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herbel Flashcards

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1
Q

To be labeled a supplement

A

The herbal product must make no claims to treat, prevent or cure a disease

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2
Q

Impact of Dietary Supplement Health Education Act

A

Restricted FDA ability to control the safe and manufacturing of herbal products

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3
Q

Why herbals initially regulated in 1920s

A

Presence of natural drugs like cocaine and opium

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4
Q

Common Problem with Herbal Medicines

A

Active Ingredient is unknown therfore saftey/side effects/drug interactions cannot be fully understood.

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5
Q

Why herbal symptoms occur (broad)

A

(1) lack of standardization (2) different purities (3) variations in plant conditions and parts

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6
Q

Two tested treatments for usage of Ginko

A

(1) Cerebrovascular insufficeny symptoms (2) Dementia

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7
Q

Tested Treatment for St. John’s Warts

A

Depression

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8
Q

Six Popular Herbal Supplements (Focus of the Lecture)

A

(1) St. John’s Wort (2) Ginko (3) Kava (4) Ephedrine (5) Omega-3-Fatty Acid (6) Turmeric./Curcumin

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9
Q

Active Ingredient St. John’s Wort

A

Hypericin

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10
Q

Prescribed use of St. John’s Wort

A

Anxiety, Depression, Insomnia (only in Germany)

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11
Q

Pharmokinetics of St. John’s Wort: Admin, Peak Blood LEvel, Half Life, Steady State

A

(1) Administered Orally (2) Peak Blood Levels at 5 hours after (3) Half Life of 25 hours (4) Steady State of 4-6 days

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12
Q

Pharmodynamics of St. John’s Wort (reduce reuptake of 3 NT, binds to 3 types of receptors, has on chemical neuronal influence)

A

(1) Reduced Reuptake of 5HT, NE, DA (2) Bind at GABA Receptors (3) Bind at Benzodiazepine Receptors (4) Blind to glutamatergic NMDA-type receptors (5) Antioxadtive

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13
Q

Clinical efficacy of St. John’s WOrt

A

Now just seend as effective in treatment of mild to moderate depression

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14
Q

What St. John’s Wort inhibits

A

(1) CYP-2D6/CYP-2C9 are inhibited by Hyperforin (2) CYP-1A2 is inhibited by Quercitin

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15
Q

In SJW inhibits CYP1A2

A

Quercitin

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16
Q

In SJW inhibits CYP2D6 and CYP2C9

A

Hyperforin

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17
Q

SJW influence on COdeine

A

SJW decreases effectiveness of codeine due to a inhibition of CYP2D6 which converts codeine into mmorphine

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18
Q

SJW influence on caffeine, tricyclics, antipsychotics

A

INcreased blood level of all three

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19
Q

SJW influence on CYP-3A4

A

Increased activivty… causing reduced levels of drugs that are cardiac and anti-inlammatory

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20
Q

Side effects of SJW

A

Mild: Sedation/Lethargy/Upset GI….. ALso photosensativity, hypomania, seotonin syndrome when combined with SSRIs (agitation, diarrhea, increased heart rate, hallucinations. nasuea, vomitting)

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21
Q

Ginko extract

A

EGb-760

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22
Q

Benefit of Ginko flavonoids and terpenoids

A

(1) Reduce free radicals implicated in the cell damage that cuases Alzheimer’s disease (2)Ginkogolide B inhibits platelet aggregation and slows blood clotting

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23
Q

Harms of GInko flavonoids and Terpenoids

A

Increased tendency to bleed and potentiate action of blood thinners…. also ainhibit CYP-1A2

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24
Q

Pharmokinetics of Ginko (Absorbtion, Peak PLasma, Half life)

A

(1) Taken orally (2) Peak plasma in 2-3 hours (3) Half life of 5 hours

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25
Q

Pharmodynamics of Ginko (homeostatic impact and brain function)

A

Egb-761 extract may act on processes involved in homeostasis of inflammation and oxidative stress ,,, (resulting in membrane protection and neurotransmission modulation)…EEG studies show increased ALPHA wave activity

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26
Q

Clinical Efficencey of Ginko

A

Ginko modestly improves cognitive functioning associated with cerebrovascular impairments but does not prevent the icidence of AD

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27
Q

Side Effects of GInko

A

(1) Mild GI upset (2) Mild Headaches [most common complaint] (3) Exacerbate bleeding problems and interacts with aspirin and other anticoagulants (4) Unknown saftey in pregnancy and lactation

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28
Q

Kava similar to

A

Ethyl alcohol–induces relaxation, improved social interaction & sleep

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29
Q

Kava inhibits

A

CYP450 liver enzyme

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30
Q

Kava most active ingredient

A

Kava Lactone

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31
Q

Kava anesthetic-like effect

A

Blocking sodium channels

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32
Q

Kava Clinical Effects

A

Seen as a short term remedy for moderate anxiety…depressive and GAD symptoms also can be improved with Kava

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33
Q

Kava Side Effects

A

(1) Drowsiness, nasea, muscle weakness, blurred vision, yellow skin, sedative effects (2) DO NOT combine with alcohol, benzoids, barbiturates, THC or CNS (3) Can result in hepatotoxcitity

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34
Q

Ephedrine course

A

Release catecholamine neurotransmitters (NE, DA, EP)

35
Q

Epedrine benefits

A

Reduce appetite, stimulate cardiac function and pyscho-stimulant

36
Q

Epderine harms

A

Release of adrenaline can increase blood pressure, heart rate, and force of cardiac contraction/cardiac output….. FATAL CARDIAC ARRYTHMIAS RESULTS

