1. Ginger for __________
    Prevention of Motion Sickness
  2. Ginger: portion of plant used ___________
  3. Origin of Ginger
    Southeast Asia/China
  4. Ginger MOA
    • Inhibits serotonin receptors (antiemetic effects)
    • Decrease vasopressin release (reduce motion-related nausea)
  5. Ginger Efficacy
    • Mixed evidence
    • 1st study: no benefit of ginger power or root over scopolamine or placebo
    • 2nd study: positive benefits with ginger pretreatment on prolonging time before nausea, shortening recovery time, and reducing basopressin levels
  6. Ginger Dosage and Standardization
    1-4 grams/day
  7. How long before a trip should you take ginger before a trip?
    • 30 min-4 hrs before
    • 1-2 days before if possible
  8. Should you continue to take ginger throughout the trip?
  9. What is the standardization of ginger?
    • 5-20% gingerols and shogoals
    • 4% volatile oils
  10. Ginger: AEs
    • Not common
    • Heartburn, diarrhea, mouth irritation
  11. Can ginger be used in pregnancy?
    • Commonly used but German Commission E recommends NO
    • Do not use more than dietary intake
  12. Ginger: Precautions
    • Fibrinolytic activity at high doses
    • Arrhythmias in animals
  13. Contraindications with Ginger
    Gallbladder disease/cholethiasis 
  14. What is the mechanism of action of ginger?

                a.  inhibits GABA receptors

                b.  inhibits serotonin receptors

                c.  inhibits dopamine receptors

                d.  inhibits H2 receptors
    inhibits serotonin receptors
  15. Ginger has been shown to:

                a.  prolong the onset of motion-induced nausea

                b.  shorten the recovery time of motion sickness

                c.  be as effective as conventional treatments

                d.  all of the above
    all of the above
  16. Which of the following is not a side effect
    of ginger?

                a.  heartburn

                b.  diarrhea

                c.  fatigue

                d.  mouth irritation
  17. Which of the following is a contraindication
    for the use of ginger?

                a.  gallbladder disease

                b.  renal insufficiency

                c.  hepatic insufficiency

                d.  pancreatic disease
    gallbladder disease
  18. Phytosterols: History
    2001: lifestyle modification with phytosterol in ATP III
  19. Phytosterols: Naturally available in
    • oils and fats
    • nuts and seeds
    • cereals 
    • vegetables
    • fruits
  20. Phytosterols: MOA
    • hydrolyzed by cholesterol reductase and replaces cholesterols in the micelles
    • not esterifiled by acyl CoA
    • accumulation of phytosterols in the enterocytes leads to upregulation of ABCA1 transporter and increased removal of phytosterols and cholesterol
  21. Phytosterols: Efficacy
    Dose of 2 g day has been proven to lower LDL cholesterol concentration by 10-11%
  22. Phytosterols: Dosaged and Standardization
    • > 1.5 g of plant sterols per day
    • Standardized by sterol content
    • Natural sesame seeds: 360 mg of phtosterols per 100g
    • Promise Active Light Spread: 1 g per tbsp
  23. Phytosterols: ADR
    • Generally well tolerated
    • Nausea
    • Indigestion
    • Gas
    • Diarrhea
    • Constipation
    • ED
    • Loss of libido
  24. Phytosterol: Contraindications
    • Pregnancy
    • Sitosterolemia
  25. Phytosterol drug interactions
    • Ezetimibe: reduced absorption of phytosterol
    • Pravastatin: reduced blood levels of phytosterol
  26. Phytosterol food and supplement interactions
    Carotene and Vitamin E both may reduce absorption and blood levels
  27. Sitosterolemia and phytosterols
    Lipid storage disease which causes increased absorption of cholesterol
  28. Phytosterols and Beta Carotene
    • may reduce absorption of beta carotenes which can lead to increased risk of chronic disease such as cancer or heart disease
    • counteract w/ diet rich in fruits and vegetables, MVI
  29. 1.     Why are phytosterols not recommended first line for reduction in LDL?

    a.     They cause too many side effects

    b.     They are a potent CYP P450 inhibitor and therefore interact with many drugs

    c.  They do not demonstrate the same capacity to lower lipids as statins

    d. They are not manufactured by a large drug
    They do not demonstrate the same capacity to lower lipids as statins
  30. 1.     Which of the following is false pertaining to phytosterols

    C.     Theyare not naturally found in many foods
  31. 1.     At a dose of ­­­_  g/day, phytosterols have been shown to lower LDL concentration by ­_ %.

