Module 5 - Blood Sugar Regulation

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  1. MO: What are big ideas for Blood Sugar Regulation?
    1. The primary organs for blood sugar regulation are pancreas, liver and adrenal glands.

    2. Never before in the history of mankind have we had an emergency need to LOWER blood sugar; not until we started consuming large amounts of sugar & refined flours.

    3. Americans are inundating their bodies with sugar and refined carbohydrates. Avg. is 140 lbs/person/year.

    4. Reducing insulin surges through adjusting macronutrient ratios will help the body utilize fats and ketones for energy rather than glucose.
  2. MO: What is interaction of pancreas, liver & adrenals?
    Endocrine portion of pancreas is a small cluster of cells called Islets of Langerhans (about 1% of pancreas).  Islets of Langerhans contain Alpha cells that make Glucagon and Beta Cells that make Insulin.  Insulin & glucagon signal the liver to either store or release glycogen.

    Liver is primary organ responding to hormone messages (insulin/glucagon/cortisol/ephinephrine)  regarding high or low blood sugar. A healthy liver is essential to good blood sugar regulation. Stores glucose as glycogen; breaks down glycogen to form glucose; makes glucose from proteins (gluconeogenesis); makes ketones.  If the liver and muscle fiber glycogen stores are full, the liver converts the remaining glucose to triglycerides and cholesterol for storage.

    Adrenals are body's emergency response system.  Produce hormones that raise blood sugar in the event glucagon is not doing its job or in other emergency situations when additional glucose is required.  Hormones are cortisol & epinephrine.
  3. MO: What is gluconeogenesis?
    The creation of glucose from primarily proteins (some fat, but insignificant proportion).
  4. MO: What is Glycogenolysis?
    The breakdown of glycogen (the stored form of sugar) to form glucose.  In the liver this glucose is released into the bloodstream; in the muscle cells this glucose is used locally.
  5. MO: What is Glycogenesis?
    The creation of glycogen (the stored form of sugar) from multiple glucose molecules.
  6. MO: Describe insulin
    • Hormone secreted by Beta cells of pancreas (Phase I initially stimulated by acetylcholine from vagus nerve before food is digested; Phase 2 based on rise in blood sugar from digested food).
    • Facilitates transport of glucose into cells for fuel or for storage; increases uptake of glucose by muscle and fat cells; does so by activating cell's GLUT transporters so they come out and grab the glucose.
    • Crucial for glycogen formation (glycogenesis); brings glucose into liver cells that make glycogen; increases amount of glycogen in muscle and liver
    • Increases fatty acid synthesis from excessive carbohydrates
    • Decreases fat breakdown and mobilization from fat tissue
  7. MO: Describe glucagon
    • Produced & secreted by the Alpha cells of pancreas. Helps maintain blood glucose levels in between meals.
    • Increases glycogenolysis in liver to convert glycogen to glucose and release it into bloodstream.
    • Increases fat breakdown and mobilization from our adipose tissue (alternate energy source in situation of low glucose)
    • Increases gluconeogenesis in liver (making glucose from mainly proteins-some fats).
  8. MO: Describe cortisol.
    • Adrenal hormone secreted by adrenal cortex
    • Released when blood sugar levels are low and not sufficiently supported by glucagon
    • Mobilizes protein from skeletal tissue--increases amount of amino acids in the blood--that is then converted in liver to glucose (gluconeogenesis)
    • Increases blood sugar through gluconeogenesis
    • Stimulates breakdown of fatty acids and release of triglycerides from adipose tissue (lipolysis)
    • Has anti-inflammatory properties
    • Bottom line: Cortisol increases blood glucose levels by telling the body to break down structures to release fat & protein into the blood. The fat & protein is then converted to glucose.
  9. MO: Describe epinephrine
    • Also called adrenalin. Released by adrenal medulla.
    • Stimulates liver to produce glucose from glycogen for release into bloodstream. Speeds up glycogenolysis!
    • Stimulates liver to produce glucose from proteins & fats for release into bloodstream.
    • Increases heart rate & blood pressure.
    • Creates a BIG SUGAR DUMP into bloodstream.
    • (Norepinephrine shuttles blood away from the deep organs and toward muscles and heart for action.)
  10. MO: Describe hypoglycemia
    Hypoglycemia is a state of blood sugar dysregulation in which blood sugar is driven too low by the pancreas, which thinks it's responding to an emergency.  When it drops, a new emergency is created in which the pancreas has to pump out glucagon and the adrenals need to fire to produce cortisol or even epinephrine to bring it back up.
  11. MO: Describe insulin resistance
    • Refers to a state in which insulin receptor sites become unresponsive to the binding of insulin.
    • Down Regulation of Insulin because of excessive exposure to Insulin.
    • Glycation where sugar is sticking to the proteins of the cell membrane affecting cell membrane's ability to receive signal from Insulin.
  12. Causes of insulin resistance.
    • Lack of Exercise and Movement
    • Over eating, Chronic Snacking
    • Eating Sugar for Pleasure
    • Chronic Prolonged Stress
    • Sugar Burning Metabolizer
  13. MO: Describe Type 1 & Type 2 Diabetes
    • Type 2 involves 2 main things:
    • 1. Loss of Beta Cell function of the pancreas due to chronic prolonged high insulin output as a result of high glycemic diet and stress.
    • 2. Elevated levels of blood sugar due to Insulin Resistance.

