Now, what are the Endocrine Glands?
 Endocrine glands are ductless structures that secrete hormones directly into extracellular spaces.
  1. From anterior and posterior pituitary glands
  2. Thyroid and parathyroid
  3. Adrenal medulla and cortex
  4. Pancreas
  5. Gonadal hormones of both sexes
  –although the reproductive organs have both endocrine and exocrine functions

 Just so you’re aware, other organs (ie stomach, small intestine, kidneys) also have hormone-producing cells (erythropoietin from the kidneys).

 B. Work on specific receptors
  1. Certain cell receptors may become “antigenic,” meaning antibodies develop against them and cause their destruction– antireceptor autoimmune disorders
   a. myasthenia gravis
   b. Grave’s disease
   c. insulin resistant diabetes
   d. some forms of asthma

  2. Regulation of bodily activities
   a. reproduction
   b. growth and development
   c. response to stress and injury
   d. maintain water/ionic balance of the blood
   e. regulate cellular metabolism
   f. control digestive activity

 C. Diabetes mellitus
   History
       1. until 1922, a progressive, wasting, fatal disease
       2. early urine testing by physicians
       3. experiments by Banting and Best in Canada
          a. wrapping canine pancreas
           b. determining that pancreas was source of insulin

       4. early insulins were what we would today call "regular"
           --required injections of up to every four hours
           --high degree of impurities
 
       5. Beta cells determined to be source of insulin in the "Isles of Langerhans"
 
 General Observations on diabetes mellitus
  1. not related to diabetes insipidus (see ADH discussion)
  2. Body’s inability to metabolize carbohydrates
  3. Polyphagia, polydipsia, polyuria; weakness
   –increased metabolisms of proteins and fats, resulting in ketosis and acidosis; ketones excreted via the breath, “fruity odor”
  4. Increased likelihood for UTIs
  5. Obesity, viral infections, autoimmune phenomena, age, genetic predisposition
  6. Long term complications–hypertension, blindness, poor healing, poor circulation, lack of sensation in periphery
  –consider the situation: the smallest capillaries become damaged or destroyed by the presence of glucose particles
  7. Type I, formerly “Juvenile Onset” “Insulin Dependent”
          –autoimmune theory: following a viral infection (ie chickenpox) the body’s antibodies attack the pancreas and destroy the beta-cells in the Isles of Langerhans
          –represents about 10% of diabetes cases
  8. Type II, formerly “Adult Onset”
  –the majority of cases; beta-cell burnout; can develop as a “rebound” effect after years of hypoglycemia
Time to recall definitions:
                        (1) polyphagia:

                        (2) polyruria:

                        (3) polydipsia:

II. Pituitary Hormones
 A. Anterior Pituitary
  1.  ACTH – adrenocorticotropic hormone
   Promotes release of glucocorticoids, androgens, and mineralocorticoids
   Deficiency: Addison’s disease
   Excess: Cushing’s disease
  2.  FSH – follicle stimulating hormone
   Stimulates ovarian follicle maturation and estrogen production (females)
   Stimulates sperm production (males)
   Deficiency: failure of sexual maturation
   Drug used to stimulate release of FSH: Clomiphene (Clomid)
  3.  GH – growth hormone
   --Stimulates uptake of amino acids, increasing muscle size
   --Stimulates synthesis of collagen
   --Stimulates glucagon release from liver, increasing glucose levels and with it, insulin release; mobilizes fat, increases triglycerides
   –may induce insulin resistance in normal adults
   –influences internal organ size, increases red cell mass
   NOTE: until recently, GH was derived from cadavers; now recombinant DNA production is used
  4. LH – luteinizing hormone
   In females, triggers ovulation
   In males, secretes androgens
  5. MSH – melanocyte stimulating hormone
   Stimulates melanin deposits
   Possible tie-in with melatonin?
  6. Prolactin
   Females: promotes lactation
   Males: potentiates testosterone?
   Excess: glactorrhea, anovulation in women; impotence in males
  7. TSH – thyroid stimulating hormone
 
