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PCOL 350 > MIDTERM > Flashcards

MIDTERM Flashcards

1
Q

magic charm for treating disease

remedy or drug

A

pharmacology

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2
Q

a book containing an official list of medicinal drugs together with articles on their preparation and use

A

pharmacopeia (drug making)

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3
Q

2 major subdivisions of pharmacology

A

pharmacokinetics and pharmacodynamics

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4
Q

what the body does to the drug

A

pharmacokinetics

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5
Q

what the drug does to the body

A

pharmacodynamics

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6
Q

an adverse effect or complication caused by a physician (resulting from medical treatment or device)

A

iatrogenic effect

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7
Q

a macromolecule whose biological function changes when a drug binds to it

A

receptor

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8
Q

the measure of propensity of a drug to bind receptor; the force of attraction between drug and receptor

A

affinity

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9
Q

dose or conc of a drug that produces 50% of maximal response

A

EC50

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10
Q

some receptors have intrinsic activity even when no ligand is bound to them

A

inverse agonist

-when a ligand binds to them, their basal activity is reduced

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11
Q

max effect produced by a drug; a measure of efficacy

A

Emax

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12
Q

ability of a bound drug to change the receptor in a way that produces an effect

A

efficacy (intrinsic activity)

-some drugs posses affinity but no efficacy

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13
Q

drugs that possess affinity and no efficacy

A

still have clinical use

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14
Q

relative position of the dose-effect curve along the dose axis

A

potency of a drug

-need 2 drugs that act by the same mechanism to compare

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15
Q

a drug which binds to the receptor and produces an effect

A

agonist

-has affinity and efficacy

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16
Q

has affinity for a receptor, but less efficacy activity

A

partial agonist

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17
Q

a drug which binds (competes for binding against other ligands), but does not activate the receptor

A

antagonist

-has affinity, but no intrinsic activity

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18
Q

a higher dose of agonist is required to produce the same effect

A

competitive antagonism

-same Emax, but shifted right

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19
Q

even a higher dose of agonist cannot produce maximal effect

A

non-competitive antagonism

-Emax will be lower

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20
Q

info that can be derived from dose response curves

A 
Emax
EC50
agonist
partial agonist
competitive antagonism
non-competitive antagonism
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21
Q

the difference between the minimum effective concs for a desired response and an adverse response

A

therapeutic window

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22
Q

quantal means

A

present or absent

-no degree of variation

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23
Q

info derived from quantal dose response curves

A

therapeutic index
therapeutic window
sensitivity

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24
Q

dose response curves shows graded response in a

A

single individual

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25
Q

quantal dose response curves show a specific response in a

A

group of individuals (population)

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26
Q

partial agonist produce

A

less than full effect when given alone

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27
Q

partial agonists act as ________ in the presence of a full agonist

A

antagonist

-it blocks the full effect

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28
Q

has lower abuse potential

less addictive than full agonists

A

partial agonists

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29
Q

provides some agonist activity and at the same time, blocks the full agonists

A

partial agonists

ex) Pindolol for high BP and abnormal heart rhythms

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30
Q

the binding sites for the agonist and the antagonist are different on the recpetor

A

allosteric interaction

-can produce inhibition or potentiation of the agonist response

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31
Q

example of allosteric interaction

A

receptor for benzodiazepines and GABA

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32
Q

4 signal transduction mechanisms

A

G-protein couples receptor systems
ion-channel receptors
enzymes as receptors
nuclear receptors

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33
Q

G-coupled receptor systems

A
  • 2nd fastest
  • uses energy obtained from GDP
  • half of all drugs work through this system
  • GPCRs, metabotropic receptors
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34
Q

ion channel receptors

A
  • fastest

- ionotropic receptors, GABA

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35
Q

enzymes as receptors

A
  • 3rd fastest
  • the interaction phosphorylates tyrosines in the intracellular region of the receptor, and the receptor becomes an active enzyme
  • tyrosine kinase, serine/threonine kinase
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36
Q

nuclear receptors

A
  • very slow, not common
  • inside cytosol of the cell
  • receptors for steroids, retinoids, and thyroid hormones
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37
Q

a drug that does not go through any of the 4 signal transduction mechanisms?