37
Q

Doping substance of herbals

A

ephedrine

38
Q

Caffeine and Ephedrine

A

Toxic combination because caffine increases the cardiovascular toxcity of ephedrine

39
Q

Psuedoephedrine

A

A synthetic steroisomer to the ephedrine molecule … must sign for it because it can be converted into methamphetamine in large doses

40
Q

Two Major Omega-3-FA

A

EPA/DHA

41
Q

Omega-3-Fatty Acids Found In

A

Wild Fish, Flax Seeds, Olive Oil, Walnuts, Dark Leafy Veggies

42
Q

Where EPA/DHA most deficent

A

(1) Western Diets (2) During Pregnancy (3) Normal Brain maturations

43
Q

EPA/DHA deficencies cause

A

Mood disorders, chronic pain syndromes

44
Q

EPA/DHA antidepressant

A

Useful in treatment of depression and BP

45
Q

ADHD link to Omega-3-FA

A

Children with ADHD consumed 50% less omega-3-FA rich food

46
Q

Normal Course of Omega-6-FA

A

Omega-6-Fatty Acids activate Aracidonic Acid which can in turn activate prostaglandins which cause inflamation

47
Q

How Omega-3-Fatty Acids impact Omega-6-Fatty Acids

A

Omega-3-Fatty Acids Inhibits the Arachidonic Acid (more specifically they inhibit the COX enzyme which converts arachidonic acid to prostagladins

48
Q

Current Westen Ratio of Omega 3 to OMega 6

A

1:8

49
Q

Ideal Ratio of Omega 3 to Omega 6

A

1:1

50
Q

OMega 3 link to Dementis

A

DHA can reduce cognitive decline

51
Q

Omega-3-Index

A

% of EPA + DHA in red blood cells… low index may mean risk for sudden cardiac death

52
Q

Recommended dose during pregnanct

A

200 mg/daty

53
Q

Suggested way of consuming DHA/EPA

A

Not through fish due to mercury but instead consider using supplements

54
Q

Benefits of Omega-3-FA in pregnancy

A

Requires for normal fetal development and optimal maternal outcome…necessary for development of neural/retinal tissues,,,, may reduce allergy susceptibility,,,, may treat depressive symptoms in pregnant females

55
Q

Benefits of Turmeric and Curcumin

A

Impact: Inflammation, cardiovascular, cancer, digestive system, anti-bacterial, anti-fungal, alzheimers, memory

56
Q

NSAIDS

A

Nonnarcotic (non-steroidal) anti-inflammatory analgesics

57
Q

Acute pain

A

Suddenly, usually self limited (opiods best)

58
Q

Chornic Pain

A

Represents a disease by itself..presists over time… leads to loss of independence, loss of interpersonal relationships, work issues, anxiety, depression

59
Q

Chronic Pain Treatment Options

A

(1) NSAIDS (2) Antidepressants with NE potentiating action (3) Mood stabilizing anticonvulsants (4) Opiod Analgesics

60
Q

NSAID impact on tissue injury

A

Reduce inflammation and reduce transmission of pain impulses

61
Q

NSAID euphoria

A

Does not produce

62
Q

NSAID course of action

A

Work by inhibiting synthesis and release of prostaglandins (body hormones that produce the local inflammatory resposne)

63
Q

Prostaglandins

A

Body hormone that produce inflammatory resposne

64
Q

NSAIDS chemical relation

A

nONE

65
Q

NSAID COX influence

A

NSAID block the COX. THey are known as COX inhibitors…

66
Q

COX role

A

Convert arachidonic acid to prostaglandins

67
Q

Cox ENzymes

A

COx 1 and COx2

68
Q

COX 1- ENzyme

A

Mediates production of prostaglandins that protect the GI tract and allow for normal platlet functioning in blood clotting

69
Q

Inhibition of COX1

A

Loss of protection for GI cells which cause ulcers …ALso Loss of platlet function which reduces ability of blood to clot… GOOD because it reduces risk of stroeks and heart attacks BAD because it causes excessive bleeding

70
Q

COX 2 Enzyme

A

INDUCED in response to inflamations. LEads to the production of prostaglandins to mediate inflammation and pain

71
Q

Asprin

A

Good for low intensity pain

72
Q

Antipyretic effect

A

(reduction of fever) due to inhibition of prostaglandin synthesis in the hypothalamus

73
Q

Key parts of aspring

A

Carboxylic acid and an ester

74
Q

Examples of nonselective COX inhibitors

A

Aspring, acetaminophen, ibuprofen

75
Q

Nonselective COX inhibitors impact

A

(1) Anti-inflammatory (2) anti-pyretic (3) Analgesic (4) inhibition of platlet aggregation (5) adverse effects on GI tract

76
Q

Asprin Benefits

A

Can bind to an inhibit blood platelets (prevent blood clotting)

77
Q

Apsring Harms

A

Gastric Upset…also if given when someone has flu can cause Rye syndrome

78
Q

Tylenol difference than Asprin

A

Does not inhibit platlet function, does not cause Rye syndrome, cause less GI distress

79
Q

Adverse effect of acetaminophen

A

Liver damage, hypertension in females

80
Q

Advil compared to tylenol and asprin

A

Advil is better tolerated than aspin.. but it does inhibit platlet aggregation like aspring

81
Q

Selective COX 2 inhibit benefit

A

Reduce risk of cancer, and reduce rate of gastric ulcers while providing same benefits as aspring

82
Q

Example of COX2 inhibitor

A

Celebrex

83
Q

Celebrex impact

A

Does not inhibit platlet aggregation so might increase incidence of heart attack BUT it reduces pain and inflammation with less GI distress

84
Q

Nitroasprins

A

Nitric oxide bound to an NSAID via an ester linkage

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