1
Q
immunogenecity
A
ability of foreign substance (ex. Antigen) to provoke an immune response in the body of a human or other animal
2
Q
Biologic Drug
A
- A substance that is made from a living organism or its products and is used in the prevention, diagnosis, or treatment of cancer & other diseases
- Biological drugs include antibodies, interleukins, and vaccines
3
Q
What is an example of a peptide drug
A
Insulin
4
Q
Insulin Lispro
A
- created by inverting the natural Pro-Lys sequence in human insulin at positions 28 & 29
- self-associates less avidly & dissociates into its monomeric form more rapidly than regular insulin
- absorbed more rapidly & has a shorter duration of action
4
Q
What is a “clot buster”
A
drugs that promote the break-up of these clots to restore normal blood flow
5
Q
Streptokinase
A
- bacterial protein produces by a group C B-haemolytic streptococci
- interacts w/ plasminogen, results in activation of plasminogen to plasmin, plasmin breaks down fibrin & fibrinogen in clots
6
Q
ends in -plase
A
- hemolytic enzyme
7
Q
Adalimumab
A
- 1st fully human monoclonal Ab
- Binds to TNFa preventing activation of TNFR2 on immune cells
- Prevents cytokine from producing inflammation
8
Q
-mab
A
Murine, high production of human anti-mouse Abs
9
Q
-ximab
A
Chimeric, 60-70% of human protein (constant domains) + 30-40% murine Abs
10
Q
-zumab
A
humanized, 5-10% murine Abs
11
Q
-mumab
A
human, 100% human
12
Q
What are the 3 mechanisms for Ab clearance
A
- target Ag mediated (on-target) and off-target binding
- Glycan receptor mediated
- FcRN receptor mediated
13
Q
Qualitative variation in Drug Response
A
- Unusual or idiosyncratic drug responses
- Response that is often dramatic & that is observed infrequently
- Typically unknown cause
14
Q
Quantitative variation in Drug Response
A
- Same response as usual, just higher or lower than expected
- Terms hyperreactive & hyporeactive are used (rather than “hypersensitive” which is a term used to denote an allergic reaction)
15
Q
Reasons for Variation in Drug response
A
- species variability
- adherence
- disease states
- age
- sex
- diet
- genetics
16
Q
Pharmacokinetic changes in Elderly that affect Drug Response
A
- Absorption - little physiological difference, higher rates of use of GI drugs including laxatives, antacids, may affect absorption of medicines in this pop
- Distribution - relative decrease in lean body mass, increase in fat %
- Metabolism - increased chance of drug interactions, general decrease in hepatic clearance
- Excretion - general decrease in kidney function
17
Q
Pharmacodynamic changes in Elderly that affect Drug Response
A
- more responsive to sedative-hypnotics & analgesics & display decreased responsiveness to B adrenergic receptor agonists
18
Q
Differences in females that affect drug response
A
- Pain perception & intensity may be higher in females
- Male respond better to NSAIDs, women respond better to opioids
- Rate of gastric emptying is slower in females
- Different levels of subcutaneous fat vs. muscle for transdermal absorption
- Smaller tidal respiratory volume in females
19
Q
Grapefruit juice inhibits…
A
Metabolic enzyme CYP3A4
20
Q
What could happen from an increase in Green Leafy Vegetables
A
- greean leafy vegetables are high in Vitamin K
- Warfarin is a Vitamin K antagonist, to reduce blood clotting
- these veggies could make warfarin less effective
21
Q
Pharmacogenetics
A
