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NPLEX II TIA > Intro to Pharm/Nutrition > Flashcards

Intro to Pharm/Nutrition Flashcards

(93 cards)

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1
Q

Risk of severe hemorrhage occurs if courmarins are combined with what?

A

any other drug that competes for albumin

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2
Q

How do sulfonamides lead to hypoglycemia?

A

they displace sulfonylureas from albumin

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3
Q

What common complication/interaction occurs with use of barbituates and another type of medication?

A

barbiturates induce P450 enzymes and enhance MAO inhibitors > ineffective depression tx

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4
Q

How can P450 induction cause unplanned pregnancy?

A

reduced oral contraceptive efficacy due to enhanced estrogen metabolism

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5
Q

What interaction occurs with steroids and MAO inhibitors?

A

they compete for P450 enzyme > reduced metabolism of MAO inhibitor > risk of overdose

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6
Q

What common condition is Aspirin contraindicated in?

A

gout; aspirin reduces renal secretion of uric acid

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7
Q

What are the pharmacokinetic reactions?

A
  • absorption
  • distributino (add or displace from albumen)
  • metabolism
  • elimination
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8
Q

What are the pharmacodynamic reactions?

A
  • antagonistic
  • synergist/agonist/additive
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9
Q

What types of absorption interactions can occur?

A
  • pH (drugs that require ionization are decreased in high pH)
  • direct block (chelating/binding agents)
  • increased or decreased motility; inc motility = inc absorption
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10
Q

Which portion of the albumen/drug complex is the bioavailable portion?

A

the “free” unbound portion

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11
Q

What is the relationship between binding level to albumen and the availability of a drug to tissues?

A

increased binding = decreased availability
decreased binding = increased availability

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12
Q

What types of cellular effects at the albumen receptor are possible?

A
  • displacement from cellular binding site
  • receptor blockade
  • enzyme modification (common with poisons)
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13
Q

Explain the following metabolic interaction types:
- induction errors
- inhibition errors
- substrate errors

A
  • induction errors: substances that INDUCE hepatic metabolism = REDUCE plasma availability of drug
  • inhibition errors: substances that** SLOW hepatic metabolism** = INCREASE plasma availability of drug
  • substrate errors: some substances supply substrate for the hepatic detox paths > induce metabolism > REDUCED plasma avbbbailability
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14
Q

What are the two hepatic detoxification pathways?

A
  • Phase 1 (cytochrome P450 paths)
  • Phase 2 (conjugation paths)
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15
Q

Describe the substances, reactions, and co-factors/substrates for phase 1 (cytochrome P450) liver detox pathways

A
  • non-polar (lipid soluble) substances > makes them polar and water-soluble
  • rxns: oxidation, reduction, hydrolysis, hydration
  • cofactors/substrates: B2/3/6/12, folate, GSH, AAs
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16
Q

What substances do phase 1 (CP450) pathways naturally create?

A

peroxide and superoxide free radicals > lipid peroxidation

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17
Q

What is the purpose of the phase 2 (conjugation) hepatic detox pathways?

A

takes intermediary (more polar) P450 metabolites and conjugates them with AAs to form excretion productions

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18
Q

At what GFR should dose adjustments be made?

A

healthy = 60+

adjustments at < 60 or above 60 with proteinuria, HTN, abn anatomy

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19
Q

Dose adjustments should be made in what cases?

A

kidney dz
liver dz
GI dz
any patient over 65

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20
Q

First order elimination properties

A
  • fast
  • logarithmic (constant percent per unit time)
  • typically what is used for half-life
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21
Q

What is the 5x rule?

A

It takes about 5x a drug’s half life for a first order eliminated drug’s serum concentration to reach steady state (this is why drugs with long half-life are started with a loading dose; to achieve the desired clinical effect more quickly) (also give it this long to see if a drug was causing SEs)

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22
Q

What is zero order elimination/michaelis-mentin kinetics?

A

circumstances in which the half-life varies with the concentration of the drug; a constant amount (rather than percent) is eliminated per unit time

implies the clearance mechanism has been saturated or overloaded

ex: aspirin, phenytoin (high dose IV vit C) and ehtanol may be consumed in high enough quantitiy to saturate metabolic enzymes in the liver so is eliminated from the body at an approximately constant rate

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23
Q

What effect do drugs that are easily displaced from albumins have on the plasma drug levels? Give examples of these types of drugs.

A

increase plasma drug level
- sulfonamides
- phenylbutazone
- tolbutamide
- coumarin

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24
Q

What effect do drugs that induce P450 have on the plasma drug levels? Give examples of these types of drugs.