A

anti-acids

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38
Q

signal transduction

A

drug binds to receptor

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39
Q

____________ tend to desensitize receptors (down-regulate)

A

agonists

  • frequent stimulation results in a decreased response
    ex) decrease in receptor number or decrease in signal transduction
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40
Q

__________ tend to up-regulate receptors

A

antagonists

  • causes a withdrawal rebound effect
  • receptor number has increased, more receptors available to agonist
  • gradually decrease dose when stopping
  • ex) beta receptor antagonist
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41
Q

the pH at which half of the drug is ionized

A

pKa

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42
Q

the fraction of an orally given drug that reaches the circulation

A

bioavailability

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43
Q

the fluid volume that is required to contain the entire drug in the body at the same conc as measured in the plasma

A

volume of distribution

=dose/Cp

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44
Q

the volume of blood from which a drug is irreversibly removed per unit of time

A

clearance

-rate of administration = rate of elimination

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45
Q

the time required for the blood (or plasma) conc of a drug to be reached by 50%

A

half-life

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46
Q

a dose of a drug sufficient to produce a plasma conc of drug that would fall within the therapeutic window after only 1 or very few doses over a short interal

A

loading dose

=Cp * Vd/F

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47
Q

the dose needed to maintain the conc within the therapeutic window when given repeatedly at a constant interval

A

maintenance dose

=Cl * Css

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48
Q

affects all process of ADME

A

lipid solubility

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49
Q

high absorption factors

A

nonionized
small
lipid soluble
nonpolar

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50
Q

factors affectting distribution

A

ionization
capillary permeability
blood flow
PLASMA PROTEIN BINDING

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51
Q

in acidic medium, like the stomach
weak acid will be
weak base will be

A

acid will be unionized, better absorbed

base will be ionized, less absorbed

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52
Q

ion trapping at steady state

A

acidic drug would accumulate on the more basic side, and

a basic drug on the more acidic side

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53
Q

clinical significance of ion trapping

A
  • breast milk
  • to increase excretion of acidic drugs (ASA), give IV sodium bicarbonate
  • to increase excretion of basic drugs, give ammonium chloride or ascorbic acid
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54
Q

if most the drug is extravascular, a change in free plasma drug conc caused by displacement from plasma protein binding would be

A

minimal

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55
Q

if most the drug is intravascular, a change in free plasma drug conc caused by displacement from plasma protein binding would be

A

very significant on the effect

ex) warfarin

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56
Q

liver and spleen have

A

leaky capillaries

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57
Q

brain capillaries have

A

tight junctions

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58
Q

high capillary permeability in

A

liver

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59
Q

low capillary permeability in

A

the brain

-exception is CTZ

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60
Q

only ________ drugs diffuse across brain capillaries

A

lipophilic

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61
Q

tight junctions between

A

endothelial cells in brain capillaries

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62
Q

to tx parkinson’s, in regards to BBB

A

it is better to give dopa than dopamine

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63
Q

high Vd

A

highly lipid soluble

-most of the drug is in the extravascular compartment

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64
Q

low Vd

A

not very lipid soluble OR highly plasma protein bound

  • most of the drug is in the vascular compartement
    ex) warfarin
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65
Q

phase 1 rxns of drug metabolism

A

functionalization: makes the drug more polar, but not necessarily inactive
- oxidation
- reduction
- hydrolytic rxns

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66
Q

phase 2 rxns in drug metabolism

A

conjugation: mostly result in drug inactivation
- glucoronidation
- sulfation
- acetylation

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67
Q

cap permeability determines

A

distribution

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68
Q

P450 monooxygenase family wich transfer electrons from

A

NADPH to an oxygen molecules and thus oxidize drugs

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69
Q

P450 enzyme characteristics

A
  • not substrate specific
  • located in ER
  • require NADPH and oxygen
  • mostly inactive drugs
  • many subfamilies -CYP3 is most common
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70
Q

the primary enzyme for metabolism

A

CYP3A4

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71
Q

increase elimination of drugs

A

inducers

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72
Q

decrease elimination of drugs

A

inhibitors

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73
Q

most common polymorphism in caucasians is

A

CYP2D6

-codeine must be metabolized by this enzyme to morphine to work

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74
Q

example of a prodrug

A

codeine

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75
Q

p-glycoprotein is an

A

efflux pump: removes drug from cell

  • broad substrate specificity
  • cancer tissue (resistance)
  • high expression by st johns wort
  • in the BBB, protects the CNS
  • CCB inhibit the pump and reverse resistance
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76
Q

enterohepatic recirculation effect

A

a compound is conjugated in the liver, excreted in the bile, deconjugated in the intestine, and is reabsorbed into circulation

  • this prolongs the duration of action (half-life)
    ex) bilirubin
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77
Q

95% of bile salts are reabsorbed and used in

A

cholesterol synthesis

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78
Q

antibiotics and CYP enzymes

A

antibiotics induce CYP enzymes that metabolize the contraceptive hormones and thus reduce their effectiveness
-they kill the bacteria that reabsorbs the estrogen

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79
Q

Cl =

A

maintenance dose (steady state)

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80
Q

creatinine Cl is used to estimate

A

GFR

-kidney function is assessed by GFR

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81
Q

when GFR is low, excretion is

A

low

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82
Q

creatinine clearance =

A

urine conc* (urine flow rate/plasma conc)