- identifying and evaluating how genetic variation alters the pharmacokinetics (well-studied) and pharmacodynamics (less well-studied) response to drugs
22
Q
Pharmacogenomics
A
using tools to survey the genome & assess multigenic determinants of drug response
23
Q
Extensive metabolizers
A
term used to describe “normal” or “typical” metabolizers often the largest group in a given pop
24
Poor metabolizers
have fewer copies or dysfunctional metabolic enzymes
25
Ultra-rapid metabolizers
typically have multiple copies of the metabolic gene
26
Metabolic enzymes that contribute to variation in drug response
* CYP450 enzymes
* phase II metabolic enzymes
* drug transporters
27
Intermediate metabolizers
functional gene but not as highly active
28
CYP2D6
* The second most common commercial drug metabolizing enzyme & is the most variable, w/ over 90 alleles
* CYP2D6 ultra-rapid metabolizer phenotype is very high in countries in the Middle-East & East Africa
* CYP2D6 variability means that codeine may be converted to morphine to different extents in different people
29
What is a Drug Interaction
* Occur when 1 drug or substance changes any parameter or effect of another drug/substance
* Drug interactions can also result in positive therapeutic effects & vast majority of drug interactions result in NO clinical impact
30
Example of Absorption DIs
* Vitamin C can increase the absorption of iron supplements
* Vitamin C prevents iron from chelating into insoluble complexes with other molecules
* Keeps it free to absorb
31
Example of Distribution DIs
* NSAID & Warfarin
* **plasma protein binding**
* Free concentration of Warfarin in plasma rises, more warfarin has access to liver, drop clotting factors further, increases INR
32
Example of Metabolism DIs
* Reversible inhibitors - Reversible interactions of the heme-iron active centre or surrounding lipophilic areas or both, Ex. Fluoroquinolones antimicrobial, azole antifungals, diltiazem
* Irreversible inhibitors (metabolite intermediate complexation & mechanism-based inactivation)
33
Example of Excretion DIs
* NSAIDs can reduce the renal clearance rate, which effects many drug levels
* oral contraceptives & antibiotics, If an antibiotic kills much of the GI tract bacteria, the drug will remain glucoronidated, will be reabsorbed back into body and excreted in the feces
34
What are Pharmacodynamic drug interactions?
* Do you have 2 drugs activating the same receptor
* Most common example would be an interaction where someone administered a GPCR agonist & antagonist
* Atropine & Acetylcholine
35
What are Physiological drug interactions
* When 2 drugs act on the same pathway to increase or oppose each others' physiological response
* Warfarin & NSAIDs, anticoagulant & antiplatelet -> both reduce clotting
* Benzodiazepines & opioids have synergistic
36
Supra-additive
* synergistic
* C > A + B
* sume of the whole is greater than the parts
37
Differentiation
* One cell type (ex. Stem cell) is differentiating into another cell type (ex. Kidney cell)
* Drugs can impact these processes in the fetus but not in the child/adult
38
Principles of Teratology
1. Genetics & envmt contribute to teratogenicity
2. Teratogenesis involves specific developmental stage
3. Teratogen acts in a specific pathway or specific mechanism, & a specific negative outcome
4. The agent causes specific adverse effects
5. Identifies the 4 manifestations: death, malformation, growth retardation, & functional deficit
6. Dose dependence
39
A Teratogen ...