 B. Posterior Pituitary
  1. Oxytocin – during childbirth and in lactation

  2. Antidiuretic hormone ADH, or “Vasopressin”
   –while an anti-diuretic hormone; it does exert some effect on blood pressure in the liver and spleen
   –hyposecretion results in Diabetes Insipidus: large amounts of dilute urine–polyuria–with polydipsia; no effect on blood glucose levels
   –effect on the GI system
    Increases tone
    Used postop for abdominal distension, esophageal varicies; dispel gas that may interfere with X-rays

  3. Related drug: desmopressin “DDAVP”
   a. synthetic analog of ADH or vasopressin
   b. used for long-term therapy of diabetes insipidus
   c. also for primary nocturnal enuresis
   d. nasal spray or injection forms available
   e. in factor VIII deficiencies (Hemophilia A or von Willebrand’s disease) to control bleeding; injection used

III. Parathyroid and Thyroid
 A. Parathyroid and calcium’s role
  1. Calcitonin (Miacalcin); salmon source; used as a nasal spray to prevent osteoporosis
 B. Thyroid
  1. Variations between Hyper- and Hypothyroidism

Metabolism                                       decreased glucose metabolism                      Hypercatabolism of glucose
                                                         Elevated cholesterol/trigly.                            Protein catabolism

CNS                                                 Mental dulling                                               irritability, excitability
                                                         Sleepiness                                                    insomnia
 
Cardiovascular                                  decreased cardiac output                              tachycardia, increased cardiac
                                                                                                                             output

GI                                                     Depressed GI tone                                       frequent stools, diarrhea

Skin                                                  Pale, thickened, dry                                      flush, thin, moist
                                                         Nails hard                                                    nails soft

Reproductive                                    depressed ovarian function                            depressed ovarian function
                                                         Depressed lactation                                      men: impotence/gynecomastia

Muscular system                               cramps, decreased vigor                                 protein catabolism; atrophy
Skeleton                                           arthralgia                                                       demineralization

  2. Thyroid preparations
   a. levothyroxine (Levothroid, Synthroid); pure T4
    These preparations are measured in micrograms–and this can lead to dosing confusion.
    Common strengths are 50mcg, 100mcg, 200mcg, 300mcg; when expressed as milligrams, these doses become 0.05mg, 0.1mg, 0.2mg, 0.3mg.
   b. dessicated thyroid; animal sources, T4 and T3
    The original “thyroid.”  “Armour” thyroid.
    These doses are expressed in milligrams or grains.
    1 grain = 60 to 65mg (depending on which conversion chart you find)
    Tablets come in 1 grain (1gr), 2 grain (2gr), 3 grain (3 gr)
   c. liothyroinine (Cytomel); pure T3
    25-50mcg doses
   d. liotrix (Euthroid, Thyrolar); synthetic combination of T4 and T3
    “1" delivers equivalent to 65mg of dessicated thyroid
   e. thyroglobulin (Proloid); purified hog extract of T4 and T3
    mg to mg equivalent to dessicated thyroid

  3. Preparations for hyperthyroid states “Antithyroid drugs”
   a. propylthiouracil (PTU or Propacil)
   –will eliminate thyroid activity within 8-12 weeks
   –can cause transient symptoms of “thyroid storm” as destroyed thyroid cells distribute throughout the body

 C. Hyperthyroidism
  1. Grave’s disease
   –also, “diffuse toxic goiter” or “exopthalmic goiter”
   a. often precipitated by changes in hormonal makeup, therefore women more prone to the condition than men (Barbara Bush)
   b. long-acting thyroid stimulator with immune disturbances, especially in T cell production

 D. Function of Iodine
  1. high vs low levels of iodine
   Iodine is required in the conversion of thyroglobulins into T3 and T4
   If iodine is not present, TSH levels continue to elevate without production of thyroid hormones; hyperplasia of the thyroid occurs.  This hyperplasia is known as simple or colloidal goiter.

