Module 5 - Blood Sugar Regulation Flashcards

1
Q

glycogenesis

A

insulin stimulates liver to convert glucose to glycogen and store it.

(genesis = creation)
-glycogenesis = creation of glycogen

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2
Q

insulin

A
  • hormone secreted by beta cells of pancreas
  • stimulates uptake of glucose into cells
  • insulin crucial for glycogen formation
    • brings glucose into liver cells that make glycogen
  • job is to facilitate transport of glucose into cells.

*imagine insulin being the key to the gate that lets glucose into the cell.

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3
Q

primary organs that regulate blood sugar

A
  • pancreas
  • liver
  • adrenal glands
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4
Q

glucagon

A

liver converting glycogen into glucose

  • alpha cells of pancreas produce and secrete glucagon
  • helps maintain blood glucose levels in btwn meals and during sleep by increasing blood glucose and returning it to normal levels
    • liver receives signal from hormone glucagon and in 2 ways makes sugar:
      1. glucagon promotes breakdown of glycogen to glucose, which is released into circulation (glycogenolysis)
      2. glucagon signals for another activity in our liver that will generate glucose: amino acids (protein) will be taken up from our circulation by our liver and used to make glucose (gluconeogenesis)
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5
Q

glycogenolysis

A

glucagon promotes breakdown of glycogen to glucose, which is released into circulation.

("lysis"= breakdown/loosening of)
glycogenolysis = breakdown of glycogen to glucose
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6
Q

gluconeogenesis

A

amino acids, from the body’s circulation, will be taken up by the liver and used to make glucose.

done during sleep

(neo = new; genesis = creation)
gluconeogenesis = creation of new glucose through protein
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7
Q

big ideas of blood sugar regulation

A
  1. primary organs of blood sugar regulation: liver, pancreas, adrenals
  2. NEVER before in history of mankind have we had an emergency eed to LOWER blood sugar (until we started consuming large amts of refined carbs/sugars)
    - refined sugar current event (30-40 yrs)
    - pancrease overcompensating by dumping as much insulin as possible in body, casuing blood sugar to go down excessively, which means glucagon, cortisol, epinephrine all racing to bring sugar up again.
    • the fact that our bodys have 3 hormones to raise blood sugar and only 1 hormone to lower it suggests that our body’s primary functions were never meant to consume this much sugar.
  3. american are inundating their bodies w/sugar and refined carbs
    - avg is at least 140 lb of refined sugar in a year
  4. reducing insulin surges through adjusting macronutrient ratios will help body utilize fats and ketones for energy rather than glucose
    - bring up fat macro
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8
Q

pancreatic hormones

A

insulin
- increases uptake of glucose by muscle and fat cells
- increases amt of glycogen in muscle and liver
- increases fatty acid synthesis from excessive carbs
- decreases fa breakdown and mobilization from fat
tissue
glucagon
- increases liver glycogen to glucose release into blood
- increase fat breakdown and mobilization from fat tissue
- increases gluconeogenesis

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9
Q

liver

A
  • filters blood in digestive track before sending it to the rest of the body
  • responsible for maintaining blood glucose level over short and long periods of time
  • responsive/healthy liver critical for blood sugar regulation
  • stores glucose as glycogen (glycogenesis: glucose -> glycogen)
  • produces glucose from glycogen fro circulation (glycogenolysis: glycogen -> glucose)
  • converts protein into glucose (gluconeogenesis)
    creates ketones

** liver receiving signals from pancreas to convert glucose/glycogen

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10
Q

adrenals

A

2 glands: medula (middle) and cortex (bark/outer layer)

cortex has 3 zones that each produce separate hormones:

  • glomerulosa (outer layer)
    • aldesterone
  • fasciculata
    • cortisol (glucocorticoid)
  • reticularis
    • sex hormones
      • testosterones, progesterones, estrogen
  • body’s “buffer zone”
    • helps us cope w/stress
    • helps us to perform and adapt flexibly to demands of everyday life
    • enables us to go beyond normal physicality when needed (adrenaline rush)
    • helps us to recover within reasonable time
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11
Q

coritsol

A
  • adrenal hormone secreted by adrenal cortex (outer layer)
  • released when blood sugar levels low and not sufficiently supported by glucagon (liver converting glycogen into glucose)
  • mobilizes proteins from skeletal tissue that’s converted in liver into glucose (gluconeogenesis) -> through catabolism
  • replenish glycogen storage (glycogenesis)
  • stimulates breakdon of triglycerides and release of fatty acids from adipose tissue (lipolysis: breakdown for fats)
  • anti-inflammatory properties (cortisol shots)
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12
Q

epinephrine

A

epinephrine (adrenaline)