    • Type 1:
    • 1. Caused by destruction of Beta Cells of the pancreas by a virus or autoimmune attack.
    • 2. Requires administration of insulin for life ("insulin-dependent diabetes").
  14. Describe Metabolic Syndrome.
    • Chronically elevated blood sugar (preceded by development of insulin resistance)
    • High triglycerides (over 150)
    • Weight gain/can’t lose weight
    • High blood pressure.
  15. MO: What is glycation?
    Glycation is glucose reacting with proteins to form “sticky proteins” or AGEs (Advanced Glycation End Products)
  16. MO: Describe how glycation damages the body and the impacts of high refined carb consumption.
    • Glycation forms sticky, damaged proteins that cannot be used by the cells for structure or communication within the cell or to other cells.
    • The proteins covered in sticky sugar become cross-linked and begin to harden, forming AGEs.
    • Clinical implications of having tissues hardened by sugar-protein cross links are far reaching. The surface of arteries, organ’s tissue, joints, cell membranes, all become hardened by glycation.
    • Also interferes with insulin's ability to do its job, glycated proteins can block insulin receptor sites, so blood sugar stays high and vicious cycle is created.
    • Glycation is accelerated by elevated blood sugar levels, which are caused by high refined carb consumption.
    • There is always some glycation occurring because there is always some glucose in the blood.  Glycated proteins cleared via the kidneys.  Problem is with chronically high glucose levels... clean-up system is overwhelmed.
  17. What are AGEs?
    • Associated Glycation End Products
    • AGEs are proteins that have been damaged by sugar.
    • AGEs cross link normally mobile proteins.
    • Clinical implications of having tissues hardened by sugar-protein cross links are far reaching. The surface of arteries, organ’s tissue, joints, cell membranes, all become hardened by glycation.
  18. MO: Should we be sugar burners or fat burners?
    • Our metabolisms were designed to be energized by fats and glucose (primarily fat).
    • Fat burning, using fat for energy, is the normal and preferred metabolic state of the human body.
    • Our culture is primarily living off the energy of glucose.
    • Sugar Burning Metabolizing turns off our Fat Burning Metabolism.
  19. MO: How do you evaluate a sugar burner?
    • A Sugar-Burning Metabolizer can’t effectively access stored fat for energy.
    • Those who primarily burn sugar for energy can’t effectively access dietary fat for energy.
    • A sugar-burner depends on a “kindling wood,” quick burning source of energy
    • A Sugar-Burning Metabolizer will burn through glycogen fairly quickly during exercise.
    • Signs and Symptoms of a Sugar-Burning Metabolizer:
    • – Less able to be satiated
    • – Insistent hunger
    • – Impaired beta-oxidation of fat
    • – Increased carbohydrate cravings and intake
    • – Difficulty burning fat for weight loss
  20. MO: How do you evaluate a fat burner?
    • Fat Burning Metabolizers burn stored fat for energy throughout the day.
    • Able to effectively oxidize dietary fat for energy.
    • Have plenty of a energy on hand.
    • Can rely more on fat for energy during exercise, sparing glycogen for when it is needed.
    • Have no change in energy after meals.
    • Sustained energy between meals.
  21. MO: Test points for Blood Sugar Regulation
    • Ragland's Postural Hypotension
    • Paradoxical Pupillary Reflex
    • Chapman Adrenals (LNT)
    • Posterior Ilium/Short Leg (LNT)
    • Inguinal Ligaments (LNT)
    • Chapman Pancreas/Spleen (7th L) (LNT)
    • Right Thenar Pad
    • T6/T7 Close to Spine on Right
    • Murphy's Sign
    • Chapman Liver/Gallbladder (6th R) (LNT)
    • Liver Point (3rd Rib) (LNT)
  22. MO: Test points for Sugar Handling Functional Evaluation - ADRENALS
    • 1. Ragland's Postural Hypotension
    • Poor adrenal function is often manifested by dizziness upon standing up too quickly. This is because the body normally compensates for gravity by briefly increasing blood pressure upon standing; this function is controlled by the adrenals.