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83
Q

net removal of a drug by the kidney =

A

filtered + secreted - reabsorbed

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84
Q

filtration

A

passive

-only free drug

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85
Q

secretion

A

active

-mainly in the proximal tubule

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86
Q

reabsorbed

A

passive and active

-happens unless the drug is very polar

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87
Q

1st order rate of elimination

A

a constant fraction of drug is eliminated per unit of time

-metabolizing enzyme is not saturated

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88
Q

zero order rate of elimination

A

a constant amount of drug is eliminated per unit of time

  • depends on metabolism
  • the metabolic mechanism for most drugs will be saturated only at high concs
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89
Q

it takes about ________ half-lives for more than 90% of a drug to be effectively eliminated

A

5

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90
Q

any chemical agent that affects living processes

A

drug

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91
Q

3 different types of drug interactions

A

drug-drug
drug-food
drug-herb

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92
Q

drug-drug interaction example

A

NSAIDs and warfarin

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93
Q

drug-food example

A

grapefruit juice

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94
Q

2 drugs affecting the same system

A

pharmacodynamic interaction

ex) 2 sedative drugs producing more sedation

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95
Q

one drug changing the ADME of another

A

pharmacokinetic interaction

ex) Ca supplements reduce absorption of thyroxine metabolism

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96
Q

one drug affecting the ___________ of another drug is the most common form of drug-drug interactions

A

metabolism

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97
Q

almost always involved in drug-drug interactions

A

CYPs

-CYP3A4

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98
Q

4 mechanisms involved in DDIs between NSAIDs and warfarin

A
  1. protein bound warfarin is displaced by warfarin (pharmacokinetics)
  2. NSAIDs suppress platelet formation, which adds to anticoagulation effect (pharmacodynamics)
  3. NSAIDs prevent metabolism of warfarin by competition for metabolizing enzyme (pharmacokinetics)
  4. NSAIDs cause gastric injury and warfarin can cause gastric bleeding (pharmacodynamics)
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99
Q

mechanisms of other drugs interacting with warfarin

A
  • altered platelet formation
  • GI injury
  • vit K synthesis altered
  • warfarin metabolism altered
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100
Q

during which trimester of pregnancy causes the most damage from drug use

A

first

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101
Q

factors that affect drug transfer across the placenta

A 
MW
pKa
protein binding
degree of ionization
placental drug transporters
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102
Q

where is p-glycoprotein located

A

on the apical membrane

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103
Q

role of p-glycoprotein in placental drug transport

A

placental expression of drug transporters, like p-glycoprotein, protects the fetus by efflux of drug from the fetal to maternal circulation

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104
Q

risk levels of drugs for use during pregnancy

A 
A = safe
B = likely safe
C = uncertain
D = likely unsafe
X = unsafe
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105
Q

parasympathetic nerves originate from the

A

adrenal medulla and sacral spinal cord

-craniosacral outflow

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106
Q

sympathetic nerves originate from the

A

thoracic and lumbar spinal cord

-thoracolumbar outflow

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107
Q

what is released at preganglionic parasymp nerves at their ganglia

A

Ach

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108
Q

what is released at preganglionic symp nerves at their ganglia and at their synapses in adrenal medulla

A

Ach

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109
Q

what is released from postganglionic parasymp nerves at their organs/tissue receptors

A

Ach

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110
Q

what is released from somatic motor nerves at the neuromuscular junction in the skeletal muscle

A

Ach

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111
Q

what is released from postganglionic symp nerves at their organ/tissue

A

NE

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112
Q

postganglionic symp fibers innervat all sweat glands, except

A

in the palms and skeletal blood vessels

-release Ach

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113
Q

adrenal medulla releases 80% ______ into circulation when stimulated by pregang symp nerves

A

epi (adrenaline)

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114
Q

adrenal medulla releases 20% ______ into circulation when stimulated by pregang symp nerves

A

NE

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115
Q

phaeochromocytoma

A

a tumor of the adrenal medulla that releases large amounts of epi and NE into circulation
-the BP and HR are increased

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116
Q

2 clinical conditions where alpha blockers are used

A

hypertension and BPH

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117
Q

urinary bladder: dominant tone

A

parasympathetic

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118
Q

urinary bladder: parasymp agonists

A

muscarinic agonists will contract the detruser muscle and relax the sphincter to empty the bladder
ex) methacholine, cholinesterase inhibitors

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3
4
5
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119
Q

urinary bladder: symp agonists

A

alpha1 agonists will contract the sphincter to prevent bladder emptying

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120
Q

urinary bladder: clinical relevance

A

urinary incontinence - want to reduce activity so give muscarinic blocker
urinary retention - use muscarinic agonist

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121
Q

tracheal & bronchial smooth muscle: parasymp

A

muscarinic agonists will contract the bronchial smooth mucles and increase bronchial secretions