  • stimulates liver to convert glycogen back to cluose (glycogenolysis) for release into bloodstream (speeds up process)
  • stimulates liver to produce glucose from proteins and fats (gluconeogenesis) and release into bloodstream
  • increases heart rate and blood pressure
  • adrenal medulla sends out epinephrine
  • stimulation to sympathetic system

norepinephrine (noradrenaline)

  • shuttles blood away from deep organs and to muscles and heart for action
  • works in conjunction w/epinephrine
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13
Q

adrenal hormones

A

epinephrine

  • increases glycogen breakdown in liver and skeletal muscle
  • increases liver glycogen to glucose release into blood
  • increases fat breakdown and mobilization from fat tissue
  • heart rate increases, blood flow to heart, muscles and liver increases, dilates airways by triggering sympathetic response in ANS (autonomic nervous system)
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14
Q

glycation

A
  • glucose reacting w/protins resulting in “sticky proteins” (think fingers [proteins] and taffy [sugar]. hard to move, but doable, unless your fingers are stuck in taffy for a while and no movement for a while)
  • proteins can’t be used by cells for structure or communication within cell or to other cells
    • sugars start to glue over proteins and can’t send/receive signals
  • process is accelerated by elevated blood sugar levels
  • proteins covered in sticky sugar become cross-linked and begin to harden (glue)
  • every time blood sugar spikes, AGEs (associated glycation end products) are created
  • surface of arteries, organs’ tissue, joints, cell membranes all become hardened by glycation
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15
Q

effects of 3 organs if glucose unstable

A

pancreas
- eventually wears out, producing insufficient quantities or quality of insulin (pancreatic fatigue)

liver

  • difficulty converting glycogen and proteins/fats to glucose (gluconeogenesis)
  • if liver is overworked and uses up nutrients/ability to do its job, if you’re eating bad fats/lots of fructose, liver becomes fatty and starts to dysfunction even more

adrenals

  • go into state of exhaustion
    • affected by blood sugar going up and down
      • when adrenals exhausted, it will keep dropping blood sugar levels
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16
Q

hypoglycemia

A

abnormally low glucose levels

- sugar can drop below 50

17
Q

primary issues of hypoglycemia

A
  • fatigue
  • insomnia
  • depression
  • infertility (bc of effect on adrenals)
  • slow metabolism and weight issues
  • endocrine issues
18
Q

signs and symptoms of hypoglycemia

A
  • craving sweets
  • irritable if meals are missed
  • depend on coffee
  • feels lightheaded if meals are missed
  • jittery and shaky
  • easily upset, nervous
  • memory issues
  • blurred vision
19
Q

hypoglycemic behavior

A
  • use of high glycemic snacks or chronic snacking
  • use of caffeine or nicotine to suppress cravings
  • eating sweets instead of meals
  • lack of fat and protein and fiber in meals
  • easily irritable
  • highly fluctuating energy
20
Q

insulin resistance

A
  • state which insulin receptor sites become unresponsive to binding of insulin
    • insulin is signalling but receptors on cell membrane not responding.
  • down regulation of insulin bc of excessive exposure to insulin
    • receptors closed its doors bc too much insulin wants to come in
  • glycation where sugar is sticking to proteins of cell membrane affecting cell membrane’s ability to receive signal from insulin
    • glycation starts to glue over receptors and can’t receive signal
  • glucose levels +124
21
Q

primary issues of insulin resistance

A
  • fatigue
    • if receptor sites are blocked, glucose (energy) can’t get into cell
  • can’t lose weight
    • insulin resistance first happns in liver, then in muscles (if liver closes doors), then settles in fat cells (if muscles reject), and will keep adding to fat until it plateaus and blood sugar spikes, resulting in type 2 diabetes.
  • joint issues
  • depressed and mood disorder
  • thyroid issues
  • fertility
  • endocrine imbalances
  • slow healing
  • premature aging
    • more glucose = more glycation rising in body
  • memory failing
22
Q

causes of insulin resistance

A
  • lack of exercise and movement
  • overeating, chronic snacking
  • eating sugar for pleasure
  • chronic prolonged stress
    • adds more glucose by constantly breaking down muscle
  • sugar burning metabolizer
23
Q

signs and symptoms of insulin resistance

A
  • fatigue after meals especially high carb meals
  • craving sweets
  • weight gain and difficulty losing weight
  • must have desserts after eating
24
Q

type 2 diabetes

A
  • loss of beta cells fuction of pancreas caused from chronic prolonged demands of high insulin output as a result of high glycemic diet and stress
  • elevated levels of blood sugar bc of insulin resistance (cells of body have become nonresponsive to insulin)
  • non-insulin dependent
  • glucose level tend to be well over normal (+124)
25
Q

type 1 diabetes

A
  • client loses ability to make insulin
  • caused by destruction of beta cells of pancreas by virus or autoantibody attack
    • pancreas no longer working
26
Q