    • Procedure: Ask the client if they know their normal blood pressure and whether there is any reason not to take BP, like recent breast surgery, lymph node removal, stents...  Measure client's blood pressure supine.
    • Ask client if they ever get dizzy when standing quickly; advise that if they should become dizzy during the test, you will have hold of their arm for support.  Pump the cuff up 15-20 mm/Hg higher than the first systolic reading and, while supporting the client’s arm, have them stand up quickly. As they are standing quickly release the BP cuff valve to get a second BP reading. You must take the reading within 5 seconds of their feet hitting the floor for accuracy. If you take longer than 5 seconds you miss the “event” which is the adrenal response for a need to raise/stabilize blood pressure when you stand quickly from a resting position. The indicator is the Systolic reading only.

    • Scoring:
    • Optimal = +6 to +10 points.
    • Fair = + or - 0
    • Poor = -1 to -10 points
    • Fail = -10 to -20
    • Exhaustion = Over -20

    • 2. Paradoxical Pupillary Reflex
    • Procedure:  Ask for contraindications:  history of head trauma within last 2 years, cataracts, lasik surgery, neurological dysfunction, psychotropic drugs (pot) or colored contact lenses. Darken room and let client's pupils dilate for a minute. Instruct client to look straight ahead and try not to blink. Shine a pen light (bring around from side of head) at about a 45-degree angle and 6-12" away into the eye.

    • Scoring:
    • Excellent = Constricts & holds for 20 seconds
    • Fair = Constricts and holds for 10 sec then pulses
    • Poor = Constricts & pulses, then enlarges after 5-10 sec
    • Fail = Constricts & pulses, then enlarges almost immediately
    • Exhaustion = Constricts & immediately enlarges or fails to constrict.

    • 3. Chapman Reflex Adrenals
    • Client supine with abdominal muscles tightened by lifting the head as if looking at toes.  Palpate 2 anatomical inches lateral and 2 anatomical inches superior to the umbilicus bilaterally. Palpate with one finger A>P  as you are feeling for small “pea-like” nodules that sit on top of the abdominal muscle. Ask for tenderness rating. Record each side.  LNT.

