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Pharmacology > KAPLAN > Flashcards

KAPLAN Flashcards

1
Q

What processes do pharmacokinetics concern?

A

Absorption
Storage/distribution
Metabolism
Excretion

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2
Q

What processes do pharmacodynamics concern?

A

Dynamics/mechanisms of action of drugs

Side effects of drugs

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3
Q

What do pharmacokinetics describe?

A

What body does to drug

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4
Q

What do pharmacodynamics describe?

A

What drug does to body

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5
Q

What factors does drug permeation depend on?

A

Solubility
Concentration gradient
Surface area and vascularity

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6
Q

Where are drugs more rapidly absorbed? Stomach or large intestine? Why?

A

Small intestine based on larger surface area and microvilli

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7
Q

How are drugs more rapidly absorbed? IM or subQ? (Muscles vs. Fat) Why?

A

IM because muscles are a more vascular tissue

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8
Q

What are common weak acid drugs?

A

Aspirin
Penicillins
Cephalosporins
Loop and thiazide diuretics

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9
Q

What are common weak base drugs?

A

Morphine
Local aenesthetics
Amphetamines
PCP

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10
Q

If you want to get rid of a weak base, put it in____

A

Acid

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11
Q

If you want to get rid of a weak acid, put it in____

A

Base

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12
Q

If you want to absorbs a drug, put it in ____

A

“like”

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13
Q

If you want to absorb a weak acid put it in ____

A

Acid

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14
Q

If you want to absorb a weak base, put it in ____

A

Base

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15
Q

What is stomach pH?

A

1-2

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16
Q

What is small intestine pH?

A

6

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17
Q

What is blood pH?

A

7.4

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18
Q

What is urine pH?

A

5.8

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19
Q

How is lactulose useful in hepatic encephalopathy?

A

Gut bacteria convert it to lactic acid which acidifies fecal masses and traps NH3 in the form of NH4+. Decreases levels of circulating NH3, NH4+ clears.

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20
Q

Gut bacteria convert this drug to lactic acid which acidifies fecal masses and traps NH3 in the form of NH4+. Decreases levels of circulating NH3, NH4+ clears.

A

Lactulose

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21
Q

What forms of drug are filtered?

A

Free
Unbound
Both ionized and nonionized

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22
Q

Which form of a drug undergoes active secretion and active or passive reabsorption?

A

Nonionized

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23
Q

Acidification of urine—>Increases ionization of___—->Increases _____

A

Weak bases

Renal elimination

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24
Q

Alkalinization of urine—>Increases ionization of___—->Increases _____

A

Weak acids

Renal elimination

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25
Q

What do you use to acidify urine?

A

NH4Cl
Vitamin C
Cranberry juice

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26
Q 
What do you use 
NH4Cl
Vitamin C
Cranberry juice
for?
A

Acidification of urine

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27
Q

What do you use to alkalinize urine?

A

NaHCO3

Acetazolamide (historically)

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28
Q

What do you use
NaHCO3
Acetazolamide (historically)
for?

A

Alkalinization of urine

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29
Q

The glomerulus is a good size filter, but a poor ___ filter

A

charge

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30
Q

Any system that uses a carrier can be ______

A

Saturated

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31
Q

What is
Tubular secretion of penicillins and diuretics in proximal tubule
an example of?

A

Active transport

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32
Q

IV administration does not involve _______

A

Absorption

There is no loss of drug

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33
Q

What is bioavailability through IV?

A

100%

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34
Q

What is the fastest route of absorption?

A

Inhalation

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35
Q

How do you know if administration is extravascular?

A

It gets absorbed

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36
Q

What two drugs are examples of oral administration first-pass effect?

A

Lidocaine

Nitroglycerin

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37
Q

How is Lidocaine administered to avoid first-pass effect? Nitroglycerin?

A

IV

Sublingual

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38
Q

Competition between drugs for plasma protein-binding sites may increase the _____, possibly enhancing the effects of the _____

A

Free fraction

Drug displaced

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39
Q

What two drugs are involved in the development of kernictus in neonates? What is the MOA?

A

Sulfonamides and Bilirubin
Both bind to albumin, when add sulfonamides they displace the bilirubin and increase bilirubin [ ] = kernictus = brain dysfunction

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40
Q

Warfarin is usually ____% protein-bound

What do warfarin and sulphonamides compete for? What are the effects of this competition

A

98%
Albumin
Sulfonamides displace the warfarin and thus increase warfarin [ ] in the blood= warfarin toxicity= bleeding and bruising

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41
Q

What is the better barrier, placenta or brain?

A

Brain

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42
Q

What does the placental barrier let through?

A

Most small molecular weight drugs

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43
Q

What does the BBB let through?

A

Only lipid soluble drugs or those of very low molecular weight

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44
Q

If the drug can cross the BB, it easily crosses the ____

A

Placenta

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45
Q

What factors make a drug safer in pregnancy?

A

Water-soluble
Large
Protein-bound

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46
Q

What happens when thyroid meds cross the placental barrier?