| 3 of the principles
1. Results in a characteristic set of malformations & is organ-selective
2. Exerts its affects at a specific state of fetal development
3. Is dose-dependent
40
Fetopathic
* Don't cause a specific malformation but a generalized adverse effect
* Ex. Increased risk of miscarriage or stillbirth, pre-mature birth, low birth weight etc…
41
Mechanisms of Teratogenesis
* DNA mutations
* Chromosome breaks
* Impaired mitosis
* Macro and micro-nutrient deficiency
* Specific protein interactions/inhibition
42
Pharmacokinetic changes in Pregnancy
* Changes in body water/fat content
* Changes in GI tract function
* Changes in cardiovascular function
* Changes in blood volume and extravascular compartment volume
* Reduced plasma protein concentration
* Changes in metabolism and excretion
43
Fetal Blood Trapping
* pH differences between fetal and maternal blood
* pH of fetal 7.2, maternal 7.4
* Basic drug, unionized can cross placenta barrier, so if pKa is in 7.2-7.6 range could have fetal blood trapping
* Since drug is going to slightly more acidic environment, have more basic drug in ionized form
44
Maternal Attributes that contribute to the incidence of adverse fetal outcomes
* Maternal nutrition
* Maternal disease - hypertension, diabetes & infection (ex. Hypothermia)
* Maternal genetics
* Maternal stress
45
FDA Risk Category A
* controlled studies in women showed no risk in 1st trimester (or later trimesters)
46
FDA Risk Category B
* animal studies showed no risk
* no controlled studies in women
47
FDA Risk Category C
* animal studies have revealed adverse effects on fetus, may still use if benefit outweighs risk
* Usually biggest category, most difficult clinical work
* Risk/benefit decision is not always clear
48
FDA Risk Category D
* positive evidence of fetal risk
49
FDA Risk Category X
* studies in animals & humans, have demonstrated a fetal abnormality
* risk outweighs any possible benefit
50
Pregnancy & Lactation Labeling Rule
* PLLR replaces the letter categories for drug safety in pregnancy w/ a more comprehensive approach
* drug's potential negative outcomes in pregnancy, lactation, and the effects of drugs on reproductive potential for males & females (new)
* Known risks based off available data
* Medical/disease factors that may increase risk
* Describing animal data in terms of human exposure
* Stating when no human data is available
51
Thalidomide
* most infamous case of drug-induced fetal malformation
* sedative & to prevent nausea & vomiting associated w/ pregnancy
* It is relatively safe in humans EXCEPT during the few weeks when fetal limb development (16 days) is occurring
* Has now been tested in 19 species & has mixed effects
52
Diethylstilbestrol
* A synthetic, non-steroidal estrogen used to prevent miscarriage by stimulating hormonal production in the placenta
* The cancer was linked to maternal use of DES prior to 18 weeks of ages was correlated to development of vaginal cancer in the female offspring
* There were also adverse effects in males including reduced sperm counts & poor semen quality
53
Retinoids
* Retinoid acid-related compounds that bind the hormone retinoid acid receptor (this can dimerize w/ other hormonal receptors)
* Retinoid receptors heterodimerize with thyroid receptors, other crucial hormone receptors
* Vitamin A deficiency causes malformations
* Knocking out retinaldehyde dehydrogenase in mice leads to malformations
* Knocking out retinoic acid receptors in mice leads to malformations
* Excess ligand (e.g. Accutane, very high-dose vitamin A) causes malformations
54
Tobacco Smoking Teratogen
* Strongest association w/ smoking tobacco & lower birth weights (also the strongest association w/ cannabis smoking)
* causative factor for lower birth weights are the aromatic hydrocarbons instead of nicotine/cannabinoids
55
Alcohol Teratogen
* fetal alcohol syndrome (FAS)
* teratogenic & fetopathic effects
* Craniofacial abnormalities
* CNS dysfunction
* Pre- and/or post-natal stunting of growth
56
Folic Acid Teratogen
* Folic acid is inversely-associated w/ neural tube defects
* Shown to decreases the incidence of neural tube defects including spina bifida if taken during pregnancy
* Supplementation is recommended prior to conception, b/c neural tube defects occur approx 1 month (23-26 days) after conception (before pregnancy might be identified)
57
Gross fetal abnormalities occur at a base rate of ____%
1%
58
Prolactin
* causes alveoli to take nutrients from blood supply & turn them into breastmilk
59
Oxytocin
* causes muscle contractions that pushes breastmilk out of the Alveoli and through the milk ducts
* Release will also cause uterine contractions which helps return the uterus to pre-pregnancy size
60
Infant risk vs. embryo/fetus risk
* The developed infant is relatively less susceptible to drug toxicity than the embryo or fetus
61
milk/plasma ratio is 1
* drug transfers readily into the milk & [ ]'s in the plasma & milk are the same
62
milk/plasma ratios greater than 1
* Drugs that accumulate in milk at higher [ ]'s than the plasma have
63
Relative infant dose (RID)
* gives a % dose to the infant based on the maternal dose & the milk/plasma ratio
64
What is a Minor Ailment
* Short term health conditions that can be managed w/ minimal treatment/self-care
65
What is Allergic Rhinitis?