A

decrease plasma drug levels
- alcohol
- barbituates
- phenytoin
- rifampicin

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25
What effect do drugs that are inhibit P450 have on the plasma drug levels? Give examples of these types of drugs.
increases plasma drug levels - chloramphenicol - sulfonamides - phenylbutazone
26
What effect do drugs that compete for renal transporters have on the plasma drug levels? Give examples of these types of drugs.
increase plasma drug levels - uric acid - probenecid - penicillins - sulfonamides - salicylates - thiazides
27
NEVER combine aminoglycosides (gent., tobra, streptomycin) with these drugs:
- neuromuscular blockers (enhanced block) - loop diuretics (compounds ototoxicity)
28
NEVER combine MAO inhibitors with these drugs:
- levodopa (hypertensive crisis) - amphetamine (hypertensive crisis) - tricyclic antidepressants
29
What are the most common drug(s)/substance(s) to cause the following side effect: **anaphylactic shock**
penicillin foreign proteins
30
What are the most common drug(s) to cause the following side effect: **hepatotoxicity**
isoniazid halothane
31
What are the most common drug(s) to cause the following side effect: **renal toxicity**
phenacetin other NSAIDs cyclosporin
32
What are the most common drug(s) to cause the following side effect: **ototoxicity**
aminoglycosides
33
What are the most common drug(s) to cause the following side effect: **drug-induced lupus**
procainamide hydralazine
34
What are the most common drug(s) to cause the following side effect: **photosensitivity of skin**
tetracyclines sulfonamides sulfonylureas
35
What are the most common drug(s) to cause the following side effect: **cutaneous flushing**
niacin
36
What are the most common drug(s) to cause the following side effect: **hemolysis in pts with G6PD deficiency**
sulfonamides primaquine
37
What are the most common drug(s) to cause the following side effect: **bone marrow suppression**
chloramphenicol ganciclovir zidovudine (AZT)
38
What is the common antidote for intoxication with acetominophen
NAC
39
What is the common antidote for intoxication with opiates
Naloxone
40
What is the common antidote for intoxication with benzodiazepines
flumazenil
41
What is the common antidote for intoxication with methanol/ethylene glycol
ethanol
42
What is the common antidote for intoxication with CO
100% O2
43
What is the common antidote for intoxication with cyanide?
amyl nitrate
44
What is the common antidote for intoxication with organophosphates?
atropine, pralidoxime
45
What is the common antidote for intoxication with iron
deferoxamine
46
What is the common antidote for intoxication with lead
EDTA
47
What is the common antidote for intoxication with coumarins
vitamin K
48
What is the common antidote for intoxication with heparin
protamine
49
What does the prefix cholinergic represent?
= ach receptor
50
What are the types of Ach receptors?
- muscarinic: found at postsynaptic PS locations, sweat glands - nicotinic: autonomic ganglia, adrenal medulla, neuromuscular junction
51
What does the prefix Adren- represent?
"adrenal acting" receptor; epi, norepi
52
What are the adrenal acting receptor types?
Beta 1 & 2: cardiopulm postsynaptic sympathetic Alpha 1 & 2: GI, vascular, CNS presynaptic sympathetic
53
What does the suffix -mimetic represent?
mimics/acts like the physiologic substance ex: sympathomimetic substances
54
What does the suffix -lytic represent?
blocks the action of the physiologic substance ex: parasympatholytic substances
55
SNS general activity/actions
- generally stimulating (GI & GU depressing) - sympathomimetic (drugs like epi mimics SNS activity > act receptors) - sympatholytic (drugs like reserpine block/decrease catecholamines and increase PS tone)
56
PNS general activity/actions
- generally relaxing (GU & GI stimulating) - parasympathomimetic (drugs like pilocarpine mimic PS activity) - parasympatholytic (drugs like atropine block PS receptors and incerase sympathetic tone)
57
IC vs EC concentration in excitable membrane physiology
ICF: high K, Mg; small Na, Ca ECF: high NA, Ca, Cl, small K, Mg
58
What enzyme breaks down ACH into choline and acetate?
ach esterase (defect = inc ach in muscles = teatany) (ach esterase is in a lot of pesticides)
59
Give detailed explanations of the adrenergic receptor type: **alpha 1**
- postsynaptic sympathetic - generally excitatory (vasoconstriction) except in GI tract / inhibititory
60
Give detailed explanations of the adrenergic receptor type: **alpha 2**
- presynaptic sympathetic: dec catecholamine release - CNS: decrease sympathetic tone - "emergency brake" on SNS
61
Give detailed explanations of the adrenergic receptor type: **beta 1**
- postsynaptic sympathetic (cardiac) excitatory (chronotrope, dromotrope, inotrope)
62
Give detailed explanations of the adrenergic receptor type: **beta 2**
- postsynaptic sympathetic (all others besides cardio) = inhibitory (vasodilation, bronchodilation)
63
Pharamcognosy of *Rauwolfia serpentina*