  2. Radioactive iodine 131I as diagnostic tool.

V. Pancreas/Diabetes

                                Ketoacidosis                       Hyperglycemic Coma                           Hypoglycemia

Onset                       hours to days                       days                                                     minutes to hours

Pt appearance          very sick                              sick                                                      healthy but confused

Skin                         flushed, dry                          dry                                                      pallor, moist

Respiration              hyperventilation                      normal                                                shallow, rapid

Glycosuria or
Polyuria                    Present                                present                                                 absent

Glucose levels              high                                    very high                                              low

Ketoacidosis              present                                absent                                                   absent
 
 Treatment                  insulin, fluids                       insulin, fluids                                          Oral and IV glucose

 B. General secretions
  1. 1-2 units/hour
  2. 4-6 units after meals or when blood sugar exceeds 100mg/ml
  3. 40-60 units/24 hours

 C. In normal situations
  1. fasting, insulin levels low, stored glucose and amino acids are used for energy
  2. after meals, insulin increases in a few minutes, peaks in 30 minutes, and returns to baseline in 3 hours

  D. Release and fate
  1. after release from pancreas, enters portal circulation, to liver
  2. half is used in the liver or metabolized; the other half enters the body to exert effect
  3. circulates unbound and is transported to most body cells

 E. Cellular level
  1. binds and activates cell membranes of about 80% of cells
  2. Primary sites of action
   a. liver cells-- decrease the breakdown of glycogen (glycogenolysis), formation of new glucose from fatty acids and amino acids, formation of ketone bodies; increase synthesis and storage of glycogen and fatty acids
   b. muscle cells-- decreases protein breakdown and increase amino acid uptake, protein synthesis, and glycogen synthesis
   c. adipose cells-- decreases breakdown of fats, increases production of glycerol and fatty acids
  3. Binding with the cells, the insulin-receptor interaction results in
   a, increase in permeability for glucose
   b. increase in permeability for amino acids, fatty acids, potassium magnesium and pohsphate ions

  4. This results in
   a. stimulates anabolic effects
   b. inhibition of catabolic processes
  5. metabolized in liver, kidneys, plasma and muscle; severe renal impairment slows the clearance of insulin from the blood

 F. Stimulates insulin secretion
  1. glucose, amino acids, fatty acids, vagal stimulation, beta-2 stimulation
  2. hormones
   a. glucagon
   b. growth hormone
   c. cortisol, progesterone, estrogen

 G. Inhibits insulin secretion
  1. stimulation of alpha-2 adrenergic receptors
  2. hypoxia
  3. hypothermia
  4. surgery
  5. severe burns

Type of onset                      Abrupt                                                                      Gradual
Family History                     Usually little family history of diabetes                       Positive history of diabetes is common

Etiology                               Unknown, postulated causes include
                                            autoimmune diseases or viral infections                     Heredity is a highly associated occurrence

Body Weight                     Usually thin and undernourished                                   Obesity is common

Insulin                                 Secretion is markedly diminished early in the
                                           disease and may be totally absent later in the
                                            disease; insulin therapy is mandatory                         Levels may be low (indicating deficiency),
                                                                                                                           normal, or high (indicating insulin resistance);
                                                                                                                            insulin therapy may not be required

Clinical Symptoms                 Polydipsia, polyuria, polyphagia                             May be asymptomatic, polyuria and/or
                                                                                                                            polydipsia may be present

Ketosis                                 Frequent (unless diet, insulin, and
                                            exercise are properly coordinated)                         Infrequent (except in the presence of
                                                                                                                            infection or stress)

II. Diabetes mellitus
 A. Background
 B. Type I (formerly insulin dependent diabetes IDDM)
 C. Type II (formerly non-insulin dependent diabetes NIDDM)
  1. impaired glucose tolerance
  2. gestational diabetes

