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NPLEX II TIA > Intro to Pharm/Nutrition > Flashcards

Intro to Pharm/Nutrition Flashcards

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
Q

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

A

increases plasma drug levels
- chloramphenicol
- sulfonamides
- phenylbutazone

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26
Q

What effect do drugs that compete for renal transporters have on the plasma drug levels? Give examples of these types of drugs.

A

increase plasma drug levels
- uric acid
- probenecid
- penicillins
- sulfonamides
- salicylates
- thiazides

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27
Q

NEVER combine aminoglycosides (gent., tobra, streptomycin) with these drugs:

A
  • neuromuscular blockers (enhanced block)
  • loop diuretics (compounds ototoxicity)
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28
Q

NEVER combine MAO inhibitors with these drugs:

A
  • levodopa (hypertensive crisis)
  • amphetamine (hypertensive crisis)
  • tricyclic antidepressants
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29
Q

What are the most common drug(s)/substance(s) to cause the following side effect: anaphylactic shock

A

penicillin
foreign proteins

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30
Q

What are the most common drug(s) to cause the following side effect: hepatotoxicity

A

isoniazid
halothane

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31
Q

What are the most common drug(s) to cause the following side effect: renal toxicity

A

phenacetin
other NSAIDs
cyclosporin

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32
Q

What are the most common drug(s) to cause the following side effect: ototoxicity

A

aminoglycosides

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33
Q

What are the most common drug(s) to cause the following side effect: drug-induced lupus

A

procainamide
hydralazine

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34
Q

What are the most common drug(s) to cause the following side effect: photosensitivity of skin

A

tetracyclines
sulfonamides
sulfonylureas

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35
Q

What are the most common drug(s) to cause the following side effect: cutaneous flushing

A

niacin

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36
Q

What are the most common drug(s) to cause the following side effect: hemolysis in pts with G6PD deficiency

A

sulfonamides
primaquine

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37
Q

What are the most common drug(s) to cause the following side effect: bone marrow suppression

A

chloramphenicol
ganciclovir
zidovudine (AZT)

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38
Q

What is the common antidote for intoxication with acetominophen

39
Q

What is the common antidote for intoxication with opiates

40
Q

What is the common antidote for intoxication with benzodiazepines

A

flumazenil

41
Q

What is the common antidote for intoxication with methanol/ethylene glycol

42
Q

What is the common antidote for intoxication with CO

43
Q

What is the common antidote for intoxication with cyanide?

A

amyl nitrate

44
Q

What is the common antidote for intoxication with organophosphates?

A

atropine, pralidoxime

45
Q

What is the common antidote for intoxication with iron

A

deferoxamine

46
Q

What is the common antidote for intoxication with lead

47
Q

What is the common antidote for intoxication with coumarins

48
Q

What is the common antidote for intoxication with heparin

49
Q

What does the prefix cholinergic represent?

A

= ach receptor

50
Q

What are the types of Ach receptors?

A
  • muscarinic: found at postsynaptic PS locations, sweat glands
  • nicotinic: autonomic ganglia, adrenal medulla, neuromuscular junction
51
Q

What does the prefix Adren- represent?

A

“adrenal acting” receptor; epi, norepi

52
Q

What are the adrenal acting receptor types?

A

Beta 1 & 2: cardiopulm postsynaptic sympathetic

Alpha 1 & 2: GI, vascular, CNS presynaptic sympathetic

53
Q

What does the suffix -mimetic represent?

A

mimics/acts like the physiologic substance

ex: sympathomimetic substances

54
Q

What does the suffix -lytic represent?

A

blocks the action of the physiologic substance

ex: parasympatholytic substances

55
Q

SNS general activity/actions

A
  • 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
Q

PNS general activity/actions

A
  • generally relaxing (GU & GI stimulating)
  • parasympathomimetic (drugs like pilocarpine mimic PS activity)
  • parasympatholytic (drugs like atropine block PS receptors and incerase sympathetic tone)
57
Q

IC vs EC concentration in excitable membrane physiology

A

ICF: high K, Mg; small Na, Ca
ECF: high NA, Ca, Cl, small K, Mg

58
Q

What enzyme breaks down ACH into choline and acetate?

A

ach esterase
(defect = inc ach in muscles = teatany)
(ach esterase is in a lot of pesticides)

59
Q

Give detailed explanations of the adrenergic receptor type: alpha 1

A
  • postsynaptic sympathetic
  • generally excitatory (vasoconstriction) except in GI tract / inhibititory
60
Q

Give detailed explanations of the adrenergic receptor type: alpha 2

A
  • presynaptic sympathetic: dec catecholamine release
  • CNS: decrease sympathetic tone
  • “emergency brake” on SNS
61
Q

Give detailed explanations of the adrenergic receptor type: beta 1

A
  • postsynaptic sympathetic (cardiac) excitatory (chronotrope, dromotrope, inotrope)
62
Q

Give detailed explanations of the adrenergic receptor type: beta 2

A
  • postsynaptic sympathetic (all others besides cardio) = inhibitory (vasodilation, bronchodilation)
63
Q