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122
Q

tracheal & bronchial smooth muscle: symp

A

beta2 agonists will relax the bronchial muscle

ex) albuterol or epi

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123
Q

tracheal & bronchial smooth muscle: clinical relevance

A

asthma, COPD

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124
Q

tracheal & bronchial smooth muscle: notes

A

non-selective beta blockers to tx hypertension, will contract bronchial muscle
-not used in asthma pts

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125
Q

GI tract smooth muscle: dominant tone

A

parasymp

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126
Q

GI tract smooth muscle: parasymp

A

muscarinic agonists will contract the GI muscle (stimulate peristalsis), relax sphincters, and increase secretions

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127
Q

GI tract smooth muscle: symp

A

beta and alpha agonists will relax the GI muscle (inhibit peristalsis), and inhibit secretions

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128
Q

GI tract smooth muscle: clinical significance

A

diarrhea and IBS - give muscarinic blocker

gastric atony and paralytic ileus - give muscarinic agonist

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129
Q

salivary & parotid glands: dominant tone

A

parasymp

130
Q

salivary & parotid glands: parasymp

A

muscarinic agonists will stimulate salivary gland secretions

131
Q

salivary & parotid glands: symp

A

alpha1 agonists will stimulate salivary secreation

132
Q

salivary & parotid glands: clinical relevance

A

muscarinic blockers are used for intubation

133
Q

liver: dominant tone

A

symp

134
Q

liver: symp

A

beta2 agonist will cause glycogenolysis and gluconeogenesis

-increase plasma glucose

135
Q

liver; clinical relevance

A

type 1 DM

-do not give a DM pt a non-selective beta-blocker

136
Q

uterus: dominant tone

A

symp

137
Q

uterus: symp

A

beta2 agonist will cause relaxation of uterine smooth muscle

138
Q

uterus: clinical relevance

A

prevent premature labor

139
Q

eyes: dominant tone

A

parasymp

140
Q

eyes: parasymp

A

muscarinic agonists will cause contraction of circular fibers of the iris and miosis (narrowing of the pupil)
M3, M2

141
Q

eyes: symp

A

alpha1 agonists will cause mydriasis (dilation of pupil)

142
Q

eyes: clinical relevance

A

glaucoma

-muscarinic blockers will cause mydriasis (dilation)

143
Q

glaucoma definition

A

increase in intraocular pressure

  • increased of aqueous humor
  • decreased outflow (drainage) of aqueous humor
144
Q

skeletal muscle: dominant

A

motor neurons

145
Q

skeletal muscle: stimulation of motor neurons

A

nicotinic agonists will stimulate contraction of the muscle

146
Q

skeletal muscle: 2 types of neuromuscular blockers

A

competitive - tubocurarinel

depolarizing - succinylcholine

147
Q

succinylcholine causes

A

persistant stimulation and depolarization, so the muscle cannot recover and becomes paralyzed

148
Q

brain: receptors

A

cholinergic & adrenergic

149
Q

brain: stimulation of muscarinic receptors

A

plays a role in memory and control of muscle contraction

150
Q

brain: tx Alzhiemer’s

A

indirect cholinergic agonists (ChE inhibitors)

151
Q

brain: tx Parkinson’s

A

muscarinic antagonists (Ach blocker/antagonists)

152
Q

parasymp effects can be mimicked by

A

muscarinic receptor agonists

acteylcholinesterase inhibitors

153
Q

parasymp effects can be blocked by

A

muscarinic receptor antagonists

skeletal neuromuscular junction blockers

154
Q

4 therapeutic uses of parasympathomimetics

A
  1. reduce intraocular pressure in glaucoma
  2. increase the motility (peristalsis) of the GI tract
  3. increase the motility of urinary tract
  4. increase salivary secretions
155
Q

2 types of cholinesterase

A

AchE and BuChE

156
Q

BuChE metabolizes

A

succinylcholine

157
Q

compounds that bind to cholinesterase can produce one of 3 types of chemical rxns

A
  1. acetylation - recovers rapidly
  2. carbamylation - recovers more slowly
  3. phosphorylation - poisons the enzyme
158
Q

botylinum toxin

A
  • used to paralyze skeletal muscle in cases of excessive involuntary skeletal muscle
  • blocks Ach release
159
Q

belladonna alkaloids

A

atropine and scopolamine

160
Q

semisynthetic and synthetic

A

oxybutynin and glycopyrrolate

161
Q

scopolamine

A

great fraction present in an unionized form at physiological pH
-duration of 3 days