 D. Epidemiology
  1. between 1990 and 1998, diabetes rose by 70% in age group 30-39
  2. up 40% in group 40-49
  3. up 31% in group 50-59
  4. 33% with insulin dependent (type I) are undiagnosed
  5. 55% with non-insulin dependent (type II) are undiagnosed
  6. In terms of comparison, in the 1970s, 10% of diabetic patients were type I; this is now 5%
  7. leading cause of adult blindness, end-stage renal disease, non-traumatic lower extremity amputations
  8. 65% of patients with type II will die of cardiovascular complications
  9. African-Americans, Hispanics, Amerinds lead groups with diabetes (1 in 4); 18 million nationwide

 E. It is different than diabetes insipidus, which is a condition involving antidiuretic hormone production
 

 G. Syndrome “X”
  1. aka “insulin resistance syndrome” or “metabolic syndrome”
  2. 36 million Americans affected
  3. Risk factors
  –increased age, low birth weight, polycystic ovary syndrome, central obesity (spare tire), sedentary lifestyle, gestational diabetes, impaired glucose tolerance or elevated fasting blood sugar, hypertension, elevated triglycerides, lower HDL cholesterol

III. Complications
 A. Diabetic ketoacidosis
 B. Hyperglycemic Hyperosmolar Nonketotic Coma
 C. Cardiovascular
 D. Nephropathy
 E. Retinopathy
 F. Neuropathy
 

IV. Drug therapy-- Insulin
 Insulin is the only effective treatment for type I diabetes.
 Insulin is required for 20-30% of type II diabetic patients who cannot control their disease with diet, weight control, and oral agents.
 In non-diabetic patients, insulin is used to prevent or treat hyperglycemia induced by IV hyperalimentation solutions; it can also be used in hyperkalemia (IV insulin with dextrose solutions cause potassium to move from the blood into the cell; it does not eliminate potassium from the body).

 A. Traditional
  –until 1922, there was no insulin, only theories on its function
  1. pork and beef sources
  2. phased out in 1999
 B. Synthetic
  1. use recombinant DNA technology to duplicate human insulin
  2. all insulins presently made in this manner today

 C. Unique combinations
  1. mixtures of regular and NPH-type insulins
  2. pen delivery systems
  3. lisinpro insulin (Humalog) insulin– very rapid onset of activity

 D. Investigational insulins
  1. nasal spray, buccal administration, inhaled insulins
  2. limitations on oral administration (German study showing promise, however)

V. Drug therapy-- Oral hypoglycemics
 A. General modes of action
  1. stimulate insulin production
  2.. inhibit carbohydrate utilization
  3. enhance insulin utilization

 B. Stimulating Insulin Production–THE SULFONYLUREAS
  –crossover allergies possible with patients allergic to sulfa drugs
  –weight gain seen with all sulfonylureas
  1. First generation sulfonylureas
   a. acetohexamide (Dymelor)
   b. chlorpropamide (Diabinese)
   c. tolazamide (Tolinase)
   d. tolbutamide (Orinase)

  2. Second generations sulfonylureas
  --new generation sulfonylureas (a bit of a disconcerting note: DuPont uses varieties of sulfonylureas as herbicides)
   a. Amaryl (glimiperide) 1mg, 2mg, 4mg tablets (Hoechst Marion Roussel)
   –can be given in combination therapy with insulin
   –dosage range of 1-8mg daily; once daily dosing is possible
 
   b. glipizide (Glucotrol)
   c. glyburide (Diabeta, Micronase)

  3. Nutritional depletions
   a. sulfonylureas cause depletion of CoQ 10

 C. Inhibiting Carbohydrate Utilization (alpha-glucosidase inhibitors)
  To be effective, these agents must be taken with the first bite of the meal; waiting even 30 minutes will render drug ineffective.
  A. Precose (acarbose), 25mg, 50mg, 100mg (Bayer Pharmaceuticals)
   –an alpha glucosidase inhibitor; meaning, it inhibits the breakdown of carbohydrates; for non-insulin dependent diabetes
    may also be used in combination with a sulfonylurea when diet plus either PRECOSE or a sulfonylurea do not result in adequate glycemic control
   –must be taken with the first bite of the meal; ineffective if forgotten until later
   –biggest side effects–gas, bloating, and diarrhea
   –abuse in “carbohydrate-free” diets? Note from the company literature: “The use of PRECOSE must be viewed by both the physician and patient as a treatment in addition to diet, and not as a substitute for diet or as a convenient mechanism for avoiding dietary restraint.”
   –contraindicated with ketoacidosis, cirrhoiss, inflammatory bowel disease, colonic ulceration or partial intestinal obstruction; doses over 100mg three times a day may be associated with increased transaminase levels (that means liver damage)
   –side effects: gas, bloating, diarrhea; worse during the first 8 weeks of therapy