A

Cretinism

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47
Q

What are the manifestations of cretinism?

A

Decrease in size
Limbs
Retardation

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48
Q

What are the effects of anticonvulsants when cross the placental barrier?
Examples:

A

Teratogenicity
Phenytoin
Carbamazepine
Valproic acid

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49
Q

Volume of Distribution equation

A 
Vd= Dose/C0
Co= plasma concentration at time zero
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50
Q

Vd is low when a high percentage of a drug is _____

A

Bound to plasma proteins

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51
Q

VD is high when a high percentage of a drug is _____

A

Sequestered in tissues

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52
Q

If most of the drug is in plasma, Vd is ____

A

Low

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53
Q

If most of drug is outside of plasma, Vd is ____

A

High

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54
Q

Why is thiopental’s (IV anaesthetic) half life 9 hours when it reaches the brain in less than a minute?

A

Redistribution: Drug goes into the brain quickly, leaves quickly, gets redistributed into the fat where sequestered for a long time (does not have an effect during this time)

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55
Q

What are the phase I reactions of biotransformation?

A

Oxidation
Reduction
Hydrolysis

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56
Q

Where are CytP450 enzymes located?

What do they have an absolute requirement for?

A

SER

Oxygen and NADPH

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57
Q

Substrate example of 1A2

A

Theophylline

Acetaminophen

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58
Q

Theophylline

Acetaminophen

A

Substrate example of 1A2

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59
Q

Inducers of 1A2

A 
Aromatic hydrocarbons (smoke) (benzopyrenes)
Cruciferous vegetables
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60
Q 
Aromatic hydrocarbons (smoke) (benzopyrenes)
Cruciferous vegetables
A

Inducers of 1A2

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61
Q

Inhibitors of 1A2

A

Quinolones

Macrolides

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62
Q

Quinolones

Macrolides

A

Inhibitors of 1A2

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63
Q

2C9 substrate examples

A

Phenytoin

Warfarin

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64
Q

Phenytoin

Warfarin

A

2C9 substrate examples

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65
Q

Inducers of 2C9

A

General Inducers

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66
Q

What are the general inducers?

A

Anticonvulsants: barbiturates (phenobarbital), phenytoin, carbamazepine
Antibiotics (rifampin)
Chronic alcohol
Glucocorticoids

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67
Q

Anticonvulsants: barbiturates (phenobarbital), phenytoin, carbamazepine
Antibiotics (rifampin)
Chronic alcohol
Glucocorticoids

A

General Inducers

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68
Q

2D6 substrate examples

A

Many CV and CNS drugs

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69
Q

Many CV and CNS drugs

A

2D6 substrate examples

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70
Q

Inhibitors of 2D6

A

Haloperidol

Quinidine

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71
Q

3A4 substrate examples

A

60% of drugs

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72
Q

Inducers of 3A4

A

General Inducers

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73
Q

General inducers induce:

A

2C9 and 3A4

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74
Q

Inhibitors of 3A4

A

General Inhibitors + GF juice

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75
Q

What are general inhibitors?

A

Antiulcer medications (cimetidine, omeprazole)
Antibiotics (chloramphenicol, macrolides (erythromycin), ritonavir (protease inhibitors in HIV), ketoconazole (antifungal),
Acute alcohol

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76
Q

What compounds are metabolized by hydrolysis?
What kind of genetics polymorphism exists with this kind of metabolism?
What does this result in?

A

Esterases and Amidases
Pseudocholinesterase
Increased [ ] of succinylcholine which is a sk. m. relaxant (that is metabolized by pseudocholinesterase)

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77
Q

What do MAOs metabolize?

A 
Endogenous amine neurotransmitters (dopamine, serotonin, and NE)
Exogenous compounds (Tyramine)
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78
Q

Where is tyramine found?

A

Found in beer, red wine, cheese, and fish

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79
Q

What are the types of conjugation in phase II metabolism?

A

Glucoronidation
Acetylation
Glutathione conjugation

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80
Q

What are morphine and chloramphenicol metabolized by?

A

Phase II Glucoronidation

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81
Q

What is chloramphenicol toxicity a result of?

A

The inability of a neonate to effectively metabolize the drug because neonate has low levels of glucoronyl transferase so can’t metabolize effectively

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82
Q

What diseases are as a result of a deficiency in glucoronyl transferase?

A

Gilbert and Crigler-Najjar syndrome

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83
Q

What is drug-induced SLE caused by?

A

By slow acetylators in the use of hydralazine, pracainamide, and isoniazid

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84
Q

Caused by slow acetylators in the use of hydralazine, pracainamide, and isoniazid

A

Drug-induced SLE

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85
Q

What’s the commonality and the difference between drug-induced and non-drug induced SLE?

A

Commonality: butterfly malar rash
Difference: non induced has +ANA and antihistones

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86
Q

What is acetaminophen hepatotoxicity associated with?