Pharamcognosy of Rauwolfia serpentina

A
  • acts by dec activity of neuronal storage vesicles
  • CNS: dec catecholamines
  • PNS: dec Norepi and serotonin
64
Q

```

~~~

Pharamcognosy of Digitalis lanata (leaf)

A
  • 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
Q

Pharamcognosy of Chincona (bark)

A

two primary chincona alkaloids; mild to moderate anticholinergic effects, direct toxic effects:
- quinine: antispasmodic (nocturnal leg crampss), antipyretic, ameobacide
- quinidine (antiarrythmic)

66
Q

Pharamcognosy of atropa belladonna

A

acetylcholine antagonist (parasympatholytic)
- muscarinic receptor blockage (post synaptic PS)
- slows digestion, dec secretions, dilates pupils

67
Q

Pharamcognosy of Calabar (bean)

A
  • physotigmine
  • reversible inhibition of ach esterase > inc ach levels (parasympathomimetic) > inc secretions, digestion, constricts pupils
68
Q

Pharamcognosy of pylocarpus mycrophyllus/jaborandi

A
  • pilocarpine
  • cholinergic (parasympathetomimetic)
  • used as eye drop in glaucoma tx
69
Q

Pharamcognosy of erythroxylon coca

A
  • cocaine
  • dilates pupils
  • anesthetic to mucous membranes
  • inc dopamine (reuptake inhibition), esp active in nucleus accumbuns/pleasure centers
70
Q

Pharamcognosy of eschscolizia californicum

A
  • california poppy
  • used in pain control formulas
71
Q

Pharamcognosy of papaver somniferum

A

opium, codeine, morphine (opiates)
- analgesic pain meds, centrally acting
- also block PS activity

**papaverine (papaver alkaloid)
**
- used for angina (vasodilation)

72
Q

Pharamcognosy of claviceps purpurea

A
  • ergot - rye or wheat fungus
  • primarily vasoconstrictive agents (ergonovine, DHE, etc)
  • postpartum, abortive hemorrhage
  • also bromocriptine (dopamine agonist) and LSD family
73
Q

Why would a pt get headaches or dizziness with AA supplementation?

A

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
Q

Carnitine is used where therapeutically?

A

places using high energy at mitochondrial level - heart, nervous system, liver, skeletal muscle etc to allow fats into mitochondria for burning

75
Q

What is the primary cofactor for transaminating?

76
Q

How should therapeutic AAs be dosed?

A

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
Q

Function & deficiency state of vitamin A

A

function: rhodopsin/vision
def: night blindness

78
Q

Function & deficiency state of vitamin D

A

function: GI (inc Ca absorption)
def: rickets/osteomalacia

79
Q

Function & deficiency state of vitamin E

A

function: antioxidant
def: ataxia

80
Q

Function & deficiency state of vitamin K

A

function: carboxylation (of glutamate), ca chelation with glutamate
def: factor 2/7/9/10 bleeding disorders

81
Q

Function, deficiency state, and sources of vitamin B1

A

function: aldehyde transfer/decarboxylation
def: beriberi

wheat germ, fish, meat, eggs, milk, cereal, green veggies

82
Q

Function, deficiency state, and sources of vitamin B2

A

function: H+ transfer/ FMN-FAD (flavins)
def: cheilosis, glossitis

fish, meat, eggs, milk, greens

83
Q

Function, deficiency state, and sources of vitamin B3

A

function: H+ transfer / NAD-NADP
def: pellegra (dementia, diarrhea, dermatitis)

wheat germ, fish, liver, peanuts

84
Q

Function, deficiency state, and sources of vitamin B5

A

function: acyl group transfer / coA
def: burning feet, HA, nausea

def not common; ubiquitous in foods

85
Q

Function, deficiency state, and sources of vitamin B6

A

function: amino group transfer, de&trans aminations
def: microcytosis, neuropathy

cereals, fish, meat, eggs, greens

86
Q

Function, deficiency state, and sources of vitamin B12

A

function: methyl transfer / methionine synth
def: macrocytosis, pernicious anemia, neuropathy

meat, dairy, fermented foods

87
Q

Function & deficiency state of vitamin C

A

function: H+ transfer, hydroxylation of proline and lysine
def: scurvy

88
Q

Function & deficiency state of biotin

A

function: carboxylation
def: sebb derm, nervous disorders, bound by avidin (in egg white)

89
Q

Function & deficiency state of folate

A

function: methyl transfer
def: macrocytosis, glossitis, colitis

90
Q

B6 dosing considerations

A
  • high doses can cause peripheral neuropathy (500mg+ chronically without def)
  • some ppl tolerate better at night
91
Q

Therapeutic effect of the following nutrient: flavinoids

A

antioxidant
antihistaminic (quercetin, rutin, hesperidin)

92
Q

Therapeutic effect of the following nutrient: CoQ10

A

antioxidant
in ETC; energy production
preserves vit E

93
Q

Therapeutic effect of the following nutrient: ALA

A
  • cofactor for mitochondrial energy rxns
  • substrate production for krebs cycle
  • antioxidant
  • chelation support

NPLEX II TIA (21 decks)

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