162
Q

glycopyrrolate

A

given preoperatively to inhibit excessive salivary secretions

163
Q

pirenzepine

A

selective for M1 receptors

-used to reduce gastric acid secretions in pts with peptic ulcers

164
Q

parkinson’s tx

A

muscarinic receptor antagonists

ex) trihexyphenidyl and benztropine

165
Q

muscarinic receptor antagonist side effects

A
  • urinary retention
  • constipation
  • mydriasis
  • blurred vision
  • tachycardia
  • inhibition of sweating
166
Q

neuromuscular junction blockers: competitive

A

curare

-no intrinsic activity

167
Q

partially imparied when __________ receptors are occupied

A

75-80%

168
Q

inhibited totally when __________ receptors are occupied

A

90-95%

169
Q

competitive neuromuscular blockers side effects

A
  • ganglionic blockade (low BP, high HR)
  • block of vagal responses
  • histamine release (bronchospasm)
170
Q

depolarizing neuromuscular blocker side effects

A
  • hyperkalemia

- malignant hyperthermia

171
Q

therapeutic uses of neuromuscular blockers

A

in surgical anesthesia to obtain relaxation of skeletal muscle

172
Q

sympathetic effects can be mimicked byb

A
  • adrenergic receptor agonists
  • NE uptake blockers
  • monoamine oxidase and COMT inhibitors
  • NE releasing agents
173
Q

monoamine oxidase and COMT inhibitors cause an ________ in N E conc

A

increase

174
Q

sympathetic effects can be blocked by

A

-adrenergic receptor antagonists

175
Q

NE can activate

A

alpha and beta1 receptors

-very little effect on beta2

176
Q

when treating asthma, epi vs NE

A

very little bronchodilation when NE is used

-use epi when treating asthma

177
Q

epi: alpha1 and beta2

A

alpha1 is vasoconstrictor

beta2 is vasodilator

178
Q

clinical uses of agrenergic drugs

A
  • allergic rnxs (epi)
  • bronchodilators (albuterol)
  • as pressor agents - hypotension (epi or NE)
179
Q

clinical uses of adrenergic receptors blockers

A

-hypertension
-glaucoma
-MI
-HAs
(metoprolol, propranolol)

180
Q

main difference between beta blocker and choinesterase inhibitor?

A
  • cholinesterase increases drainage (outflow)

- beta blocker reduces production

181
Q

autocoids

A

local hormones

-have a brief lifetime and act near their site

182
Q

autocrine

A

histamine, prostaglandins, serotonin, leukotrienes

183
Q

paracrine

A

NO, ET-1

184
Q

endocrine

A

hormones

-insulin, thyroxine, estradiol

185
Q

where is histamine stored in the body

A

mast cells and basophils

186
Q

mast cells

A

gut and lungs

187
Q

histamine works on two receptors

A

in neurons (CNS) and in peripheral nerves (H1)(minor allergies)

188
Q

directly released by certain drugs that displace histamine in mast cells

A

morphine and d-curarine

189
Q

agents that inhibit the release of histamine from mast cells are

A

cromolyn
theophylline/aminophylline
beta agonists

190
Q

3 types of histamine receptors

A

H1, H2, H3

191
Q

H1 receptors

A

contribute to rhinitis, urticaria

-contribute to minor allergic rxns - hay fever

192
Q

H2 receptors

A

gastric acid secretions

-activation causes increase gastric acid secretion

193
Q

H3 receptors

A

central neurotransmitter role

-G-protein coupled

194
Q

histamine will contribute to bronchial _____

A

constriction

195
Q

4 types of antihistaminics

A
  1. dimenhydrinate (gravol) sedative and has anticholinergic fx
  2. diphenhydramine (benadryl) same
  3. cyclizine (motion sickness) same
  4. loratadine (claritin) nonsedative and no anticholinergic fx
196
Q

main use of antihistaminics

A

to tx allergy rxn sx

-hay fever, urticaria, rhinitis, cold and drug rxns

197
Q

2nd generation agents

A

loratadine

  • do not cross BBB
  • no sedation
  • more potent
  • less side fx
  • no anticholinergic fx
198
Q

H2 blockers are given to reduce

A

gastric acid secretion

ex) ranitidine

199
Q

NSAIDs inhibit ______

A

COX enzyme

200
Q

serotonin distribution

A

GIT, platelets, brain

201
Q

distribution of serotonin in GIT

A

enterochromaffin cells

  • carcinoid syndrome
  • 90% of 5-HT is found here
202
Q

distribution of serotonin in platelets

A

5-HT found here contribute to platelet aggregation

5-HT released from platelets contribute to vasoconstriction and increase BP

203
Q

distribution of serotonin in brain

A

5-HT is one of the major neutrotransmitters in the brain

-regulates sleep, temp, depression, and anxiety

204
Q

serotonin agonists

A

buspirone (5-HT1a) - tx anxiety, depression

sumatriptan (5-HT1b/1d) - tx HAs and migraines

205
Q

serotonin antagonists

A

cyrproheptadine (blocks histamine, H1, and serotonin, 5-HT) - tx carcinoid syndrome, urticaria, pruritus
ondansetron (5-HT3) - tx nausea and vomiting (anti-emetic)
ketanserin (5-HT2) - antihypertensive