  B. Glyset (miglitol), also 25mg tid with meals

 D. Enhancing Utilization of Insulin–THE BI-GUANIDES
  1. Glucophage (metformin)
   a. 500mg, 850mg, 1000mg
   b. prolonged use can result in B-12 depletion
   c. one of those mysteries: metformin has been available worldwide for 4 decades– yet it is just now coming off patent (3 March 2000) after 510 million dollars in annual sales
   d. Sustained release version released 2001
   e. generic expected on regular-release 2001

  2. MIXING ‘Em Up! (and extend the patent)
   Glucovance: Glucophage (metformin) with Diabeta (glyburide)
   –dosage is 1 to 4 tablets, in divided doses, daily with meals
Pricing “advantage” being promoted
   Glucovance 1.25/250  47.85/100 (wholesale)
   Glucovance 2.5/500  58.22/100
   Glucovance 5/500  58.22/100

   Glucophage 500mg  56.64/100
   Glyburide 5mg   8.25/100  3. Recommendations with Glucovance
   a. again, like Glucophage, not for patients at risk for lactic acidosis
   b. renal function test prior to initial therapy, then annually

  4. biguanides cause depletion of vitamin B-12

 E. Thiazolinediones – also causes notable weight gain
  “Insulin sensitizers,” reducing insulin resistance in skeletal muscle, adipose tissue, and liver
  Liver function must be assessed while on these drugs
  1. troglitazone (Rezulin) withdrawn in 2000 for deaths – liver failure
  2. pioglitazone (Actos)
  3. rosiglitazone (Avandia)
 
 F. Meglitinides – less pronounced weight gain
  1. STARLIX (nateglinide) – new 2001 entry
   a. monotherapy and in combination with methformin (Glucophage)
   b. amino acid derivative; thought to break the cycle of mealtime hyperglycemia before it begins
   c. mild hypoglycemia side effect reported

  2. repaglinide (Prandin)

VI. Monitoring diabetes
 A. Glucometers
 –before the general inexpensive availability of glucometers, it was thought “good practice” to maintain a certain level of hyperglycemia to insure against the dramatic side effects of hypoglycemia....urine testing was the only means possible to generally test blood sugar “ranges” up until then, and they would only work if the blood glucose was over 180 and glucose was spilling over.  Until glucometers, there was no simple method to determine hypoglycemia.
 –early “home unit” meters were about the size of a small suitcase and cost $600.  They measured glucose levels by “color reflectance” – the color being proportional to the amount of sugar present.  These have been replaced by sensor meters, which use an electrochemical process to determine blood sugar.  These newer units are not affected by environmental temperature or hematocrit.

  1. frequency testing problems
   a. only 40% of type I diabetics are testing at least daily
   b. only 26% of type II patients using insulin test at least once daily; 5% or fewer on oral hypoglycemic agents are testing blood glucose levels
   c. women have best compliance
   d. education education education!
  2. logbook use
   a. to determine surrounding situations involving abnormal blood sugar
   b. bring to each physician, nurse practitioner, or dental visit

  3. pattern management
   –one to two units of insulin is equivalent or a rise or reduction of 30 to 50mg/dL in blood glucose
  4. limitations
   a. patients concerned about cost of strips and materials
   b. denial and fear of needle sticks
   c. no non-invasive glucose meter is currently available on the market
 B. HbA1c
  1. glucose binds to hemoglobin, forming “glycosylated hemoglobin.”
  2. the more glucose present, the greater the HBA1c present
  3. hemoglobin lives 8-12 weeks before replacement; HbA1c indicates the glucose level average over the previous 8-12 weeks
  4. normal non-diabetic HbA1C is 3.5-5.5% -- In diabetes 4-6% is acceptable.
  5. generally if  diabetes is controlled (an HbA1C lower than 7%), check every 6-12months.
  6. The HbA1C level changes slowly, over 10 weeks, so it  can be used as a 'quality control' test.
 