A

Depletion of GSH in the liver

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87
Q

A constant amount of drug is eliminated per unit time

A

Zero-order elimination

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88
Q

Rate of elimination is independent of plasma concentration

A

Zero-order elimination

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89
Q

No fixed half-life

A

Zero-order elimination

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90
Q

Drugs with zero-order elimination

A

Phenytoin
Ethanol
Aspirin

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91
Q

A constrant fraction of the drug is eliminated per unit time

A

First-order elimination

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92
Q

Half life is constant

A

First-order elimination

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93
Q

Rate of elimination is directly proportional to plasma level- the higher the amount, the more rapid the elimination

A

First-order elimination

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94
Q

What is zero-order elimination due to?

A

Saturation of elimination mechanisms

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95
Q

Rate of elimination equation

A

= GFR + active secretion - reabsorption

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96
Q

CL=GFR when?

A

There is no reabsorption or secretion and no plasma protein binding

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97
Q

CL=

A

free fraction x GFR

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98
Q

If CL< GFR then

A

drug is reabsorbed

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99
Q

if CL> GFR then

A

drug is actively secreted

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100
Q

Maintenance dose equation

A

C (steady state) x CL x tau / f

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101
Q

The time to reach steady state is dependent ONLY on

A

Elimination half life

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102
Q 
How many half lives does it take to get to 
50% steady state
90% steady state
95% steady state
100% steady state
A

1 half life
3.3 half lives
4-5 half lives
>7 half lives

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103
Q

CLINICAL steady state is accepted to be reached at how many half lives?

A

4-5 half lives

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104
Q

Loading dose equation

A

= Vd x plasma conc. / f

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105
Q

Half life equation

A

= .7 x Vd/CL

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106
Q

Infusion rate equation

A

= CL x Conc. (steady state)

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107
Q

What does a partial agonist act as in the presence of an agonist?

A

Antagonist

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108
Q

What is an example of a partial agonist that acts as an antagonist in the presence of epinephrine?

A

Pindolol (B blocker)

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109
Q

Causes a parallel shift to the right in the D-R curve
Can be reversed by increasing the dose of the agonist
Appears to decrease the potency of the agonist

A

Competitive antagonist

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110
Q

Cause a nonparallel shift to the right
Can be only partially reversed by increasing the dose of the agonist
Appear to decrease the efficacy of the agonist

A

Noncompetitive antagonist

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111
Q

Examples of noncompetitive antagonists

A 
Phenoxylbenzamine (alpha blocker)
Digoxin (blocks Na K ATPase)
Allopurinol- XO
PPIs- proton pump
Aspirin- COX
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112
Q 
Phenoxylbenzamine (alpha blocker)
Digoxin (blocks Na K ATPase)
Allopurinol- XO
PPIs- proton pump
Aspirin- COX
A

Examples of noncompetitive antagonists

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113
Q

Drugs with low therapeutic index (dangerous)

A

Theophylline
Digoxin
Warfarin
Lithium

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114
Q

Theophylline
Digoxin
Warfarin
Lithium

A

Drugs with low therapeutic index (dangerous)

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115
Q

Therapeutic index equation

What does it mean

A

TI= Therapeutic Dose 50/ Effective Dose 50

x how many recommended doses you can take before toxicity

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116
Q

Examples of intracellular receptors

A

Glucocorticoids
Thyroid hormones
Gonadal steroids
Vitamin D

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117
Q

Glucocorticoids
Thyroid hormones
Gonadal steroids
Vitamin D

A

Examples of intracellular receptors

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118
Q

Examples of membrane receptors directly coupled to ion channels

A

Nicotinic receptor for ACh coupled to Na+K+ ion channel

GABA receptor in the CNS coupled to a chloride channel

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119
Q 
Receptors for:
Catecholamines (Beta)
Dopamine (D1)
Glucagon
Histamine (H2)
Prostacyclin
Some serotonin subtypes
A

Gs protein drugs

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120
Q

Gs protein drugs

A 
Receptors for:
Catecholamines (Beta)
Dopamine (D1)
Glucagon
Histamine (H2)
Prostacyclin
Some serotonin subtypes
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121
Q

Adrenoreceptors (alpha-2)
ACh (M2)
Dopamine (D2)
Opioid and serotonin subtypes

A

Gi protein drugs

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122
Q

Gi protein drugs

A

Adrenoreceptors (alpha-2)
ACh (M2)
Dopamine (D2)
Opioid and serotonin subtypes

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123
Q

Ach (M1 and M3)
NE (alpha 1)
Angiotensin II
Serotonin subtypes

A

Gq protein drugs

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124
Q

Gq protein drugs

A

Ach (M1 and M3)
NE (alpha 1)
Angiotensin II
Serotonin subtypes

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125
Q

M1 M3 A-1 receptor mechanism

A

Gq activation of phospholipase C

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126
Q

M2 A-2 D2 receptor mechanism

A

Gi inhibition of adenylyl cyclase

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127
Q

B-1 B-2 D1

A

Gs activation of adenylyl cyclase

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128
Q

Which ANS receptors use Gq activation of phospholipase C

A

M1 M3 A-1 receptor mechanism

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129
Q

Which ANS receptors use Gi inhibition of adenylyl cyclase

A

M2 A-2 D2 receptor mechanism

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130
Q

Which ANS receptors Gs activation of adenylyl cyclase

A

B-1 B-2 D1

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131
Q

Mechanism of vasodilators

A

Increase the synthesis of NO by endothelial cells. NO activates guanylyl cyclase thus increasing cGMP in smooth muscle. cGMP facilitates dephospho rylation of myosin light chains, preventing their interaction with actin and thus causing vasodilation.