- acts by dec activity of neuronal storage vesicles - CNS: dec catecholamines - PNS: dec Norepi and serotonin
64
# ``` ``` Pharamcognosy of *Digitalis lanata (leaf)*
- decreases aberrant SA to AV conduction - pos inotrope and dromotrope (blocks NA/K ATPase > inc IC Ca > elongated plateau on cardiac AP) - improves atrial dysfunction
65
Pharamcognosy of *Chincona (bark)*
two primary chincona alkaloids; mild to moderate anticholinergic effects, direct toxic effects: - quinine: antispasmodic (nocturnal leg crampss), antipyretic, ameobacide - quinidine (antiarrythmic)
66
Pharamcognosy of *atropa belladonna*
acetylcholine antagonist (parasympatholytic) - muscarinic receptor blockage (post synaptic PS) - slows digestion, dec secretions, dilates pupils
67
Pharamcognosy of *Calabar (bean)*
- physotigmine - reversible inhibition of ach esterase > inc ach levels (parasympathomimetic) > inc secretions, digestion, constricts pupils
68
Pharamcognosy of *pylocarpus mycrophyllus/jaborandi*
- pilocarpine - cholinergic (parasympathetomimetic) - used as eye drop in glaucoma tx
69
Pharamcognosy of *erythroxylon coca*
- cocaine - dilates pupils - anesthetic to mucous membranes - inc dopamine (reuptake inhibition), esp active in nucleus accumbuns/pleasure centers
70
Pharamcognosy of *eschscolizia californicum*
- california poppy - used in pain control formulas
71
Pharamcognosy of *papaver somniferum*
**opium, codeine, morphine (opiates)** - analgesic pain meds, centrally acting - also block PS activity **papaverine (papaver alkaloid) ** - used for angina (vasodilation)
72
Pharamcognosy of *claviceps purpurea*
- ergot - rye or wheat fungus - primarily vasoconstrictive agents (ergonovine, DHE, etc) - postpartum, abortive hemorrhage - also bromocriptine (dopamine agonist) and LSD family
73
Why would a pt get headaches or dizziness with AA supplementation?
they are dehydrated and/or are deficient in cofactors; no GI/neuro SE with AA in bowel dysbiosis, beta AAs are formed and perpetuate poor GI flora. increases the B6 need and taurine loss in urine.
74
Carnitine is used where therapeutically?
places using high energy at mitochondrial level - heart, nervous system, liver, skeletal muscle etc to allow fats into mitochondria for burning
75
What is the primary cofactor for transaminating?
B6
76
How should therapeutic AAs be dosed?
away from other AAs and protein foods; in divided doses if over 1000mg, with cofactor therapy - be sure to correct hypothyroidism (t3 stim BBB AA transport) - dose with small carb to help inc amino acid uptake (by insulin release)
77
Function & deficiency state of vitamin A
function: rhodopsin/vision def: night blindness
78
Function & deficiency state of vitamin D
function: GI (inc Ca absorption) def: rickets/osteomalacia
79
Function & deficiency state of vitamin E
function: antioxidant def: ataxia
80
Function & deficiency state of vitamin K
function: carboxylation (of glutamate), ca chelation with glutamate def: factor 2/7/9/10 bleeding disorders
81
Function, deficiency state, and sources of vitamin B1
function: aldehyde transfer/decarboxylation def: beriberi wheat germ, fish, meat, eggs, milk, cereal, green veggies
82
Function, deficiency state, and sources of vitamin B2
function: H+ transfer/ FMN-FAD (flavins) def: cheilosis, glossitis fish, meat, eggs, milk, greens
83
Function, deficiency state, and sources of vitamin B3
function: H+ transfer / NAD-NADP def: pellegra (dementia, diarrhea, dermatitis) wheat germ, fish, liver, peanuts
84
Function, deficiency state, and sources of vitamin B5
function: acyl group transfer / coA def: burning feet, HA, nausea def not common; ubiquitous in foods
85
Function, deficiency state, and sources of vitamin B6
function: amino group transfer, de&trans aminations def: microcytosis, neuropathy cereals, fish, meat, eggs, greens
86
Function, deficiency state, and sources of vitamin B12
function: methyl transfer / methionine synth def: macrocytosis, pernicious anemia, neuropathy meat, dairy, fermented foods
87
Function & deficiency state of vitamin C
function: H+ transfer, hydroxylation of proline and lysine def: scurvy
88
Function & deficiency state of biotin
function: carboxylation def: sebb derm, nervous disorders, bound by avidin (in egg white)
89
Function & deficiency state of folate
function: methyl transfer def: macrocytosis, glossitis, colitis
90
B6 dosing considerations
- high doses can cause peripheral neuropathy (500mg+ chronically without def) - some ppl tolerate better at night
91
Therapeutic effect of the following nutrient: flavinoids
antioxidant antihistaminic (quercetin, rutin, hesperidin)
92
Therapeutic effect of the following nutrient: CoQ10
antioxidant in ETC; energy production preserves vit E
93
Therapeutic effect of the following nutrient: ALA
- cofactor for mitochondrial energy rxns - substrate production for krebs cycle - antioxidant - chelation support

NPLEX II TIA (21 decks)

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