X.  Hypoglycemia
 A. If patient is unconscious, treat for
 hypoglycemia
 B. If conscious, give oral carbohydrate
 C. CAUSES
  1. missing or delayed meals
  2. too much insulin
  3. exercising or working more than usual
  4. stress (dental visits?!) or illness
  5. ethanol

XI. DKA “diabetic ketoacidosis”
 A. Severe insulin deficiency
 B. not sudden
 C. cannot use glucose for fuel–body uses fats with ketone production and acidosis resulting
 D. “fruity breath”
 E. nausea, vomiting, anorexia, thirst, polyuria, dehydration
 F. Treat
  1. insulin
  2. IV of NS with potassium
  3. sodium bicarbonate (buffer)
  4. identify source of potential infection–often a cause
   

 A. Interaction problems with
  1. ephedrine
           general concern with fad diets
           governmental concern tied to campaign contributions?
  2. glucosamine
           arthritis therapy and problems with maintaining blood sugars

 B. Promoted as “natural diabetic agents”
  1. bitter melon
  2. Gymnema sylvestre
  3. fenugeek seeds

1. BITTER MELON
 a. other names: African Cucumber, Balsam-Apple, Balsambirne, Balsam Pear, Balsamo, Bitter Apple, Bitter Cucumber, Bitter Gourd, Bittergurke, Carilla Gourd, Chinli-Chih, Cundeamor, Karela, Kuguazi, K'u-Kua, Lai Margose, Momordique, Pepino Montero,  P'u-T'ao, Sorosi, Wild Cucumber.
 b. PREGNANCY: LIKELY UNSAFE The juice can stimulate menstruation and cause abortion.
 c. Adverse  Reactions– None reported.  Theoretically, concomitant use of bitter melon can enhance hypoglycemic drug effects and alter blood glucose control. Monitor blood glucose levels if bitter melon is used. Insulin dosage adjustments might be necessary due  to the hypoglycemic effects of bitter melon.
 d. Dosage and Administration– ORAL: People typically use 1 to 2 grams of powdered leaf in tablets or capsules daily. Bitter melon is also taken as a 4:1  tincture in a dose of 1 to 3 mL twice daily.

 2. Gymnema sylvestre
         a. other names:Gur-Mar, Gurmar,Gurmarbooti, Merasingi, Meshashringi.
              b. Orally, gymnema leaf is used to treat diabetes.   In combination with other products, gymnema is used for metabolic control .    In Ayurvedic medicine, gymnema is a component in the Tribang shila compound, which contains tin, lead, zinc,  gymnema leaves, neem leaves, jambul seeds, and Enicostemma littorale . Traditionally, gymnema has been used as an antimalarial, digestive stimulant, laxative, and diuretic. It has also been  used traditionally for coughs and as a snake bite antidote.
              c. The applicable part of gymnema is the leaf. Gymnema lowers  blood sugar , serum triglycerides, total cholesterol, and VLDL and LDL cholesterol in animals . The constituent,  gymnemic acid, inhibits the ability to taste bitter (quinine) or  sweet (sugar) without affecting the ability to taste sour,  astringent, or pungent flavors .
             d. Gymnema can enhance the blood glucose lowering effects of these drugs, and blood glucose levels  should be monitored closely.
  e. Dosage and Administration ORAL: For lowering blood sugar, the typical dose of the extract  GS4 is 400 mg daily.
  f. note: actually shown to cause an increase in beta-cell generation in the pancreas!