AGEs

A

Associated Glycation End Products

  • proteins that have been damaged by sugar
  • changes bread from soft and pliable to hard and stiff c proteins and sugars form cross-links
    • same thing happens inside body as AGEs cross-link normal mobile proteins
  • clinical implications of having tissues hardened by sugar-protein cross-links are far reaching. surface of arteries, organ’s tissue, joints, cell membranes all become hardened by glycation
27
Q

how to evaluate a sugar burning metabolizer

A
  • can’t effectively access stored fat for energy
    • can’t use beta for oxidations. can only go 2-3 hrs without food before going crazy hungry; can’t skip meal.
  • can’t effectively access dietary fat for energy
    • if they’ve eaten fat, can only use the sugar portion for energy; can’t burn fat
  • depends on “kindling wood”, quick burning source of energy
    • burns glycogen quickly; more dietart fat being stored than burned
  • burns through glycogen fairly quickly during exercise
    • uses goos to restore glycogen
    • most susceptible to hittng wll/getting bonked during workouts
  • less able to be satiated
  • insistent hunger
  • impaired beta-oxidation of fat
    • can’t break down fat for energy
  • increased carb cravings and intake
  • difficulty burning fat for weight loss
28
Q

how to evaluate fat burning metabolizer

A
  • burns stored fat for energy throughout the day
    • can skip meals w/o being cranky
  • able to effectively oxidize dietary fat for energy
    • if you add lots of fat to a sugar metabolizer, they can’t burn the fat and will gain weight
  • have plenty of energy on hand
  • can rely more on fat for energy during exercise, sparing glycogen for when you need it
    • don’t need goo
  • have no change in energy after meals
  • sustained energy btwn meals
  • fat burners can still burn sugars when needed, but sugar burners can’t burn fat when needed
  • can handle some carbs along w/some fat
  • can empty glycogen storage throughout intense exercise
  • refill those stores
  • burn whatever dietary fat isn’t stored
  • easily access and beta oxidize fat that’s stored when it’s needed
    burn energy like a big fat log in a fireplace
29
Q

test points for adrenals

A
  • Ragland’s Test
    • blood pressure (lying down then quickly standing up)
  • Paradoxical Pupillary Response
    • eye’s adaption to light in dark room
  • chapman reflex
    • 2” , ^ of umbilicus
  • posterior ilium/short leg
    • pulling on legs
  • inguinal ligament tenderness
    • btwn ASIS and lateral edge of pubic bone
30
Q

Ragland’s Test

A

purpose
- determine presence/severity of adrenal dysfunction

procedure

  • tell client to lie on back
  • place blood pressure cuff on arm of choice and determine systolic pressure
  • pump up cuf again 15 mm/hg higher than systolic pressure
  • while supporting their arm, tell client to stand up quickly
  • immediately release valve to determine standing systolic pressure w/i seconds of client arising

scoring

  • excellent: 6-10 pt rise in systolic upon standing
  • fair: systolic stays the same
  • poor: systolic drops up to 10 pts
  • failure: systolic drops 11-20 pts
  • exhaustion: systolic drops +20 pts
31
Q

Paradoxical Pupillary Response

A

purpose

  • determine ability of eyes to adapt to light
  • indication of adrenal dysfunction

procedure

  • darken room and wait 15 secs
  • tell client to look at fixed point and not blink
  • position light by client’s ear and hold light 6-12 inches from head
  • move light towards eye and aim light at pupil at app. 45 degree angle
  • observe reaction of pupil for 20 secs

scoring

  • excellent: pupil constricst/holds tight for 20 secs w/o pulsing
  • fair: pupil holds, but pulses after 10 secs
  • poor: pupil pulses and becomes larger after 5-10 secs
  • failure: puil pulses and becomes gradually larger over first 10 secs
  • extreme exhaustion: puil immediately becomes larger or fails to constrict
    • rule out drugs or neurological dysfunction
32
Q

test points for pancreas

A
  • chapman reflex
    • left 7th intercostal
  • right thenar pad tenderness
    • right thenar pad (hand)
  • t6/t7 tender close to point
    • back, under shoulder bone
33
Q

test points for liver

A
  • dr. dejarnette’s digns

- 3rd rib

34
Q

explain the damage caused to our bodies by glycation and the blood sugar impacts of a diet high in refined carbs and low in fats and proteins

A
  • *overburdens organs of blood sugar regulation due to high blood glucose and due to lack of blood glucose metabolism modulators
    • high carb foods – even sprouted and properly prepared whole grains or starchy veggies – all have an effect on blood glucose. after eating meal high in carbs and low in fats/proteins, the digestive tract breaks down carbs and turns them into sugar.
      • proteins and fats not turned into glucose by same processes, so they have little to no effect on blood glucose level
  • pancreas under constant stress to produce more insulin
    • too much insulin secretion over time can cause high blood pressure, high levels of triglycerides, obesity, etc.