obesity Flashcards

1
Q

cause of obesity

A

disbalance between energy intake and expenditure

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2
Q

metabolic disorders that characterize obesity

A

insulin resistance, type 2 diabetes, fatty liver disease, atherosclerosis, hypertension, hypercholesterolemia

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3
Q

hunger

A

CNS/hypothalamus receives info when blood sugar is low from Ghrelin

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4
Q

hunger hormones/peptides

A

hypothalamic peptides (neuropeptide Y)
Ghrelin (from empty stomach; binds to G receptors)
Dopamine stimulates appetite

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5
Q

hunger stimulation

A

hypothalamic secretion of thyroid and adreno-corticoids cause metabolism and utilization of food stuffs

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6
Q

satiety

A

CNS receives inhibitory signals from leptin which antagonizes ghrelin

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7
Q

satiety hormones/peptides

A

CCK + PYY + GLP-1; from the GI
Insulin
Leptin (from adipose tissue)
Lipid metabolism byproducts such as ketones

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8
Q

CCK

A

secreted in duodenum when protein and fat are present to trigger feedback mechanism

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9
Q

lipid metabolism byproducts such as ketones

A

shut off mechanism for hunger
can cause metabolic acidosis

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10
Q

keto diet

A

high lipids and protein and little to no carbs
- less intake due to quicker satiety
- more energy stores broken down to satisfy requirements
- risk of ketoacidosis

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11
Q

how keto diet works

A

based on hunger inhibitory mechanisms; quick satiety due to CKK inhibitory action when released in response to protein/fat in duodenum
- puts person in state of ketosis
- high protein breakdown strains renals
- caloric intake low

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12
Q

ketosis

A

when there arent enough carbs to burn for energy so body burns fat

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13
Q

causes of decreased hunger

A

sympathetic stimulation (pain, stress, trauma)
GI pathologies
Low iron (=low ghrelin)

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14
Q

simple carbs

A

better for athletes because they provide fast energy

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15
Q

fiber

A

not digested but provides satiety and no glucose so its good for diabetic patients

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16
Q

calorie use in obese patients

A

excess nutrients stored as glycogen and triglycerides in adipose cells which leads to weight gain

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17
Q

BAT (brown adipose tissue)

A

exists to insulate and create energy; has lots of mitochondria; “thermogenic organ”
- born with it and then declines over time
- people living in cold climates may have more

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18
Q

BAT synthesis

A

myogenic origin and more similar to skeletal muscle than to WAT
- differentiated differently than WAT

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19
Q

WAT (white adipose tissue)

A

an endocrine organ
provides energy, insulation, and protection; can be subcutaneous and visceral
- highest in obese, female, and elderly

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20
Q

WAT synthesis and secretion

A

leptin, adiponectin, cytokines

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21
Q

adipose cell composition

A

triglycerides and organelles

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22
Q

adipose cell function

A

uptake of excess nutrients –> transformed into triglycerides –> release 3 fatty acids and glycerol (then to glucose) for energy use

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23
Q

fat location in males

A

controlled by testosterone
- usually goes to abdomen

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24
Q

fat location in females

A

controlled by oestrogen
- usually goes to hips

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25
Q

leptin

A

satiety hormone
- decreased distribution and receptor binding creating resistance when WAT is high and increases hunger signaling

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26
Q

if total numbers of leptin are elevated

A

will lead to alternate binding sites –> pro inflammatory mediation and degradative connective tissue enzymes created which creates risk for arthritis, osteoarthritis, joint deformity and back pain

27
Q

adiponectin

A

hormone that suppresses fatty acid influx to liver, enhances insulin function, and acts as an anti inflammatory

28
Q

relation between high WAT and adiponectin

A

decreased synthesis and secretion which leads to
- increased fatty acid deposition
- insulin resistance
- inflammation indicated by C-reactive protein
and all these put at risk for cardiac disease, cholecystitis, hyperglycemia, DM II

29
Q

relation between high WAT and cytokines

A

increases levels of cytokines due to increased number of cytokine synthesizing adipose cells and puts at risk for inflammatory diseases, atherosclerosis, metabolic resistance= insulin resistance

30
Q

body fat accumulation

A

high sugar increases dopamine which causes person to eat more
low estrogen
genetic predispositions

31
Q

firmicutes (bacterial phylum)

A

f=fat cells and fat cells=firmicutes
- high in obese patients=higher digestion= higher absorption of fats