    a.     15 g/day; 10-11%

    b.     1.5 g/day; 21-67%

    c.    2g/day; 10-11%

    d.     10-11 g/day; 2%
    c.    2g/day; 10-11%
  32. 1.     Although phytosterols are generally well tolerated, an adverse effect commonly noted in patients is

    C.     GIupset (nausea, dyspepsia, constipation, flatulence)
  33. 1.     Phytosterols supplementation may reduce the absorption and transportation of which of the

    a.     LDL

    b.     HDL

    c.     Hydrocarbon carotenes

    d.    Both a and c
    d.    Both a and c
  34. 1.     Phystosteral supplementation should be avoided in which disease states

    a.     Diabetes mellitus

    b.     Acid reflux

    c.     Morbid obesity

    d.    sitosterloemia
    d.    sitosterloemia
  35. Curcumin Indication
    Parkinson's Disease
  36. First use of curcumin
  37. Curcumin MOA
    • a)   MOA: protects specific (MES23.5) dopaminergic
    • cells from 6-hydroxydopamine (6-OHDA) induced neurotoxicity

    • i)    Acts as a free radical scavenger/antioxidant
    • ii)   6-ODHA causes neurotoxicity by 2 mechanisms:

    • 1.  Forms free radicals
    • 2.  Potential inhibitor of mitochondrial respiratory chain complexes I and IV

    Scientists also hypothesize curcumin helps reduce glutathione-depleted oxidative dopaminergic neurons by increasing glutathione levels
  38. Curcumin efficacy profile
    • No human clinical trials
    • All hypothesized effects are result of speculation and animal tests
  39. Curcumin AE
    • dermatitis
    • bitter taste
    • GI disturbances (with chronic use): dyspepsia, nausea, vomiting, dizziness, diarrhea
  40. Curcumin Contraindications
    • Hypersensitivity to tumeric/curcumin
    • Bile duct obstruction/gallstones
    • Gastric ulcer
    • Surgery (risk of bleeding)
    • Pregnancy/lactation (emmenagogue/uterine stimulant effects)
  41. Curcumin Drug Interactions
    • Anticoagulation/antiplatelet: increased risk of bleeding, medium risk
    • Diabetes medications: may increase risk of hypoglycemia
    • H2RAs and PPIs: may block mechanism of action to result in increased acid secretion
  42. Curcumin Food interactions
    • Cinnamon: Increased risk of bleeding
    • Monitor: potential for interaction
  43. Curcumin disease interactions
    Bile duct obstruction/gallstones: may cause gallbladder contractions
  44. Curcmin Dosing
    • Typically 1-3 500 mg capsules daily w or w/o food
    • Dosage depends on taking curcumin
  45. When should you D/C curcumin? (s/sx)
    • Breathing problems
    • Tightness in throat/chest
    • Chest pain
    • Skin hives
    • Itchy/swollen skin
  46. 1.     What is the basic mechanism of action for how curcumin is suspected to reduce the progression of
    Parkinson’s Disease?

    A.  Decreases oxidative stress to prevent degradation of
    dopaminergic neurons

    B. Increases oxidative stress to stimulate glutathione conjugates in the liver

    C.  Increases intracranial blood flow to increase oxygen supply to the brain

    D.  Stabilizes the myelin sheath around neurons to enhance signal transduction 
    A.  Decreases oxidative stress to prevent degradation ofdopaminergic neurons
  47. Which of the following is NOT a contraindication to curcumin?

    A. Pregnancy
    B. Surgery
    C. Hypertension
    D. Gastric Ulcers
  48. Which of the following medications would result in a drug-interaction with curcumin?

    A. Propranolol
    B. Warfarin
    C. Amoxicillin
    D. Simvastatin
  49. Which of the following clinical trials support the use of curcumin in
    Parkinson’s Disease?

