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401 mt > TOXIDROMES AND DIETARY SUPPLEMENTS > Flashcards

TOXIDROMES AND DIETARY SUPPLEMENTS Flashcards

1
Q

CLINICAL DIAGNOSIS

A

collect
assess
plan
implement
f/u

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2
Q

TOXIDROMES

5 main toxidromes

A

toxidromes based on…

5 main
- sympathomimetic
-anticholinergix
-cholinergic
-sedative/hypnotic
- opioid
- never ones (neuroleptic malignany syndrome, serotonin syndrome

2 larger classes toxidromes
- fast and furious: sympathomimetic and anticholinergic
- downers: sedative-hypnotics, opioids

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3
Q

TOXIDROMES – VITAL SIGNS

bp, pulse, RR, temp, pupils, skin, peristalsis
other signs

A

Sympathomimetics ↑ ↑ ↑ ↑ Dilated Wet −/↑ Tremors, seizures diaphoresis

Anticholinergic +/- ↑ +/- ↑ Dilated Dry ↓ Dry mucous, flush, urinary retention

Cholinergic +/- +/- - - Small Wet ↑ Salivation, lacrimation, urination,
diarrhea, bronchorrhea,
fasciculations, paralysis

Opiates ↓ ↓ ↓ ↓ Small - ↓ Hypoflexia

Sedative/Hypnotic ↓ ↓ ↓ ↓ +/- - ↓ Hypoflexia, ataxia

Withdrawal** ↑ ↑ −/↑ −/↑ Dilated Wet ↑ Tremors, seizures diaphoresis

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4
Q

TOXICOLOGY MNEUMONIC

bradycardia PACED
tachycardia FAST

A

P - propanolol (BB), poppies (opioids)
A - anticholinesterase drugs
C - clonidine, CCB
E - ethanol, other alcohols
D- digoxin

Tachycardia (FAST)
F - freebase (cocaine)
A - anticholinergics, antihistamines, amphetamines
S -sympathomimetics, solvent abuse
T - theophylline

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5
Q

TOXIDROMES - SYMPATHOMIMETIC

causes
key signs/symptoms
common agents
tx/antidote

A

slide 10

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6
Q

TOXIDROMES - ANTICHOLINERGIC
causes
key signs/symptoms

mnemonics
common agents
tx/antidote

A

slide 11-12

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7
Q

TOXIDROMES - CHOLINERGIC
causes
key signs/symptoms
common agents
tx/antidote

A

slide 13

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8
Q

TOXIDROMES – SEDATIVE/HYPNOTIC
causes
key signs/symptoms
common agents
tx/antidote

A

slide 14

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9
Q

TOXIDROMES - OPIOID

causes
key signs/symptoms
common agents
tx/antidote

A

slide 15

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10
Q

TOXIDROMES - Serotonergic (Serotonin Toxicity)

causes
key signs/symptoms
common agents
tx/antidote

A

slide 16

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11
Q

TOXIDROMES - Withdrawal Syndromes

alcohol, sedative-hypnotic, opioid

A

slide 17

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12
Q

SALES AND REGULATION….
, Supplements

A

Natural Health Products
Under the Natural Health Products Regulations, which came into effect on
January 1, 2004, natural health products (NHPs) are defined as:
q Probiotics
q Herbal remedies
q Vitamins and minerals
q Homeopathic medicines
q Traditional medicines such as traditional Chinese medicines
q Other products like amino acids and essential fatty acids

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13
Q

PROBLEMS
Key Issues

A

§ Poorly characterized (ie., ADME)
§ Not been rigorously studied – lack of good scientific data
§ Inadequately regulated manufacturing
§ Contamination or tampering of the products
§ Potential interaction with prescription drugs
§ Narrow therapeutic range (eg. warfarin and digoxin) highest risk
§ Products decrease concentrations of daily medications such as
immunosuppressants to prevent organ rejection