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132
Q

How does cGMP cause vasodilation?

A

facilitates dephospho rylation of myosin light chains, preventing their interaction with actin and thus causing vasodilation.

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133
Q

facilitates dephospho rylation of myosin light chains, preventing their interaction with actin and thus causing vasodilation.

A

cGMP

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134
Q

Drugs activating NO

A

Nitrates (Nitroglycerin)

M receptor agonists (Bethanechol)

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135
Q

Nitrates (Nitroglycerin)

M receptor agonists (Bethanechol)

A

Drugs activating NO

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136
Q

Endogenous compounds activating NO

A

Bradykinin and histamine

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137
Q

Bradykinin and histamine

A

Endogenous compounds activating NO

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138
Q

If see increase in secretions =

A

Muscarinic agonist

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139
Q

If see drying out of secretions (dry mouth, no sweating) =

A

Muscarinic blocker

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140
Q

Hormone which can work on both innervated and non innervated tissues

A

Epinephrine

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141
Q

B2 receptors are generally not innervated so what hormone will work on them and which one will never work on them?

A

Epinephrine and NE (or other NTs)

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142
Q

Neurotransmitter at both nicotinic and muscarinic receptors in tissues that are innervated
All direct transmission from CNS (preganglionic and motor) uses this NT

A

ACh

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143
Q

ACh

A

Neurotransmitter at both nicotinic and muscarinic receptors in tissues that are innervated
All direct transmission from CNS (preganglionic and motor) uses this NT

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144
Q

NT at most adrenoceptors in organs, as well as in cardiac and smooth muscle

A

NE

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145
Q

NE

A

NT at most adrenoceptors in organs, as well as in cardiac and smooth muscle

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146
Q

Activates receptors causing vasodilation in renal and mesenteric vascular beds

A

Dopamine

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147
Q

Dopamine

A

Activates D-1 receptors causing vasodilation in renal and mesenteric vascular beds

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148
Q

Activates most adrenoceptors and is transported in the blood

A

Epinephrine

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149
Q

Epinephrine

A

Activates most adrenoceptors and is transported in the blood

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150
Q

What is the direct way of increasing BP?

A

Ach–>Nn, NE–>B-1

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151
Q

What is the direct way of decreasing BP?

A

Ach–>Nn, Ach–>M (AV node)

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152
Q

What receptor increases TPR?

A

A-1

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153
Q

What receptor decreases TPR?

A

B-2

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154
Q

What happens when TPR increases?
By what NT on what receptor?
How do you block this?

A

Reflex bradycardia
ACh on M2
M2 blocker or ganglionic blocker

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155
Q

What happens when TPR decreases?
By what NT on what receptor?
How do you block this?

A

Reflex tachycardia
ACh on B-1
B-1 blocker or ganglionic blocker

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156
Q

Blood pressure system is ONLY affected by ____ in mean BP which results in ___ in renal blood flow

A

Decrease

Decrease

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157
Q

Decreased renal pressure causes the release of ____ which promotes the formation of _____

A

Renin

Angiotensins

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158
Q

Angiotensin II increases ____ release from the adrenal cortex, which increases blood volume by____
Angiotensin also causes ____ resulting in an ___TPR

A

Aldosterone
Acting to retain sodium and water
Vasoconstriction
Increase

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159
Q

Equation for BP

A

=TPR x CO

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160
Q

Equation for CO

A

= HR x SV

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161
Q

=TPR x CO

A

Equation for BP

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162
Q

= HR x SV

A

Equation for CO

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163
Q

When you give antihypertensive drugs, the body responds by the renin-angiotensin-aldosterone system and increases BV and thus BP, how do we fight off reflexes?

A

Tachycardia: B blocker

Salt and water retention: diuretics or ACE inhibitor

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164
Q

What muscles in the eye are under muscarinic control?

A

Sphincter (contracts)

Ciliary (contracts)

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165
Q

What effects does muscarinic stimulation have on the eye?

A

Miosis

Accomodation (near vision)

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166
Q

Accomodation is purely a _____ response

A

PANS (muscarinic)

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167
Q

What effects does muscarinic antagonism have on the eye?

A

Mydriasis

Accommodation to far vision (cyclopegia) (Paralysis of accommodation)

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168
Q

What does accommodation to far vision lead to?

A

Cyclopegia (Paralysis of accommodation)

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169
Q

What muscles in the eye are under adrenergic control? What receptors?

A

Radial (A-1) (Contracts)

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170
Q

What effects do A-1 agonists have on the eye?