    A. CIPD (Curcumin in Parkinson’s Disease)
    B. TTND (Turmeric Treatment in Neurodegenerative Disorders)
    C. CMPHS (Curcumin: Managing Parkinson’s with Herbal Supplementation)
    D. None of the above: there are NO clinical trials supporting the use of curcumin in Parkinson’s Disease
    D. None of the above: there are NO clinical trials supporting theuse of curcumin in Parkinson’s Disease
  50. Maca Indication
    Menopausal symptoms
  51. Part of Maca used in medicine
  52. Maca MOA
    • Exact mechanism unknown-- does not affect concentration of hormones
    • Marker compounds Macaene and macamide (polyunsaturated fatty acids)
  53. Maca efficacy profile
    Positive benefits over the placebo effect for menopause symptoms [not due to a change in estrogen or androgen content]
  54. Maca compared to conventional medicine
    Less efficacy but also fewer side effects
  55. Maca dosage and standardization
    • > 0.6% glucosinolates, o.6% macamides and macaenes
    • Dosage in clinical trials: 2 g/day
  56. Maca AE
    • None verified
    • Case reports: budd-chiari, attention disturbances, weight loss, agitation, abdominal pain, epistxis, gingival bleeding, HA, vomiting, and abdominal lifer function [none directly related to Maca]
  57. Maca’s mechanism of action is which of the following:
    a.  unknown
    b. stimulates GABA receptors in the brain
    c. increases adrenal stimulation of alpha and beta receptors
    d. Increases levels of nitrous oxide systemically
  58. Maca’s commonly reported side effects are?

    C. There are no commonly reported side effects
  59. Where does Maca originate from?
    a. Peru
    b. United States
    c. Russia
    d. China
  60. Maca is used to treat which of the following?
    a. Menopause
    b. Diabetes
    c. Pain
    d. Muscle wasting
  61. Saw Palmetto Indication
  62. Saw Palmetto: Part of the plant used
    whole berries or oily flesh of the berry
  63. Saw Palmetto MOA
    • poorly understood
    • antiandrogenic, antiproliferative, and anti-inflammatory properties
    • inhibition of 5-alpha reductase --> decrease growth of prostate
    • slow prostate cell proliferation: inhibition of fibroblast growth factor and epidermal growth factor, apoptosis
    • Inhibition of alpha-adrenergic receptors
    • Placebo effect
  64. Saw Palmetto Efficacy Profile
    showed no significant statistical improvement in symptoms or prostate size reduction in patients with BPH treated with Saw Palmetto
  65. Saw Palmetto Dosage and Standardization
    • 160 mg capsule BID (clinical trials)
    • or 
    • 320 mg of a lipophilic extract containing 80-90% fatty acids
  66. Saw Palmetto AE
    • Common: dizziness, nausea, HA, vomiting, constipation, diarrhea
    • Less common: asthenia, loss of libido, ejaculation disorders, orthostatic hypotension
  67. Saw Palmetto precautions
    • Antiplatelet and anti-estrogen effects
    • Surgery: D/C 2 weeks prior to surgery
  68. Saw Palmetto Drug Interactions
    • Anticoagulants: increase risk of bleeding
    • Antiplatelets: increase risk of bleeding
    • Oral Contraceptives: anti-estrogenic effects
    • Estrogens: anti-estrogenic effects
  69. Saw Palmetto Lab Test Interactions
  70. Saw Palmetto Interactions with Other CAM
    antiplatelet effects: angelica, clove, danshen, garlic, ginger, ginkgo, panax, ginseng
  71. 1.   What is the most common use of Saw Palmetto?

    a.   pruritus caused from an allergic reaction

    b.  memory loss

    c.lower urinary tract symptoms associated with benign
    prostatic hyperplasia

    d. wart caused by tinea pedis

    e.   appetite suppressant
    lower urinary tract symptoms associated with benignprostatic hyperplasia
  72. 1. Which of the following medications is most
    likely to interact with Saw Palmetto?

    a. metoprolol tartrate
    c. fluconazole
    d. warfarin
    e.none of the above
  73. 1.      
    What is the most commonly proposed mechanism
    of Saw Palmetto?

    a.      inhibitor of HMG-CoA reductase

    b.     inhibitor of 5-alpha reductase

    c.      alpha-2 agonist

    d.     inhibition of prostaglandin synthesis

    e.     both a & b
    inhibitor of 5-alpha reductase
  74. Did the systematic review favor Saw Palmetto
    for the treatment of BPH?

    a.      Yes, because Saw Palmetto proved to be
    effective in the treatment of BPH