* An allergen-dependent inflammation of the lining of the nose associated w/ conjunctivitis
* May be chronic, recurrent or seasonal
66
Examples of 1st gen Anti-histamines
* Ethanolamine ethers -> Diphenyhydramine
* Alkyl amines -> Chlorpheniramine, Brompheniramine, Dexbrompheniramine
67
Ethanolamine Ethers (Diphenhydramine)
* oldest antihistamine used today
* Nonselective, reversible H1-receptor antagonists
* Lipophilic molecules that can pass the BBB
* CNS side effects - sedation, drowsiness
* Cholinergic aide effects - dryness of mouth, blurred vision
68
Alkyl Amines (Chlorpheniramine, Brompheniramine)
* Carbon atom replaces the heteroatom spacer
* Long duration of action, decreased CNS & cholinergic side effects compared ethanolamine ethers
* BUT still has CNS & cholinergic side effects
* S-enantiomers exhibit greater affinity toward H1-receptors
* Alkyl chain w/ amine on the right of the molecule
* Benzene ring can have Cl or Br
69
SAR of 1st Gen Anti-histamines
* aromatic rings at Ar1 & Ar2 provide optimum H1 receptor binding
* X can be carbon or CHO (ether) or nitrogen
* 2 or 3 carbon spacer provides optimum activity
* R1 & R2 can be alkyl groups (Me) or alkyl chains
70
Why use 2nd Gen over 1st Gen Anti-histamines
* Exhibit increased tolerability & safety, decreased CNS & cholinergic side effects
* selective, peripheral H1-receptor binding as opposed to H1-receptor binding in the CNS
* Rapid onset of action
* Zwitter ionic (amphoteric) in nature & are unable to cross the BBB
* slow dissociation from H1-receptors & exhibit long duration of action
71
Terfenadine & Fexofenadine
* Terfenadine was withdrawn in the 1990's due to increased risk of cardiac arrhythmias
* Fexofenadine (Allegra) is the carboxylic acid metabolite of Terfenadine & lacks the cardiovascular side effects
* Carboxylic group undergoes oxidation
* Polar group, less likely to get into brain, less CNS SEs, non-drowsy
72
Loratadine (Claritin)
* Related to 1st gen tricyclic antihistamines
* Desloratadine is the more potent antihistamine (H1-selective) active metabolite of loratadine & is marketed are Clarinex
* Piperadine ring
* NH2+ -> highly polar, won't get into brain
* Nonsedating & lack cardiovascular toxicity
73
Bilastine
* H1 receptor binding affinity similar to cetirizine
* Lacks CNS & cardiovascular SE
* Benzimidazole ring -> enhances H1 binding affinity
* Piperidine & carboxylic acid group -> highly polar, doesn't go to brain in high enough [ ] -> no drowsiness
74
Rupatadine
* Fused tricyclic/piperidine derivative
* H1 receptor antagonist & inhibitor of platelet-activating factor (PASF)
* Chemical structure is highly lipophilic drug
* But when taken orally, undergoes conversion to multiple metabolites which are highly polar
* Lacks CNS & cardiovascular SE
75
Fluticasone Furoate
* Steroid derivative
* Bind glucocorticoid (GR) receptors
* Fluticasone furoate & propionate exhibit potent anti-inflammatory activity
* Furan ring, fluorenes, thiofluromethyl -> enhance binding affinity towards glucocorticoid receptors
76
Steroid Derivative Nasal Sprays
* steroids: 4 rings -> A, B, C, D, 3 cyclohexanes & 1 cyclopentane
* Allergy in chronic phase has inflammation & inflammation mediators -> steroid based drugs