A 
Mydriasis
No cyclopegia (there are no A-1 receptors on ciliary muscle, only under M control)
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171
Q

Miosis + blurred vision=

A

M agonist

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172
Q

Mydriasis + blurred vision=

A

M antagonist

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173
Q

What does hemicholinium do?

A

Inhibits uptake of choline

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174
Q

Inhibits uptake of choline

A

hemicholinium

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175
Q

What does Botulinum toxin do?

How?

A

Prevents Ach release by binding to synaptobrevin (which allows docking of vesicles onto membrane)

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176
Q

Prevents Ach release by binding to synaptobrevin (which allows docking of vesicles onto membrane)

A

Botulinum toxin

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177
Q

What does synaptobrevin do?

A

allows docking of vesicles onto membrane

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178
Q

Reversible AChE inhibitors

A

Edrophonium
Physostigmine
Neostigmine

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179
Q

Edrophonium
Physostigmine
Neostigmine

A

Reversible AChE inhibitors

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180
Q

Irreversible AChe inhibitors

A

Echothiophate
Malathion
Parathion

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181
Q

Echothiophate
Malathion
Parathion

A

Irreversible AChe inhibitors

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182
Q

What are the medical uses of botulinum toxin?

A

Blepharospam (involuntary contraction of eyelid)
Strabismus (lazy eye) (paralyzes extraocular muscles)
Hyperhydrosis (sweatiness) (decreases secretions by decreasing ACh)
Dystonia (painful menstrual cramps)
Cosmetics

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183
Q

Blepharospam (involuntary contraction of eyelid)
Strabismus (lazy eye) (paralyzes extraocular muscles)
Hyperhydrosis (sweatiness) (decreases secretions by decreasing ACh)
Dystonia (painful menstrual cramps)
Cosmetics

A

medical uses of botulinum toxin

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184
Q

Decreased CV function
Increased secretions
Increased smooth muscle contractions

A

M receptor activation

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185
Q

Results of M receptor activation

A

Decreased CV function
Increased secretions
Increased smooth muscle contractions

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186
Q

What M receptors are in the eye? What parts of the eye? What are they coupled to? How do they work?
What effect does agonism of these receptors have?

A 
Sphincter m= M3
Ciliary m= M3
Gq-coupled
Increase Ca in smooth muscle= contraction
Miosis and Accommodation for near vision
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187
Q

What M receptors are in the heart? What parts of the heart? What are they coupled to? How do they work?
What effects does agonism of these receptors have? What changes on the EKG?
Where are sympathetic R NOT found in the heart (only sympathetic R)

A 
SA node= M2
AV node= M2
Gi-coupled
Inhibit adenylyl cyclase
SA node= decrease heart rate (bradycardia)
AV node= decrease conduction velocity
Increases PR interval
Ventricular muscle
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188
Q

What M receptors are in the lungs? What parts of the lungs? What are they coupled to? How do they work?
What effects does agonism of these receptors have?
When shouldn’t you use M agonists based on these effects?

A 
Bronchioles=M3
Glands= M3
Gq-coupled
Increase Ca in smooth muscle= contraction
Bronchioles= Contraction=bronchospasm
Glands= Increased secretion
Decreases the FEV/FVC ratio
Those are COPD symptoms. Shouldn't use it on patients with asthma or CF
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189
Q

What M receptors are in the GI tract? What parts of the GI tract? What are they coupled to? How do they work?
What effects does agonism of these receptors have?
When shouldn’t you use M agonists based on these effects?

A 
Stomach= M3
Glands= M1
Intestine= M3
M1 and M3 coupled to Gq
Increase Ca in smooth muscle= contraction
Stomach= Increased motility-cramps
Glands= Increased acid production
Intestine= Contraction=diarrhea, involuntary defecation
Patients with PUD
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190
Q

What M receptors are in the bladder? What are they coupled to? How do they work?
What effects does agonism of these receptors have?

A 
M3
Gq-coupled
Increase Ca in smooth muscle= contraction
Contraction in the detrusor
Relaxation in the trigone/sphincter
=
Voiding and urinary incontinence
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191
Q

What M receptors are in the sphincters?
What are they coupled to? How do they work?
What effects does agonism of these receptors have?

A

M3
Gq-coupled
Increase Ca in smooth muscle= contraction
Relaxation except lower esophageal which contracts

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192
Q

What M receptors are in the glands?
What are they coupled to? How do they work?
What effects does agonism of these receptors have?

A

All glands are M3 except in the GI tract (M1)
Gq-coupled
Increase Ca in smooth muscle= contraction
Secretion-sweat (thermoregulatory), salivation, and lacrimation

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193
Q

What M receptors are in the blood vessel endothelium?
What effects does agonism of these receptors have?
What is the exception to what can activate these receptors? Why?

A

M3
Dilation (via NO/EDRF)
Indirect agonists will NOT work because there is no parasympathetic innervation in vasculature, it is solely sympathetic. So, only direct M agonists will work.

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194
Q

What is the response of activating Nn receptors in the adrenal medulla?