32
Q

bacteroidetes (bacterial phylum)

A

higher in lean patients=lower fat absorption

33
Q

treatment of firmicutes and bacteroidetes

A

probiotics to balance host flora as well as dietary fiber

34
Q

lean adipose tissue effects

A

increase in anti-inflammatories, antioxidants, insulin sensitivity, angiogenesis

35
Q

obese adipose tissue effects

A

increase in inflammation, oxidative stress, insulin resistance, dysfunctional angiogenesis

36
Q

men waist circumference for obesity

A

if greater than 102cm then they are greatly at risk/obese

37
Q

women waist circumference for obesity

A

if greater than 88cm then they are greatly at risk/obese

38
Q

drug interactions in obese patients

A

increased half life and elimination due to meds going to fats

39
Q

cholecystitis

A

gallbladder inflammation
high fat intake–> low fatty acid oxidation d/t low adiponectin–> pro inflammatory state–> high cholesterol in bile –> gallstone formation

40
Q

cholecystectomy

A

surgical excision of gallbladder

41
Q

obesity complications of cholecystectomy

A

impaired wound healing due to dysfunctional angiogenesis
pro inflammatory state
opioids are lipophilic so it can cause addiction or require higher doses due to increased half life and elimination

42
Q

osteoarthritis

A

degenerative disorder of articular cartilage
- ‘wear and tear’ affecting type II collagen fibril and proteoglycan

43
Q

osteoarthritis pathology

A

decreased proteoglycans and collagen–>tissue destruction due to pro-inflammatory mediators –> tissue destruction causing bone-bone articulating surface

44
Q

osteoarthritis treatment

A

NSAID’s and glucocorticoids (cortisone)

45
Q

DM type II

A

insulin deficiency or resistance due to inflammatory state
- low adiponectin and high cytokines

46
Q

sulfonylureas

A

antidiabetic for DM II
- increase beta cell insulin release; can cause hypoglycemia
- glyburide (Diabeta); used instead of metformin

47
Q

Glyburide (Diabeta)

A

a sulfonylurea used for DM II

48
Q

Biguanides

A

antidiabetic for DM II
- decrease glucose release
- Metformin (Glucophage)

49
Q

Metformin (glucophage)

A

a biguanide used for DM II
- number one drug of choice
- monitor liver

50
Q

thiazolidinediones

A

antidiabetic for DM II
- increase cellular blood glucose uptake
- Rosiglitazone

51
Q

rosiglitazone

A

a thiazolidinedione used for DM II
- monitor weight gain

52
Q

SGLT2 inhibitors

A

antidiabetic for DM II
-increase glucose excretion
- sanagliflozin (invokana)

53
Q

sanagliflozin (invokana)

A

a SGLT2 inhibitor

54
Q

GL1 receptor agonists

A

antidiabetic for DM II
- slow GI absorption and decrease appetite
- Dulaglutide (trulicity), Ozempic

55
Q

dulaglutide (trulicity)

A

a GL1 receptor agonist used for DM II
- monitor N&V as well as anorexia

56
Q

metabolic syndrome

A

group of reversible risk factors for CV disease and DM II
- can be the silent killer for people with obesity because while test values may appear normal they are on the higher end

57
Q

5 diagnostic components of metabolic syndrome

A
  • large waist circumference
  • elevated BP
  • low plasma HDL
  • elevated triglycerides
  • elevated fasting plasma glucose
58
Q

lipase inhibitors

A

decrease fat and triglyceride absorption in intestines through inhibition of lipase
- Orlistat (xenical)

59
Q

orlistat (xenical)

A

lipase inhibitor
- watch for decrease in lipophilic medications, fecal fat and leakage, GI bloating

60
Q

contrave (buproprion + naltrexone)

A

anorexiant (antidepressant with opiate antagonist)
- can be addictive so only good short term

61
Q

bariatric surgery

A

limits food intake/absorption by making stomach smaller cause less ghrelin production
-BMI must be over 40 to qualify for surgery

62
Q

post bariatric surgery

A

take vitamin and mineral supplements to ensure patient does not become malnourished due to bypass from duodenum where nutrients and vitamins are absorbed

63
Q

dumping syndrome

A

food exits stomach too quickly before it can be digested; high insulin release and sudden hypoglycemia
- watch for N&V, cramping, hypoglycemia
- can occur post bariatric surgery or with bolus feeding

64
Q

dumping syndrome treatment

A

smaller food amount and low simple suagr foods