    b.     No, because there are too many risks involved
    in using Saw Palmetto

    c.     No, the studies in the systematic review did not
    favor Saw Palmetto

    d.     Yes, but only favored one dosage form of Saw
    Palmetto over another
    No, the studies in the systematic review did notfavor Saw Palmetto
  75. Cranberry Indication
  76. Cranberry Portion Used
    Fruit Portion
  77. Cranberry MOA
    • Interferes with bacterial adherence to urinary tract epithelial cells
    • Proanthocyanidins wrap around pathogens
  78. Cranberry Juice Efficacy Profile
    • NMCD "possibly effective"
    • May reduce risk of recurrent UTI but should not be used to treat active UTI
    • Not sure if juice or percentage is effective
  79. Dosage and Standardization
    • Cranberry juice 300-480 mL 
    • Cranberry capsule 400-800 mg BID
  80. Cranberry AE
    • N/V
    • Diarrhea
  81. Cranberry Precautions
    Drinking 1 L/day for extended period can increase urice acid kidney stone formations
  82. Cranberry contraindications
    • ASA allergy
    • Atrophic gastritis
    • Diabetes
    • Hyochlorydria (decrease in B12 absorption)
    • Hx of kidney stones
  83. Cranberry Drug Interactions
    Warfarin: Increase INR
  84. Cranberry Lab Interactions
    Increases serum and urine salicylate levels
  85. Cranberry Disease Interactions
    • ASA allergy
    • Atrophic Gastritis
    • Diabetes
    • Hypochlorhydria
    • Kidney Stones
  86. What are possible adverse effects of using cranberry?

    D) GI side effects
  87. Cranberry is contraindicated in all of the following EXCEPT

    a)   Diabetes

    b)   Aspirin allergy

    c)    History of kidney stones

    d)   Penicillin allergy
    PCN allergy
  88. Which of the following about the effectiveness of cranberry is FALSE?

    a)   It is unclear whether cranberry juice and capsule form are equal in effectiveness.

    b)   To prevent UTIs an exact dose of cranberry has been recommended.

    c)    Some studies have shown a decrease in recurrent UTIs as a result of taking cranberry.  

    d)   The Natural Medicines Comprehensive Database has listed Cranberry as “possibly effective” for UTIs.
    To prevent UTIs anexact dose of cranberry has been recommended.
  89. What is the active ingredient responsible for the MOA of Cranberry against bacterial pathogens?

    a)   Anthocyanidins

    b)   Fructose

    c)    Flavonoids

    d)   Water
  90. Fenugreek Indication
    Type 2 Diabetes
  91. Fenugreek MOA
    Three proposed mechanisms: slows the absorption of food from the GI tract, direct pancreatic beta-cell stimulation, promotes insulin sensitivity
  92. Fenugree Efficacy
    • Fenugreek in combo with sulfonylurea vs. sulfonylurea
    • 0.35 g fenugreek TID after meals 
    • Significant reductions in FBG, 2h PBG, and HbA1c compared to placebo group
  93. Fenugreek Dosage and Standardization
    • No standardized dosage among products
    • 4 g of Fenugreek seed recommended
  94. Fenugreek AE
    • flatulence
    • bloating
    • diarrhea
    • mild abdominal distention
    • hypoglycemia
  95. Should Fenugreek be used in pregnant women? nursing women? children?
    • No
    • Use caution in nursing women and children
  96. Fenugreek Drug Interactions
    • Anticoagulants: enhances effects of anticoagulants
    • Conventional antidiabetic meds: enhance glucose lowering properties
  97. a.     In which of these patients would you most likely recommend the use of fenugreek?
    i.  Diabetic patient                                            
    ii. Pregnant patient                                            
    iii. Nursing mother
    iv. Pediatric patient
    Diabetic patient
  98. a.     What part of the plant has therapeutic effects?
    i.    The leaf                              
    ii.    The root                                              
    iii.    The stem                                               
    iv.    The seed
    The Seed
  99. Which of the following is a common adverse effect of fenugreek?
    i.    Somnolence
    ii.    Muscle cramps
    iii.    Tinnitus
    iv.    GI upset
    GI upset
  100. In making an argument ‘For’ the use of fenugreek, which of the following is true?
    i.    Fenugreek should always be used in combination
    with other diabetic agents.
    ii.    Fenugreek may be used as an oral supplement to lower blood glucose and HgbA1c and to increase insulin sensitivity.
    iii.    Fenugreek will have no effect on PPG if mixed
    with food and consumed.
    iv.    Fenugreek may be used as an oral supplement to lower blood glucose and HgbA1c, but it will decrease insulin
    Fenugreek may be used as an oral supplement to lower blood glucose and HgbA1c and to increase insulin sensitivity.
  101. Cat's Claw for _________
  102. Part of Cat's Claw used for medicinal purposes
    Roots (bark)
  103. Cat's Claw MOA
    Inhibits production of prostaglandin E1 and TNF-alpha in vitro (anti-inflammatory)
  104. Cat's Claw Efficacy
    • Effective in osteoarthritis of the knee vs. placebo
    • Pain relief only with activity, not at rest
  105. Cat's Claw Dosage and Standardization
    • None
    • Both 100 mg daily and 60 mg daily were used in clinical trials
  106. Cat's Claw AE
    • HA
    • dizziness
    • GI complaints
  107. Cat's Claw in Pregnancy?
    Avoid: used to prevent and abort pregnancy
  108. Cat's Claw Contraindications
    • Renal dysfunction
    • Pts. using immunosuppressants
  109. Cat's Claw Precaution
    • Pts. with active bleeds
    • Hx of bleeding
    • Hemostatic disorders (D/C 14 days before surgery or dental procedures)
  110. Cat's Claw Drug Interactions
    • Anticoagulants/antiplatelets: due to potential antiplatelet effects
    • Antiarrhythmics: antiarrhythmics effects in vitro
    • Antihypertensives
    • Diuretics
    • Immunosuppressants
    • CYP 450 metabolized agents
    • Herbs or supplements with hypotensive effects
    • Chemotherapeutic agents
  111. In what formulations is Cat’s Claw Prepared
    i.    Liquid extracts
    ii.    Capsules
    iii.    Teas