A

Secretion of epinephrine and NE

195
Q

What is the response of activating Nm receptors at the neuromuscular junction?

A

Stimulation- twitch/hyperactivity of skeletal muscle

196
Q

Blood vessels are solely innervated by the _____, so stimulation of autonomic ganglia results in ______

A

SANS

Vasoconstriction

197
Q

GI tract is dominated by ____ so ganglionic stimulation causes ______

A

PANS

Increased motility and secretions

198
Q

What is ileus? When does it occur?
When does urinary retention occur?
What drug is used for these conditions? What kind of drug is it?

A

When the gut is not moving (no peristalsis) Post-op or neurogenic
As a result of peripheral neuropathy that diabetics suffer from
Bethanechol
DIRECT-ACTING Cholinomimetic working on M1 and M3

199
Q

When is methacholine used?

What kind of drug is it?

A

Used for diagnostic procedure: it triggers wheezing in a person with bronchial hyperreactivity
DIRECT-ACTING Cholinomimetic woking on M receptors

200
Q

When is pilocarpinen used?

What kind of drug is it?

A

In glaucoma (topical-eye drops)
Xerostomia (dry mouth)
Sjoger disease (fibrosis of lacrimal and salivary glands)
DIRECT-ACTING Cholinomimetic working on M receptors

201
Q

What is myasthenia? What drugs are used for its differentiation from cholinergic crisis? What drugs are used for its treatment?

A

Autoimmune disease where auto antibodies block N receptors of skeletal muscles so patient has facial weakness and ptosis as a result of paralysis of muscles from lack of stimulation from ACh.
Edrophonium
Neostigmine and Pyridostigmine

202
Q

What is characteristic of physostigmine?

What is it used to treat?

A 
Tertiary amine (enters CNS)
Glaucoma and antidote for atropine (M antagonist) overdose
203
Q 
Tertiary amine (enters CNS)
Used in Glaucoma and antidote for atropine (M antagonist) overdose
A

Physostigmine

204
Q

What is characteristic of neostigmine and pyridostigmine?

What are they used to treat?

A 
Quaternary amines (cannot enter CNS)
Ileus
Urinary retention
Myasthenia
Reversal of nondepolarizing NM blockers
205
Q 
Quaternary amines (cannot enter CNS)
Used to treat:
Ileus
Urinary retention
Myasthenia
Reversal of nondepolarizing NM blockers
A

neostigmine and pyridostigmine

206
Q

What are donepezil and tacrine used to treat?

A

Alzheimer’s

207
Q

What indirect-acting cholinomimetics are used to treat Alzheimer’s?

A

donepezil and tacrine

208
Q

What is characteristic of organophosphates?

How are they used?

A

Irreversible inhibitors
Used in glaucoma (echothiophate)
Used as insecticides (malathion, parathion) and as nerve gas (sarin)

209
Q

Irreversible inhibitors
Used in glaucoma (echothiophate)
Used as insecticides (malathion, parathion) and as nerve gas (sarin)

A

Organophosphates

210
Q

Acute AChE inhibitor poisoning symptoms-Muscarinic effects

A 
DUMBBELSS
Diarrhead
Urination
Miosis
Bradycardia
Bronchoconstriction
Excitation (CNS/muscle)
Lacrimation
Salivation
Sweating
211
Q 
DUMBBELSS
Diarrhead
Urination
Miosis
Bradycardia
Bronchoconstriction
Excitation (CNS/muscle)
Lacrimation
Salivation
Sweating
A

Acute AChE inhibitor poisoning symptoms- Muscarinic effects

212
Q

Skeletal muscle excitation followed by paralysis

CNS stimulation

A

Acute AChE inhibitor poisoning symptoms- Nicotinic effects

213
Q

Acute AChE inhibitor poisoning symptoms- Nicotinic effects

A

Skeletal muscle excitation followed by paralysis

CNS stimulation

214
Q

How do you manage Acute AChE inhibitor toxicity?

A

Atropine (antimuscarinic) for muscarinic effects

Pralidoxime (2-PAM) for the regeneration of AChE

215
Q

How does 2-PAM work?

A

It takes the phosphate that attached to AChE and binds it to itself

216
Q

How does chronic AChE inhibitor poisoning present itself?

A

Peripheral neuropathy causing muscle weakness and sensory loss
MS symptoms: foot drop, wrist drop, scanning speech, diplopia

217
Q

Peripheral neuropathy causing muscle weakness and sensory loss
MS symptoms: foot drop, wrist drop, scanning speech, diplopia
are symptoms of?

A

chronic AChE inhibitor poisoning

218
Q

What are the atropine side effects?

A

Decreased secretions (salivary, bronchiolar, sweat, dry mouth)
Mydriasis and cycloplegia
Hyperthermia (with resulting vasodilation)
Tachycardia
Sedation
Urinary retention and constipation
Behavioral excitation and hallucinations

219
Q

Decreased secretions (salivary, bronchiolar, sweat)
Mydriasis and cycloplegia
Hyperthermia (with resulting vasodilation)
Tachycardia
Sedation
Urinary retention and constipation
Behavioral excitation and hallucinations

A

atropine side effects

220
Q

When is the atropine side effect of decreased secretions used?