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14
Q

PHARMACOLOGICAL PRINCIPLES

5

A
  1. Volatile oils – Aromatic plants (ethereal or essential oils), evaporate at RT, odor, many
    are mucus membrane irritants, CNS activity, eg., catnip, chamomile, garlic
  2. Fixed oils – Esters of long-chain fatty acids and alcohols, used as emollients,
    demulcents, bases of other products, generally least dangerous, eg., olive and peanut oils
  3. Resins – Complex mixtures of acrid resins, resin alcohols, resinol, tannols, esters,
    resenes, strong GI irritants, eg., dandelion, elder
  4. Alkaloids – Heterogenous group of alkaline and nitrogenous cmpds, found throughout plants, many active and toxic compds, eg., acotnium, goldenseal, Jimson weed
  5. Glycosides – Esters that contain a sugar component (glycol) and a nonsugar (aglycone)
    - Saponins: licorice, ginseng (mucus membrane irritants, cause hemolysis, steroid activity)
    - Anthraquiones: senna, aloe (irritant cathartics)
    - Cyanogenic glycosides: apricot, cherry, peach pits (release cyanide)
    - Lactone glycosides: tonka beans (anticoagulant activities)
    - Cardiac glycosides: foxglove and oleander (cardioactive steroids – digoxin)
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15
Q

CONTAMINATION

Metal and mineral poisonings from lead,
cadmium, mercury, copper, selenium, zinc,
arsenic…

A

Mineral Clay Products
* Products used to relieve joint pain,
muscle or other chronic diseases
(osteoarthritis)
* Clay acidic extracts suppress nitric
oxide production and reduce
inflammation
* Rich in essential mineral but may also
contain arsenic, cadmium lead

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16
Q

DIETARY SUPPLEMENT-DRUG INTERACTIONS
St. John’s Wor

A

q Common herbal remedy promoted to treat anxiety, depression, gastritis,
insomnia, promote healing, HIV
q Interacts >20 different pharmaceutical products – clinical implications
A) Chronic use – induces P-gp activity, leads decrease absorption and increased
excretion
B) Induces CYP3A4, CYP2E1, CY2C19
C) Inhibits monoamine reuptake, increasing levels of serotonin, norepinephrine,
dopamine – precipitates serotonin toxicity
D) Inhibits COX-1 in platelets decreasing TxA2 (additive effect with antiplatelet
agents)

17
Q

vitamins
concerns

A
  • Consistently among the top most common categories of poisonings
  • Two general classes:
  • Water-soluble
  • Minimal toxicity -thiamin, riboflavin, pantothenic acid, folic acid, biotin, Vit B12
  • Associated toxicity - Ascorbic acid (Vit C), nicotinic acid (Vit B3) and
    pyridoxine (Vit B6)
  • Fat-soluble
  • Bioaccumulate and may have toxicity
  • Vitamins A, D and E (but not K) toxicity large overdose or chronic use
  • Adverse effects secondary to Vit K – severe/fatal anaphylactoid reaction
18
Q

Vitamin A
RDA
Adult male 900 mcg RAE/day (3,000 IU/day)
Adult female 700 mcg of RAE/day (2,300 IU/day)

pathophys

A
  • Two forms – retinol (storage form) and carotenoid (precursor)
  • Essential for growth and differentiation of epithelial cells in mucus-secreting or keratinizing tissues
  • Primarily stored in the liver

Pathophysiology
* Toxic effects at the nuclear level as retinoic acid influences gene expression (hormones, growth factors)
* Hepatoxicity (Ito cells) – hypertrophy, hyperplasia transdifferentiation -obstruction
* Evidence of idiopathic intracranial hypertension

19
Q

vitamin a
clinical manisfestations
management

A

dlinical Manifestations
* Toxic effects more frequent with chronic ingestions
* Acute O/D – hrs-2days-
* Chronic – affects skin, hair, bones, liver, brain – dry/fragile skin (yellow-orange discoloration); hair thinning/curly; nails shiny/brittle; cirrhosis/portal hypertension; severe headache/visual disturbances

Management
* Acute – GI decontam (activated charcoal)
* Discontinuation and supportive care