  3. Fenugreek seeds
a. other names: Bird's Foot, Bockshornsame, Foenugraeci Semen, Foenugreek,  Greek Hay, Greek Hay Seed, Hu Lu Ba, Methi, Trigonella.
b.  Orally, fenugreek seed is used for loss of appetite, for lowering blood glucose in  people with diabetes, constipation, atherosclerosis, high serum cholesterol and triglycerides  and for  promoting lactation.
c. Topically, fenugreek is used as a poultice for local   inflammation , myalgia, lymphadenitis, gout, wounds, leg ulcers, and eczema.  Traditionally, fenugreek has been taken to reduce fever, promote lactation, and treat mouth ulcers, boils, bronchitis,  cellulitis, tuberculosis, chronic coughs, chapped lips, and cancer. It is also used as a cure for baldness.
d. For food use, fenugreek is included as an ingredient in spice blends. It is also used as a flavoring agent in imitation maple syrup, foods, beverages, and tobacco.  In other manufacturing processes, fenugreek extracts are  used in soaps and cosmetics.
e. LIKELY SAFE ...when seed preparations are used in the amounts commonly found in foods, (maximum use level is 0.05% in meat). It has Generally Recognized as Safe (GRAS)  status in the US .
f. PREGNANCY: LIKELY UNSAFE …contraindicated for oral use in amounts greater than those found in foods because of its potential oxytocic and uterine stimulant activity.
g. Effectiveness ...when used orally for lowering blood sugar in people with diabetes and for the loss of appetite ...when used topically as a poultice for local inflammation.
h.  Mechanism  of Action--The applicable part of fenugreek is the seed. Fenugreek affects  gastrointestinal transit, slowing glucose absorption.
i.  Adverse Reactions – The oral use of fenugreek can cause diarrhea and flatulence.
URINE ODOR: Fenugreek can cause a maple syrup odor in urine.
k. Dosage and Administration
ORAL: The typical dose is 1-2 grams of the seed or equivalent three times daily  or one cup of the tea several times aday. The tea is prepared by steeping 500 mg seed in 150 mL cold water for three hours and the straining. The maximum  amount of fenugreek is 6 grams of the seed per day.
 

 C. Stevia – “controversial” sweetener Stevia rebaudiana
  1. Banned by FDA, with seizure orders, in 1991
  2. Exception made in 1995, provided it was sold only as a “food supplement”
  3. 100 times sweeter than sucrose at 10% sucrose concentration, stable for cooking
  4. no carbohydrate value
  5. also being promoted as a general miracle additive, as a weight loss aid;  traditionally, stevia leaf has been used for treating diabetes, as a contraceptive , for hypertension, heartburn, lowering uric acid levels, as a cardiotonic and diuertic; For food uses, stevia leaf has a centuries-long history of use as a sweetener in Paraguay and is used as a non-caloric sweetener in South America and Asia.
  6. ORAL: A typical dose of powdered stevia leaf is 1000 mg per day

1. What is the difference between diabetes mellitus and diabetes insipidus?
2. What are the different types of insulin
 a. by strength
 b. by source
 c. by duration of action

3. What does U-100 mean?
4. You have to administer 45 units of NPH U-100 insulin.  How much volume is this?
5. Define
 a. hypoglycemia
 b. hyperglycemia
 c. polyuria
 d. polydipsia
 e. polyphagia

6. Name a thyroid supplement.
7. What is a powerful inhibitor of ADH that is legally available to Michigan residents over the age of 21?
8. What is a treatment for diabetes insipidus?
9. What drug allergy is of concern with patients being given oral hypoglycemic drugs?
10. Where does “human” insulin come from?
11. Name a carbohydrate inhibitor.  When should it be administered?
12. Your diabetic patient has “fruity” breath.  What is possibly happening?
13. Which gland is involved with calcium use?  What salmon-source nasal spray is used to prevent calcium loss and osteoporosis?

End of Module Nine
January 2002
KCC Dental Hygiene Pharmacology
Contact and Instructor: Jim Middleton