A

In allergies, colds, intubation

side effect: dry mouth

221
Q

When is the atropine side effect of mydriasis and cyclopegia used?

A

To check for retinopathies in diabetics

Side effect: blurred vision (lack of accommodation)

222
Q

When is the atropine side effect of urinary retention and constipation used?

A

In urinary incontinence and diarrhea

223
Q

What are some other drugs with antimuscarinic pharmacology?

A 
Antihistamines
TC antidepressants
Antipsychotics
Quinidine
Amantadine
Merepidine
224
Q 
Antihistamines
TC antidepressants
Antipsychotics
Quinidine
Amantadine
Merepidine
A

other drugs with antimuscarinic pharmacology

225
Q

How do you treat acute atropy intoxication?

Why this drug?

A

Symptomatic + physostigmine

It is an AChE inhibitor that can cross the BBB

226
Q

M blockers

A 
BAITS
Benztropine, trihexyphenidyl
Atropine
Iptratropium
Tropicamide
Scopolamine
227
Q 
BAITS
Benztropine, trihexyphenidyl
Atropine
Iptratropium
Tropicamide
Scopolamine
A

M blockers

228
Q

Clinical uses and/or characteristics of atropine

A

Antispasmodic, antisecretory, management of AChE inhibitor OD, antidiarrheal, ophthalmology

229
Q

Antispasmodic, antisecretory, management of AChE inhibitor OD, antidiarrheal, ophthalmology

A

Clinical uses and/or characteristics of atropine

230
Q

Clinical uses and/or characteristics of tropicamide

A

Opthalmology (topical)- dilates the pupil

231
Q

Opthalmology (topical)- dilates the pupil

A

Clinical uses and/or characteristics of tropicamide

232
Q

Clinical uses and/or characteristics of ipratropium

A

Asthma, COPD- no CNS entry, no change in mucus viscosity (decreases secretions in volume not viscosity)
Prevents bronchospasm

233
Q

Asthma, COPD- no CNS entry, no change in mucus viscosity (decreases secretions in volume not viscosity)
Prevents bronchospasm

A

Clinical uses and/or characteristics of ipratropium

234
Q

Clinical uses and/or characteristics of scopolamine

A

Used in motion sickness, causes sedation and short-term memory blocks (anterograde amnesia)

235
Q

Used in motion sickness, causes sedation and short-term memory blocks (anterograde amnesia)

A

Clinical uses and/or characteristics of scopolamine

236
Q

What do ganglionic blockers essentially do?

A

Wipe out ANS

Prevent baroreceptor reflexes

237
Q

What are endplate nicotinic receptor blockers?

A

Tubocuranine
Atracurium
Succinylcholine

238
Q

What effectors are controlled by the SANS?

What is the effect then of a ganglion blockade?

A

Arterioles- vasodilation, hypotension
Veins- Dilation, decreased venous return, decreased CO
Sweat glands- anhydrosis (lack of sweating)

239
Q

What effectors are controlled by the PANS?

What is the effect then of a ganglion blockade?

A

Heart- FIXED tachycardia (no more ANS regulation)
Iris- FIXED mydriasis
Ciliary muscle- Cycloplegia (blurred vision)
GI tract- Decreased tone and motility= constipation
Bladder- Urinary retention
Salivary glands- Xerostoma (dry mouth)

240
Q

What step does methyl-p-tyrosine inhibit in catecholamine synthesis?

A

The rate-limiting step

Tyrosine –> DOPA

241
Q

What effect do MAO inhibitors and releasers have?

A

Increase the NE mobile pool= CV effects

242
Q

What does reuptake of NE usually do? What do reuptake blockers do? What are they used for?

A

Create concentration gradient
Block this- thus get rid of conc. gradient
Depression (keep the NE in the junction!)

243
Q

How do A-2 agonists work in the neuroeffector junction?
How does an A-2 blockade work?
Examples of A-2 agonists

A

They enhance negative feedback so decrease NE levels being released (used for hypertension)
Increase NE levels (cancels negative feedback)
Clonidine and methyldopa

244
Q

What adrenergic receptors are found in the eye?

What is the response to activation?

A

A-1 on radial (dilator) muscle

Contraction= mydriasis (without cycloplegia- no blurred vision)

245
Q

What adrenergic receptors are found in the arterioles (skin, viscera) ?

What is the response to activation?

A

A-1- makes the heart work harder
Contraction= increased TPR=increase in diastolic P, increase in after load (what the heart has to work against)
Useful in shock

246
Q

What adrenergic receptors are found in the veins?

What is the response to activation?

A

A-1

Contraction=increased venous return=increased preload=increased systolic P

247
Q

What adrenergic receptors are found in the bladder trigone and sphincter?
What is the response to activation?

A

A-1

Contraction=urinary retention

248
Q

What adrenergic receptors are found in the male sex organs?