206
Q

arachidonic acid

A 
also called eicosanoids
-class of autocoids is derived from cell membrane phospholipids
207
Q

eicosanoids types

A
  • prostaglandins (PGs): uterine/gastric motility
  • prostacyclin (PGI2): vasodilator, platelet disaggregation
  • thromboxane (TXA2): vasoconstrictor, platelet aggregation
  • leukotrienes (LTs): bronchoconstrictor
208
Q

PGF2alpha

A

increase uterine contraction labor

-potent abortificant

209
Q

leukotrienes

A

produced from arachodonic acid and potent mediators of inflammation and allergy

210
Q

montelukast blocks

A

CysLT1 receptors

211
Q

Zileuton blocks

A

5-LO

-decreases LT production

212
Q

potent bronchodilators

A

LTC4, LTD4, LTE4 (CysLTs)

213
Q

LT antagonists, CysLT1 antagonists manage

A

(montelukast and zafirlukast)

manage bronchial asthma by decreasing CysLT mediated inflammation and mucus secretion

214
Q

Zileuton inhibits the synthesis of

A

leukotrienes by inhibiting 5-LO

-decreasing the production of inflammatory mediator leukotrienes

215
Q

CysLT1 blocker (montelukast) blocks

A

leukotriene receptors

216
Q

montelukast and zileuton both promote

A

bronchodilation and are helpful in ASA-induced asthma

217
Q

st johns wort tx

A

depression

218
Q

saw palmetto tx

A

BPH

-benign prostatic hypertrophy

219
Q

ginkgo biloba tx

A

alzheimer’s disease and dementia

220
Q

3 herbals that are comparable in efficacy to respective allopathic meds

A

st johns wort
saw palmetto
ginkgo biloba

221
Q

kava kava root tx

A

anti-anxiety agent

222
Q

black cohosh tx

A

postmenopausal sx

223
Q

cinnamon bark (cinnulin) tx

A

type 2 DM

224
Q

vanadium & chromium tx

A

type 2 DM

225
Q

echinacea tx

A

cold and flu sx

226
Q

ephedrine tx

A

asthma, weight loss, nasal congestion

227
Q

st johns wort root extract comparable to

A

tricyclic antidepressant 75mg

228
Q

highest herbal sales in germany and france

A

ginkgo biloba

229
Q

ginkgo biloba comes from

A

1000 yr old trees, 10m circumference

230
Q

extract from ginkgo

A

Egb761

-shows improvement on ADAS-Cog scale

231
Q

JAMA article

A
  • shows ginkgo is effective in tx of both alzheimer’s disease and vascular dementia
  • fewer side fx than placebo
  • 2 outcome measures ADAS (cog) and GERRI (social) showed improvement
232
Q

saw paletto is comparable to

A

finasteride

233
Q

saw palmetto: 5-a-reductase converts

A

testosterone to active androgen, dihydrotestosterone

234
Q

finasteride is 5-a-reductase ___________

A

inhibitor

235
Q

both saw palmetto and finasteride _____ IPSS

A

decrease

-urgency, frequency, sensation of incomplete voiding

236
Q

kava kava is comparable with

A

benzodiazepines

237
Q

6 classes of drugs for asthma and COPD

A
  1. beta2-selective adrenergic agonists
  2. adenosine antagonist and PDE inhibitor
  3. muscarinic antagonist
  4. mast cells stabilizers
  5. corticosteriod
  6. leukotriene synthesis and LT antagonist
238
Q

examples of beta2-selective adrenergic agonists

A

albuterol (salbutamol)

salmaterol (LABA)

239
Q

examples adenosine antagonist + PDE inhibitor

A

theophylline

240
Q

examples of muscarinic antagonist

A

ipratropium and tiotropium

241
Q

examples of mast cell stabilizers

A

cromolyn, nedocromil, omalizumab

242
Q

examples of corticosteriods

A

beclomethasone, fluticasone, dexamethosone

243
Q

examples of leukotrienes synthesis inhibitors and LT antagonsits

A

zileuton and montelukast

244
Q

beta2 agonists _______ bronchioles

A

dilate

245
Q

division of anti-asthmatic drugs

A

bronchodilators

decrease inflammation and reduce bronchial hyperresponsiveness

246
Q

bronchodilators

A
  • beta selective agonists
  • phosphodiesterase inhibitor + and Adenosine antagonist
  • muscarinic antagonist
247
Q

reduce inflammation and reduce bronchial hyperresponsiveness

A
  • mast cell stabilizer
  • leukotrienes
  • corticosteriods
248
Q

phosphdiesterase inhibitor - theophylline side fx

A

seizures and cardiac arrhythmias

249
Q

antimuscarinic agents

A

inhaled increases their selectivity at localized site (bronchioles)
-minimal side fx