    • 4. Posterior Ilium/Short Leg
    • Procedure:  Position the client either face up or face down. Either GENTLY pull on the legs to help straighten their position or ask the client to push their heels together and release – this will help straighten their position. Then holding the client’s feet together, determine if one leg is shorter than the other) byplacing your thumbs or fingers on their medial malleolus (anklebones). You can compare the anklebones or compare the seams of the shoes where the heels attach.  LNTs really well.

    • 5. Inguinal Ligament Tenderness
    • Sartorius muscle governed by the adrenals.  They also influence laxity of your ligaments.  If one inguinal ligament is tighter than the other, the leg with the tighter ligament will be shorter.
    • Procedure:  Always ask permission before palpating a sensitive area. The Inguinal Ligament runs between the ASIS and the lateral edge of the pubic bone. Palpate entire ligament by drawing your fingers back and forth across it like a bow on a violin at a 90 degree angle. Press  A>P while doing so. If there is pelvic instability, the ligament on one side will be tight and the other side flaccid. Palpate both sides for tenderness and tension.  LNT.
  23. MO: Test points for Sugar Handling Functional Evaluation - PANCREAS
    • 1. Chapman Reflex Pancreas/Spleen (endocrine as opposed to exocrine digestive function)
    • 7th  intercostal space on the left, midmammary line. Find the 6th  intercostal space and move down and slightly lateral. When locating the 7th intercostal space if you move to the xiphoid, you will be below it. Single finger palpation, A>P.  LNT.

    • 2. Right Thenar Pad Tenderness
    • Draw a circle around the right thenar pad. Directly in the middle of this imaginary circle there should be a slight indentation. Probe deeply into this point. Palpate for tenderness. Often the indicator is a sharp pain.  DOES NOT LNT.

    • 3. T6/T7 Close to Spine
    • Located on the right side of the spine only! Locate the bottom of the scapula (wing) either right or left side. Cup it with the palm of your hand (palm facing up). As you roll your hand upward, and with your palm now flat against the client’s back, palpate right next to the spine (RIGHT SIDE), with your first 3 fingers. Posterior to Anterior P>A.  Check for congestion or tenderness on the right side only. Compare against the left side to determine if there is a difference. IF THEY ARE THE SAME TENDERNESS THIS IS NOT AN INDICATOR.  DOES NOT LNT.
  24. MO: Test points for Sugar Handling Functional Evaluation - LIVER
    • 1. Liver Point/3rd Rib
    • Dr. Dejarnette’s sign. Start on the clavicle, mid-mammary line, RIGHT SIDE, and count down until you are on top of the 3rd  rib. (The clavicle counts as the first rib.) On the 3rd  rib on the right move slightly laterally to the point where the bone turns to cartilage (chondracostal junction). Palpate A>P  checking for pain and rigidity. You can verify findings by checking the 3rd rib on the left to compare. IF THEY ARE THE SAME, THIS IS NOT  AN INDICATOR.  LNTs VERY WELL.

    • 2. Murphy's Sign
    • Indicates acute dysfuntion of liver/gallbladder if tender.
    • Procedure: Position client with knees bent; place finger tips 1.5-2” away from curvature of ribs; ask client to take deep breath in and when they exhale palpate A>P. Ask the client to take one more breath and on the exhale gently change the direction of your palpation more deeply, inferior to superior I>S and under therib cage. With your hand still under the ribcage, ask them to inhale one last time. This allows the diaphragm to push the gallbladder into your fingertips. Be sure to watch client’s face and stop the palpation at any point when they feel discomfort or you cannot fairly easily go further. Rate either tenderness and/or tension.  DOES NOT LNT.

    • 3. Chapman Liver/Gallbladder
    • In the right  6th intercostal space, mid-mammary line.  The 6th  is almost always under the bra band on women. One finger palpation, A>P.  LNT.
Card Set:
Module 5 - Blood Sugar Regulation
2014-06-04 04:18:48
insulin glucagon cortisol adrenals pancreas liver epinephrine hypoglycemia hyperglycemia

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