physiology Flashcards

1
Q

how do you calculate BMI?

A

weight (kg) / height squared (m)

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2
Q

what are the BMI ranges?

A
<25 = normal 
25-29.9 = overweight
30-39.9 = obese
>40 = morbidly obese
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3
Q

what are the major contributor to disease and premature mortality in obesity?

A
  • type 2 diabetes
  • high bp
  • heart attack
  • cancers eg colon
  • osteoarthiritis
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4
Q

what are the consequences of obesity?

A
  • stroke (hypertension)
  • resp disease (sleep apnea)
  • heart disease
  • gallbladder disease
  • osteroarthiritis
  • dementia
  • NAFLD (fatty liver)
  • diabetes
  • cancer
  • hyperuricemia, gout
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5
Q

how does the CNS influence energy balance and body weight?

A
  • behaviour eg feeding and physical activity
  • ANS activity eg regulates energy expenditure
  • neuroendocrine system eg secretion of hormones
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6
Q

what do satiation signals do during meal times?

A
  • increase to limit meal size
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7
Q

what are the 5 satiation signals?

A
  • cholecystokinin (CKK)
  • peptide YY (PYY3-36)
  • glucogon-like peptide 1 (GLP-1)
  • Oxyntomodulin (OXM)
  • Obestatin
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8
Q

what does CKK do?

A

– secreted from enteroendocrine cells
in duodenum and jejunum. Released in proportion to lipids and
proteins in meal. Signals via sensory nerves to hindbrain and
stimulates hindbrain directly (nucleus of solitary tract (NTS)).

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9
Q

what does PYY3-36 do?

A

– secreted from endocrine mucosal L-
cells of G-I tract. Levels increase rapidly post-prandially. Inhibits
gastric motility, slows emptying and reduces food intake (Hypo).

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10
Q

what does (GLP-1) do?

A
  • product of pro-glucagon
    gene. Also released from L cells in response to food ingestion.
    Inhibits gastric emptying and reduces food intake (Hypo, NTS
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11
Q

what does (OXM) do?

A

– Also from pro-glucagon gene and
released from oxyntic cells and L-cells of small intestine after meal.
Acts to suppress appetite – mechanism and site 2unclear.

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12
Q

what does Obestatin do?

A

– peptide produced from gene that encodes ghrelin
and released from cells lining stomach/small intestine.
Suggested to reduce food intake – may act to antagonise the
actions of ghrelin – actions unclear at present.

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13
Q

what is ghrelin?

A
  • an octanoylated peptide
  • it i sproduced and secreted in the stomach
  • increased before meals and decrease after emals
  • peripheral ghrelin stimulates food intae and decreases fat utilisation
  • ghrlin-containing neurons in hypothalamus help to control fat metabolsim and increases lipogenesis
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14
Q

where are signals produced in response to body nutritional status sensed?

A

in the hypothalamus

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15
Q

which hormones report fat status to the brain and where are they released from? (adiposity signals)

A
  • leptin = made and released from fat cells

- insulin = made and released from pancreatic cells

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16
Q

what happens when you reduce leptin?

A
  • it mimics starvation, causing unrestrained appetite
17
Q

what are the biological roles of leptin?

A
  • food intake/enegry expenditure/ fat depositiom
  • peripheral glucose homeostasis/ insulin sensitivity
  • maintenance of immune system
  • angiogenesis
  • tumourigenesis
  • bone formation
18
Q

what causes food reward pathway

A
  • dopamine
19
Q

what drugs are used for obesity?

A
  • orlistat

- contrave

20
Q

what does orlistat do?

A
  • inhibits pancreatic lipase decreasing triglyceride absoption
  • reduced efficaty of fat absorption in small intestine
  • side effects = cramping and diarrhoea
21
Q

what does contrave (mysimba) do?

A
  • combination of bupropion + naltrexones
22
Q

what is liraglutide? (saxenda)

A
  • glucagon-like peptide 1 receptor agonists (GLP-1 - a saftey peptide)
  • higher doses than used for diabetes, produces weight loss
  • concerns = thyroid and pancreatic cancer
23
Q

what is bariatric surgery?

A
  • gastric by-pass - prodces sustainable weight loss
  • high level of complete resolution of type 2 diabeteres
  • restricts calorie intake and induced malabsorption of nutrients by resolution of T2D is not due to decreased energy intake
24
Q

what is adaptive thermogenesis?

A
  • thermogenic adipocytes - increase energy expenditure uncoupling of oxidative metabolism from ATP production