250
Q

mast cell stabilizer: cromolyn

A
  • given as prophylactic prior to onset
  • not given orally
  • inhibits the secretion of mediators from mast cells
  • inhibits the release of inflammatory mediatorrs from mast cells in response to noxious stimuli
251
Q

corticosteroids

A
  • slow mechanism of action
  • acts by blocking inflammatory mediators
  • long term use is bad
252
Q

management of COPD- stages

A
  1. comb of inhalation agents: iprapropium+LABA+occasional use of ICS
  2. beclamethasone+ iprapropium+combo of all diff bronchodilators
  3. oral corticosteriod+iprapropium, consider giving vaccine
  4. all drugs and tx stated in 3 + oxygen tent/ventilation
253
Q

etanercept

A

new drugs for refractory asthma

  • tumor necrosis factor alpha receptor antibody neutralizers inflammation
  • it sits on TNF-alpha receptor so that TNF cannot sit on the receptor and act
254
Q

anti-tussives: cough suppressants

A

dextromethorphan>codeine>noscapine>benzonatate>guaifenesin

255
Q

proximal convoluted tubule

A

carbonic anhydrous inhibitors

40% Na reabsorbed (bicarbonate)

256
Q

thin descending limb

A

osmotic diuretic

257
Q

thick ascending limn

A

35% Na reabsorbed

loop diuretics

258
Q

distal convoluted tubule

A

10% Na reabsorbed

thiazides

259
Q

cortical collecting tubules

A

2-5% Na reabsorbed

K+ sparing diuretics

260
Q

examples of carbonic anhydrase inhibitors

A

acetazolamide

261
Q

examples of osmotic diuretic

A

mannitol

262
Q

examples of loop diuretics

A

furosemide, ethacrynic acid

263
Q

examples of K+ sparing diuretics

A

spironolactone, triamterene

264
Q

hydrochlorothiazide AEs

A 
hypokalemia
alkalosis
hypercalcemia
hyperuricemia
imparied glucose tolerance
265
Q

K+ sparing diuretics AEs

A

hyperkalemia
acidosis
gynecomastia

266
Q

how tolerance develops to diuretics

A

excretion of Na leads to COMPENSATORY intake of Na

-macula densa cells sense reduction in total body Na and stimulate renin release, which increases aldosterone

267
Q

how to deal with tolerance to diuretics

A

furosemide, increase its dose

and lower intake of Na and water

268
Q

combos: thiazides/loop diuretics/K+ sparing

A

HCTZ+spironolactone
HCTZ+triamterene
HCTZ+amiloride
furosemide+spironolactone

269
Q

combos: thiazides+ACEi or beta1 blockers

- for hypertension

A

HCTZ+enalapril -ACE

HCTZ+atenolol -beta1 blocker

270
Q

carbonic anhydrase inhibitor uses

A

glaucoma, petitmal seizures

  • acute motion sickness
  • edema w/ severe metabolic alkalosis
271
Q

therapeutic uses of mannitol

A

cerebral edema - decreases ICP

in actute renal failure- maintain high urine flow

272
Q

loop diuretic AEs

A 
hypokalemia
hyponatremia
hypovolemia
alkalosis
hypotension
hyperuricemia
273
Q

loop diuretics actions

A

block Na-K-Cl transport

274
Q

alkalosis vs acidosis diuretics

A

CAIs and K+ sparing = acidosis

Loop and thiazide =alkalosis

275
Q

dont use beta2 agonists in

A

hypovolemia and hyponatremia

276
Q

5 things that result from NE release from symp nerve endings

A
  1. vasoconstriction of resistance type arterioles - direct effect
  2. reabsorption of tissue fluid as a result of a decrease in cap pressure
  3. increase in venoconstriction - cap vessels
  4. release of renin and increase in renin-ang2-ald activity
  5. increase in HR and increase in cardiac contractility
277
Q

major effects following RAAS blockade

A 
-ACE inhibitors decrease ang2 level and cause a fall in BP
decrease output of symp nervous systm
increase vasodilation
decrease in retention of Na and water
increase levels of bradykinin
278
Q