* Examples: Mometasone furoate, Ciclesonide, Fluticaseon Furoate, Azelatine
76
Mometasone Furoate
* steroid derivative
* Bind glucocorticoid (GR) receptors
* Exhibit anti-inflammatory activity
* Chloromethyl group & furan ring -> enhance binding affinity for GCR
* Route of admin - nasal spray
77
Ciclesonide
* steroid derivative
* Bind glucocorticoid (GR) receptors
* Exhibit anti-inflammatory activity
* Dioxolane ring enhances metabolic stability & binding affinity to GCR
* route of admin - nasal spray
77
Azelastine
* 2nd gen anti-histamine, H1-receptor antagonist & mast cell stabilizer
* Pyridazinone ring -> binding affinity to H1 receptors
* Route of admin - nasal spray
78
Fusidic Acid
* Steroid antibiotic
* Obtained from fermentation of Fusidium coccineum
* Antibacterial agent
* Carbon-carbon DB -> not very stable from light
* Exposed to light, might undergo degradation
* Route of admin - topically to eyes
79
Lodoxamide
* Anilinio oxacetic acid derivative (symmetric diacid)
* Mast cell stabilizer
* Can chelate Ca2+ ions & prevent activation of mast cells
* Need the 2 acidic groups on either end to chelate Ca2+
* Nitrile group & chloride group are EWGs
* Route of admin - topically to eyes
80
Ketotifen
* Fused tricyclic/piperidine derivative
* Exhibit selective H1-receptor binding
* Also acts as mast cell stabilizer
* Thiophene ring
* Prodrug: tertiary amine -> secondary amine = active metabolite
* Route of admin - topically to eyes
81
Bepostastine
* Piperidine derivative
* Exhibits selective H1-receptor binding
* Also acts as mast cell stabilizer & shows anti-inflammatory activity
* Sold as the S-enantiomer
* Diphenyl ring
* Route of admin - topically to eyes
82
Oloptadine
* Fused tricyclic derivative
* Exhibit H1-receptor binding
* Also acts as mast cell stabilizers
* Have to have carboxylic acid group
* Tertiary amine can undergo metabolism to secondary amine -> not active, therefore not a prodrug
* Can change Oxapane to C, or N & molecule will still show activity
* Route of admin - topically to eye
83
Desonide
* Steroid derivative
* Desonide has anti-inflammatory activity
* Binds to glucocorticoid (GR) receptors
* Dioxolone ring -> increases binding affinity towards glucocorticoid receptors & enhances stability
* Route of admin - topically as a cream
84
Crisaborole
* Benzoxaborole derivative
* Phosphodiesterase-4 (PDE-4) inhibitor
* Boron -> oxaborolane
* EWG enhances binding affinity to phosphodiesterase enzyme
* Route of admin - topically as a cream
85
What are Decongestants
* Are a1 adrenergic receptor agonists and/or indirect sympathomimetics (NE releasing agents)
* Act in the nasal mucosa to produce vasoconstriction
* decreases volume of nasal mucosa & reduce delivery of secretions to nasal mucosa
* Results in decreased resistance to airflow & improve ventilation
86
Cough, Cold and Flu Medications include:
* An analgesic/antipyretic/antiinflammatory (typically acetaminophen or ibuprofen)
* A cough suppressant (dextromethorphan)
* A decongestant (e.g. pseudoephedrine)
* An antihistamine (typically first-generation, in the “night time” dosage form)
87
Examples of Decongestants
* Ephedrine
* Pseudoephedrine
* Phenylephedrine
88
What are Antitussives
* in cough/cold preparations include dextromethorphan or codeine