    iv. All of the above
    All of the above
  112. Cat’s claw should be discontinued _________ before medical or dental procedure.
    i.    3 days
    ii.    1 week
    iii.    14 days
    iv.    1 month
    14 days
  113. Which medications interact with Cat’s Claw?

    i.    Antibiotics

    ii.    Antipsychotics
    iii.    Oral contraceptive
    iv.    Anticoagulants
  114. Cat’s Claw was proposed for the use in what ailment?
    i.    Acne
    ii.    Osteoarthritis
    iii.    Hepatitis
    iv.    ADHD
  115. Chasteberry for ___________
    Treatment of Pre-menstrual Syndrome
  116. Portion of chasteberry used
    Dried fruit
  117. Chasteberry MOA
    • Indirectly affects hormones and neurotransmitters including dopamine, ACh, and opioid receptors
    • Higher doses inhibit prolactin release as a result of pituitary dopamine agonism
    • Linoleic acid component: selective for estrogen receptors
  118. Chasteberry Active Ingredients
    • Essential oils
    • Irioid glycosides (agnuside)
    • Flavonoids
    • Diterpenes
  119. Chasteberry Efficacy Profile
    • One trial showed no difference between chasteberry and fluoxetine
    • One trial showed efficacy vs placebo
  120. Chasteberry Standardization
    6% agnuside
  121. Chasteberry Dosage
    20-40 mg daily
  122. Chasteberry in pregnancy?
    C.I. in pregnancy and lactation
  123. Chasteberry AE
    • GI upset (N/D)
    • HA
    • Itching
    • Urticarial rash
    • acne
    • insomnia
    • irregular menstrual bleeding
    • weight gain
  124. Chasteberry Drug Interactions
    • Birth control, estrogens
    • Dopamine agonists: due to increased dopaminergic effects
    • Dopamine antagonists: due to interference with dopamine antagonism
    • Metoclopramide: due to interference with dopamine antagonism
  125. Chasteberry Disease Interactions
    • Hormone sensitive cancers/conditions
    • In-vitro fertilization: could terminate viable embryos
  126. Vitex agnus-castus (chasteberry) affects all of the
    following hormones and neurotransmitters except:

    1. Dopamine

    2. Serotonin

    3. Prolactin

    4. Acetylcholine
  127. What is the most common indication for chasteberry?

    1. Benign prostatic hyperplasia (BPH)

    2. Insect repellant

    3. Menopause

    4. Premenstrual syndrome (PMS)
  128. Chasteberry should be avoided during in-vitro fertilization because:

    1. Chasteberry causes the death of sperm cells

    2. Chasteberry causes potential hyperstimulation syndrome that terminates viable embryos

    3. Chasteberry has potential effects on estrogen levels

    4. Chasteberry’s dopaminergic effects cause spontaneous abortion
    Chasteberry causes potential hyperstimulation syndrome that terminates viable embryos
  129. All of the following medications interact with chasteberry except:

    1. Metoclopramide

    2. Antipsychotics

    3. Birth controls

    4. Antihypertensives
  130. Zinc for ________
    Treatment of Acne
  131. Zinc MOA
    Prevents granulocytes from being attracted to the vicinity of invading pathogens, thuse preventing inflammation
  132. Zinc Efficacy
    • Conflicting Data
    • In combination w/ erythromycin was more effective than erythromycin alone
    • Another trial showed the Zinc in combination with erythromycin was less effective than benzoyl peroxide + erythromycin
Card Set
Exam 2