vasopressin system restores

A

plasma volume

-reabsorption of water from collecting ducts

279
Q

bosentan is a

A

nonselective ET antagonist

280
Q

ambrisentan is a

A

selective ETa antagonist

281
Q

vascular ETa and ETb contributes to

A

vasoconstriction

282
Q

release of NO

A

decreases Ca and promotes vasodilation

283
Q

3 local (intrinsic) control systems: autocoids

A

histamines, serotonin, PGs

284
Q

nitrates examples

A

nitroglycerin
isosorbide
dinitrate

285
Q

beta-adrenergic blocker examples

A

metoprolol

atenolol

286
Q

CCBs examples

A

diltiziam
verapamil
amlodipine
nifedipine

287
Q

2 goals of therapy for coronary ischemia

A
  1. reduce oxygen demand and decrease workload on heart: give nitrates, beta-blockers, and CCBs
  2. increase oxygen supply to the heart: give nitrates and CCBs (coronary vasodilation)
288
Q

nitrates action

A
  • increase cGMP levels
  • vasodilator
  • rapid onset
  • best for acute angine
  • tolerance develops
289
Q

beta-blockers action

A

-decrease the oxygen demand to the heart
-decrease HR
-decrease contractility
-long term management of stable angine
USE WITH CAUTION IN UNSTABLE/VASOSPASTIC ANGINA

290
Q

CCBs action

A
  • inhibit Ca influx
  • vasodilation
  • decrease load on heart
  • effective in both typical and atypical angine
291
Q

sodium nitroprusside given for

A

hypertensive crisis

-cyanide release from plasma NOT GOOD

292
Q

rapid relief of acute angina by nitrates is due to

A

increase venodilation causes decreases venous return to the heart
decrease preload, decrease workload on the heart, resulting in decrease oxygen consumption

293
Q

best example of drug causing tolerance

A

nitrates

-need to give “drug holidays”

294
Q

beta-adrenergic antagonists AEs

A 
lots!
-bronchospasms
-decrease in max exercise tolerance
-asthma
-erectile dysfunction
decrease HR, decrease CO, decrease RAS
295
Q

CCBs action

A

decrease HR, decrease afterload

-higher affinity for smooth muscle than cardiac muscle

296
Q

CCBs AEs

A

in smooth muscle

  • constipation
  • urinary retention
  • HA
297
Q

Dihydropyridines

A

amlodipine and nifedipine

-used as antihypertensive agents

298
Q

diltiazem use

A

angina

299
Q

verapamil use

A

decrease AV conduction, decrease contractility

-tx arrhythmias

300
Q

features of CCBs and AEs

A

decreases workload, causes vasodilation

-AEs = cardiac depression, ankle edema, constipation

301
Q

preferred tx for both types of angina

A

diltiazem and verapamil

302
Q

tx more effective as antihypertensive

A

amlodipine

-cause a reflex increase in HR

303
Q

pentoxifylline

A

PDE inhibitor, TNFalpha inhibitor, adenosine antagonist

  • promotes red cell deformability
  • helpful in vascular dementia
304
Q

diuretics AEs

A 
hypokalemia
hypovolemia
hyperuricemia
hypercalcemia
hyperglycemia
305
Q

beta-blockers contraindications

A

lipid hostile and precipitates hypoglycemia

COPD and asthma

306
Q

CCBs AEs

A

constipation
HAs
flushing

307
Q

direct renin inhibitor (DRIs)

A

shuts off ang1 and ang2

308
Q

diff between DRI, ACE, ARB

A

ACE: increased renin, increased ang1, decreased ang2, decreased aldo, increased BK
ARB: increased renin, increased ang1, increased ang2, decreased aldo
DRI: decreased everything

309
Q

Group A: ACE/ARB, beta-blocker, DRI

Group B: CCB, diuretic

A

choose 1 from each group and combine for hypertension management

310
Q

carvedilol/labetolol, non-selective alpha/beta blocker used for

A

CHF

311
Q

phentolamine/phenoxybenzamine for

A

pheochromocytoma

312
Q

8 classes of drugs for CHF

A
  1. ACE inhibitors
  2. beta1-blockers
  3. ang2 blocker (ARB)
  4. alpha/beta adrenergic blocker
  5. tailored diuretics (lower edema)
  6. digoxin
  7. vasodilators
  8. dobutamine
313
Q

CHF: ACE inhibitors examples

A

enalapril

lisinopril

314
Q

CHF: beta1-blocker examples

A

atenolol

metoprolol

315
Q

CHF: ang2 blocker (ARB) example

A

losartan

316
Q

CHF: alpha/beta adrenergic blocker example

A

carvedilol

-has antioxidant properties

317
Q

CHF: digoxin use

A

inhibits Na pump

-narrow therapeutic window

318
Q

CHF: vasodilators examples

A

hydralazine

nitrates

319
Q

CHF: dobutamine use

A

last ditch

320
Q

goals of CHF drugs

-overall decreasing CO

A

decreasing afterload - decreasing arteriolar resistance
decreasing preload - decreasing load coming to the heart
increasing cardiac contractility

321
Q

CO =

A

HR*SV

increased preload = increased SV

PCOL 350 (1 decks)

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