sin general health (weight & muscle loss -> frail -> vulnerable to stressors)
+ impaired nutrition
+ serious disease/ advanced aging (rest home care; if home socially isolated; rely on assisted living services; food & nutrition guidelines less relevant)

54
Q

What factors contribute to nutrition-related health?

A

poverty
lack of transport
Inability to shop
Inability to prep and cook meals
Failure to cater to ethnic & food preferences
inability to self-feed
Social isolation & lack of social support

55
Q

How does digestive function change as we age?

A
  1. absorption of macronutrients remain same
  2. Liver & biliary function retained but liver is smaller
  3. No reduction in pancreatic secretions
  4. No deficiency in intestinal morphology
56
Q

How does Taste & smell change as we age?

A

+ Starts to decline after 60 + leads to decreased satiety
+ less pleasure (cant differentiate flavours)
+ cant smell spoiled food
+ 75% have impairment (women affected less than men)

+ number & structure of taste buds not affected

57
Q

What dental changes occur with age & how do they effect nutrient intake?

A

57% edentulous; 36% functional dentition; 10% had ulcerated lesions

affects chewing, swallowing & taste

58
Q

How does saliva change as we age?

A

Thicker & more viscous with age

59
Q

What is the effect of changes in saliva flow?

A

affects ability to swallow

60
Q

How does Oesophageal motility change as we age?

A

+ not to effected with age
+ rare but occur with autonomic nervous system disturbances (stroke; parkinsons)
+ slower gastric emptying  early satiety
+ reduced gastric acid output

61
Q

How does Atrophic gastric change as we age?

A
  1. reduced secretion of HCL & Pepsin (secondary infection from helicobacter pylori)
  2. Bacteria overgrowth in stomach abused by decreased HCL secretion
  3. Can’t absorb b12 (can’t be dissociated from food)
  4. bacteria colonization of upper GIT takes up B12
  5. low B12 affects folate, calcium & iron absorption
62
Q

How does Hydration change as we age?

A
  1. Diminished sense of thirst & decrease in total body water

2. Kidney function decline: less able to concentrate urine & more water lost

63
Q

What is dehydration signs & symptoms?

A 
upper-body muscle weakness
Dry mucous membranes
Speech difficulty + confusion
Longitudinal tongue furrows
Dry tongue
Sunken appearance of eyes in sockets
64
Q

What are the effects of dehydration?

A
  1. Increased resting HR
  2. Susceptibility to pressure ulcers, UTI, pneumia
  3. Leads to confusion disorientation & dimentia
65
Q

What has the biggest effect on nutritional status & physical resilience in older adults?

A

+ muscular strength peaks at 30 then declines (2-3% per decade)
+ weight stable; fat replaces muscle
+ Decreased basal metabolic rate

66
Q

What are some Sacropenial age-associated changes in body composition:

A
  1. Muscle atrophy
  2. Increase in body fat
  3. subcutaneout to visceral; fat infilitrates into skeletal muscle
67
Q

What does sarcopenia lead to?

A

Fraility & dependance?

68
Q

What is frailty?

A 
A Geatric syndrome with 3+ conditions:
1. unintentional weightloss
2. self-reported exhaustion
3. weakness
4. slowness
5. low PA
Used as a measure of biological age
69
Q

What does frailty lead too>

A
  1. these lead to diability
  2. increased risk of falls
  3. increased risk of hospitalization
  4. leads to dependence & 5 year risk of death with fraility
70
Q

How can we measure fraility?

A

Walking Speed

Grip Strength

71
Q

What factors contribute to sacrpenia?

A

Nutrition

Muscle loss

72
Q

How does sarcopenia mask obesity?

A

because they don’t look frail

as losing muscle & fat is infiltrating muscle

73
Q

What is sarcopenia obesity associated with?

A

with higher risks of mobility disability, metabolic diseases, hypertension, CVD & mortality than either alone

HUNT 243 exam (3 decks)

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