* act centrally on medulla to increase cough threshold
89
Centers involved in cough
* Pneumotaxic center
* Apneustic center
* Pons
* Medulla
* 4th ventricle
* Reticular formation
90
Opioid Antitussives
* All opioids are cough suppressants
* Codeine is both an opiate & Opioid
* Acts on opioid receptors in medullary cough centre
* May also have additional peripheral action
* does NOT require metabolism to morphine
* ADRs: sedation, constipation
91
Dextromethorphan
* D-isomer of levorphanol (chemically similar to codeine)
* No analgesic or euphoric properties
* Does NOT act through opioid receptors
* Acts centrally to elevate threshold for coughing
* Metabolized by CYP 2D6 - increased CNS effects in poor metabolizers/drug interactions w/ 2D6 inhibitors
* ADRs: Occasional dizziness, drowsiness, nausea `
92
What are Expectorants
* Helps bring mucous & other materials from the bronchi
* stimulation of respiratory tract secretions, thereby increasing respiratory fluid volumes & decreasing mucous viscosity & promoting mucociliary activity
* Ex. Gaidenesin
93
What is Arachidonic Acid
* AA & its metabolites are long-chain carbon molecules w/ a carboxylic acid functional group
* Double bonds in the carbon chain result in the molecule folding back on itself in a hairpin loop
94
Eicosanoids
* Lipid signalling molecules related to or derived from arachidonic acid
* Autocoids - includes eicosanoids as well as histamine, serotonin, kinins
* modulate the activity of smooth muscles, nerves, glands, platelets & other tissues
95
Prostanoids
* derived via the actions of cyclo-oxygenase (COX), an enzyme that converts arachidonic acid to PGH2
* AA -> PGH2 -> Prostanoids
96
Leukotrienes
* Derived from HPETE which is produced from arachidonic acid by lipoxygenase (LOX)
* synthase, hydrolase & dipeptidase enzymes then convert HPETE into additional leukotrienes
* AA -> HPETE -> Leukotrienes
97
What are Anti-pyretics
* Primary target is the cyclo-oxygenase enzyme
* Centrally produces fever-reducing (antipyretic) activity via inhibition of COX in the thermoregulatory centre
* inhibit synthesis/release of prostaglandins (PGE2) in the thermoregulatory centre of the anterior hypothalamus (to reverse some of these actions by cytokines)
98
What are NSAIDs
* used for pain (analgesic effects), inflammation (anti-inflammatory effects) and fever (antipyretic effects)
* inhibit cyclo-oxygenases (COX) to prevent conversion of arachidonic acid to PGH2, thus preventing subsequent prostaglandin production
* Inhibition of COX-2 produces (most) of the therapeutic effects
* Inhibition of COX-1 produces (most) of the AEs
* 1st NSAIDs were non-selective COX inhibitors
* COX-2 selective inhibitors -> ex. Celecoxib
99
Ibuprofen
* Common NSAID
* propionic acid derivative
* ibuprofen will cause typical NSAID adverse reactions, including GI AEs
* equipotent for COX1 & COX2
100
What are Corticosteroids
* Target 1st enzyme in the arachidonic acid cascade, phospholipase A2 (enzyme that synthesizes AA)
* shut down all arachidonic acid products including prostaglandins, bradykinins, & leukotrienes
* treatment of allergic reactions of any type, all autoimmune disorders, & any inflammatory condition (ex. Acute & chronic pain)
101
What are Opioids & How do they work?