20
Q

Vitamin D

pathophys

A
  • Deficiency – historical problems (Rickets disease)
    lack of dietary or sunshine
  • Excessive fortification of foods (milk) led to
    poisonings – balance
  • VitD must be metabolized (liver) into active form
  • Circulates, binds to receptors – regulates calcium
    Pathophysiology
  • Toxic doses – varies, no consensus
  • Hallmark toxicity is hypercalcemia, serum concentrations 25(OH)D 20x normal
21
Q

vitamin d
clinical manisfestations
management

A

Clinical Manifestations
* Early manifestations – weakness, fatigue, somnolence, irritability, muscle and bone pain,
nausea/vomiting, abdominal pain
* Chronic – polyuria and polydipsia, nephrolithiasis (kidney stones)
* Severe hypercalcemia – ataxia, confusion, psychosis, seizures, AKI, cardiac dysrhythmias
Management
* Discontinuation and supportive care, oral or IV fluids, calcitonin

22
Q

Vitamin E

pathophys
clinical manisfestations
management

A
  • Eight naturally occurring compounds 2 classes (tocopherols and tocotrienols)
  • Antioxidant properties, protects polyunsaturated FA from oxidation, binds to
    peroxyl radicals
    Pathophysiology
  • High doses it acts as prooxidant (ie., alpha-tocopheroxyl radical)
    Clinical Manifestations
  • GI symptoms – nausea, diarrhea, abdominal cramps >2000mg/day
  • Antagonizes the effects of vitamin K by increasing epoxidation to inactive form
    Management
  • Discontinuation and supportive care
23
Q

Vitamin C

clinical manisfestation
pathophys

A

Ascorbic acid, reported antioxidant properties, scurvy (reducing agent)
* Popular use for wound healing, cataracts, aging, mental attentiveness decrease
stress
* Little to no objective data to support these benefits (500mg/day supplements)
* Absorption occurs by a saturable active transport system in intestine, large
ingestions get eliminated via kidney (occurs ~3g/day)
* Co-factor in several hydroxylation and amidation reactions
* Prooxidant properties at high concentrations
Clinical Manifestations
* Conflicting data suggesting association with oxalosis and kidney stones
* GI effects at high doses (>1g/day) – localized esophagitis (prolonged mucosal
contact) and diarrhea

24
Q

Vitamin B6

pathophys
clinical manisfestations
management

A
  • Pyridoxine absorbed in intestinal tract, rapidly metabolized, renal excretion
  • Pyridoxal phosphate (PLP) is the active form – coenzyme for synthesis of γaminobutyric acid (GABA)
  • Treatment of nausea and vomiting of pregnancy
    Pathophysiology
  • Both deficiency and toxicity are characterized by neurologic effects, peripheral
    sensory system
    Clinical Manifestations
  • Chronic overdose – progressive sensory ataxia and severe distal impairment of
    proprioception and vibratory sensation
  • Reflexes diminished of absent but touch, pain, temp minimally effected
    Management
  • Discontinuation and supportive care
25
Q

Vitamin B3

pathophys

A

Nicotinic acid, or niacin, converted into nicotinamide (incorporated into cofactor NAD)
* Reduces TG synthesis and VLDL production
* Increases HDL-C and decreases LDL-C
Pathophysiology
* Deficiency causes pellagra (dermatitis, diarrhea, dementia)
* Most common ADR vasodilatory cutaneous flushing (sense of warmth) last ~1-3h,
caused by production PGD2 and PGE2

26
Q

Vitamin B3
clinical manisfestations
management

A

linical Manifestations
* Immediate release formulations develop flushing more, dyspepsia
* Extended release more GI effects and hepatoxicity (>2-3g/day)
* Elevated aminotransferases, fatigue, anorexia, nausea, vomiting, jaundice
* Severe cases fulminant hepatic failure and hepatic encephalopathy
Management
* NSAID (aspirin) prior to administration inhibit COX, take with food (avoid EtOH, spicy),
gradual increment of dosing
* Tolerance to flushing will develop – take several weeks

401 mt (12 decks)

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