* Any chemical that activates opioid receptors can be called an opioid
* 3 classes - Endorphins (beta-endorphin), Enkephalins (leu- and met-enkephalin), Dynorphins
* Opioids activate opioid receptors including u, S, and k
* directly inhibit the ascending neurotransmission of pain from the spinal cord dorsal horn
* increase the activity of "pain control" circuits that descend from the midbrain to the medulla & to the spinal cord dorsal horn
* A greater effect on pain tolerance than perception, so pts may still perceive the pain, but it won't cause as much discomfort
102
What are Topical Anesthetics
* reversible drug induced loss of sensation in a specific site
* Sensation is carried by nerve fibers arranged in bundles
* Excitable nerve cells generate action potentials which are responsible for nerve conduction
* Local anesthetics inhibit Na+ influx & block propagation of APs
103
PPIs
* Structurally related to H2 histamine receptor antagonists
* specific effects on the gastric proton pump
* administered as active drugs or prodrugs
* Metabolized by CYP2C19 -> variations in this enzyme may affect efficacy & toxicity
* PPIs accumulate in Parietal cells of the GI tract & find their way into the stomach
* Once in stomach, activated by low pH & start to covalently bind to H+/K+-ATPase by disulfide bonds
104
Antacids
* self-limited and/or intermittent GERD
* Bases are ingested, result in direct interaction w/ H+ to form salt & water
* May also stimulate prostaglandin production
105
Bismuth compounds
* Ex. Pepto-Bismol
* Coats erosions & ulcers
* Stimulates prostaglandin production
* Stimulates mucous & bicarb secretions
* Decreases GI secretions to treat diarrhea
106
Loperamide
* NOTE: opioids can cause constipation -> reverse diarrhea
* Loperamide is structurally-related to opioids but w/out significant central opioid effects (at least at typical doses) due to limited crossing of BBB
* decreases smooth muscle tone
107
Receptors involved in nausea & vomiting
* M1 muscarinic receptors
* H1 histamine receptors
* NK1 Neurokinin receptors
* 5-HT3 serotonin receptors
* D2 dopamine receptors
108
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Dermal Layers drug partitions through
In vehicle at surface -> Stratum corneum -> stratum spinosum -> Basement membrane -> Subcutaneous fat -> Bloodstream
109
Treatments for Eczema
* emollients
* topical steroids
* topical antihistamines
* topical immunosuppressants
* PDE4 inhibitors
* topical antibiotics
110
Benzyl peroxide
* treatment in acne
* Penetrates skin & is converted to benzoic acid in epidermis & dermis
* involves direct antimicrobial activity as well as epidermal turnover rate increases
111
Retinoic Acids
* treatment for acne, topical form
* result in decreased cohesion b/w epidermal cells, thus increased epidermal turnover
* induce direct inflammation & peeling
* sun avoidance & sunscreen
112
Oral Isotretinoin
* treatment for acne, oral
* may cause dry, itchy skin & lipid profile changes
* Teratogenicity
113
Melatonin
* NT derived from the AA tryptophan
* Involved in sleep-wake cycles & diurnal rhythms, released during dark cycle - 9pm to 4 am
* Melatonin 1 receptors are coupled to Gai & are thought to promote sleep when activated
* Melatonin 2 receptors are Gq-coupled & are thought to serve a coordinating function in the light-dark cycle
114
Xerostomia
* dry mouth, is a side effect of anticholinergic drugs, but can also be caused by smoking, mouth breathing, dehydration or other disease states
* treatment includes Cholinergic agonists (ex. Bethanechol, pilocarpine) or Cholinesterase inhibitors
115
What are the criteria to be an Essential Nutrient
* Required in diet for growth, health & survival
* Absence from diet or inadequate intake leads to characteristic signs of a deficiency disease & eventually death
* Signs of deficiency are prevented only by the nutrient or a precursor
* Severity of signs of deficiency is proportional to amount consumed
* The substance is not synthesized in the body
116
Toelrable upper intake level (UL)
highest level of continuing daily nutrient intake that is likely to pose no risk of adverse health effects in almost ALL individuals in the life-stage group
117
Estimated average requirement (EAR)
median usual intake value estimated to meet the requirement of 1/2 the health individuals in a specific age or gender group
118
Recommended daily allowance (RDA)
* average daily dietary intake level that is sufficient to meet the nutrient requirement of nearly all healthy individuals in a life stage & gender group
119
Fat Soluble vitamins
* Vitamin A, D, E, K
120
Water-soluble vitamins
* B vitamins, Vitamin C
121
Electrolytes
* sodium
* potassium
* chloride
122
Essential minerals
* calcium
* phosphorus
* magnesium
* iron
123
Key trace minerals
* zince
* copper
* manganese
* iodine
* slenium
* molybdenum
* chromium
PHARM 141
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