What is the response to activation?

A

A-1
Vas deferens- ejaculation
Why people don’t like to take alpha blockers lawl

249
Q

What adrenergic receptors are found in the liver?

What is the response to activation?

A

A-1 and B-2
A-1= increased glycogenolysis
B-2= increased glycogenolysis, increased gluconeogenesis, increased lipolysis
Beta receptors are more sensitive (until high doses of A)

250
Q

What adrenergic receptors are found in the kidney?

What is the response to activation?

A

A-1 and B-1
A-1= decreased renin release
B-1= increased renin release
Beta receptors are more sensitive (until high doses of A)

251
Q

What adrenergic receptors are found in the pre junctional nerve terminals?
What is the response to activation?

A

A-2

Decreased transmitter release and NE synthesis= decreased A-1 stimulation= decreased contraction

252
Q

What adrenergic receptors are found in the platelets?
What is the response to activation?
What hormone works on these receptors?
When do you not want A-2 side effects? (AKA whom do you not want to prescribe A-2 agonist to?)

A

A-2
Aggregation
Epinephrine- plays role in aggregation of platelets and thrombosis during bleeding
If patient is hypertensive or has atherosclerotic plaques

253
Q

What adrenergic receptors are found in the pancreas?
What is the response to activation?
When is it not best to give an A-2 agonist then?

A

A-2 and B-2
A-2= decreased insulin secretion
B-2= Increased insulin secretion
Beta receptors are more sensitive (until high doses of A)
To a diabetic patient if it further suppresses insulin secretion!

254
Q

What adrenergic receptors are found in the heart?
What is the response to activation?
What can this cause?

A

B-1
SA node= Increase in HR
AV node= increase in conduction velocity
Atrial and Ventr. muscle= increased force of contraction, conduction velocity, CO and oxygen consumption
His-Purkinje= increased automaticity and conduction velocity
Worsen angina, worsen M.I, can’t use chronically

255
Q

What is characteristic of B-2 receptors?
What does this mean in terms of what can and cannot work on it?
What is the physiological basis for this?

A

They are mostly not innervated
Neurotransmitters (NE) cannot reach it
In fight or flight, NE constricts vessels= no O2 to the heart, brain, or muscles (which you need!)
Epinephrine opposes this silly reaction by vasodilating all the blood vessels
B-2 receptors are more sensitive than A-1 to stimulation

256
Q

What adrenergic receptors are found in all blood vessels?

What is the response to activation?

A

B-2 receptors

Vasodilation- decrease in TPR=decrease in diastolic P=decrease in afterload

257
Q

What adrenergic receptors are found in the uterus?
What is the response to activation?
When is it used?

A

B-2
Relaxation
To prevent premature labor

258
Q

What adrenergic receptors are found in the bronchioles?
What is the response to activation?
When is it used?

A

B-2
Dilation
Asthma

259
Q

What adrenergic receptors are found in skeletal muscle?

What is the response to activation?

A

B-2

Increased glycogenolysis= contractility (tremor)

260
Q

Where are D-1 receptors found?

What is the response to activation?

A

Renal, mesenteris, coronary vasculature

Vasodilation- in kidney= increased RBF, increased GFR, increased Na secretion

261
Q

What kind of drug is phenylephrine?

What is it used for?

A

Direct A-1 agonist

Nasal decongestant and ophthalmologic use (mydriasis without cycloplegia)

262
Q

Direct A-1 agonist

Nasal decongestant and ophthalmologic use (mydriasis without cycloplegia)

A

phenylephrine

263
Q

What kind of drug is methoxamine?

What is it used for?

A

Direct A-1 agonist
Paroxysmal atrial tachycardia through vagal reflex
Needs to slow SA and AV node so increases BP to get a reflex bradycardia

264
Q

What kind of drugs are clonidine and methyldopa? What are they used for?

A

A-2 agonists

Hypertension

265
Q 
What kind of drugs are 
albuterol
salmeterol
terbutaline ?
What are they used for?
A

Selective B-2 agonists

Asthma

266
Q

What kind of a drug is ritodrine?

When is it used?

A

Selective B-2 agonist

Premature labor

267
Q

What kind of a drug is isoproterenol?

What it is used for?

A

B-1=B-2 agonist

Used for bronchospasm, heart block, and bradyarrhythmias

268
Q

Direct A-1 agonist
Paroxysmal atrial tachycardia through vagal reflex
Needs to slow SA and AV node so increases BP to get a reflex bradycardia

A

methoxamine

269
Q

A-2 agonists

Hypertension

A

clonidine and methyldopa

270
Q

Selective B-2 agonist

Premature labor

A

ritodrine

271
Q

B-1=B-2 agonist

Used for bronchospasm, heart block, and bradyarrhythmias

A

isoproterenol

272
Q

What kind of a drug is dobutamine?

When is it used?

A

B-1>B-2 agonist

CHF

273
Q

B-1>B-2 agonist

CHF

A

dobutamine

274
Q

What receptor does NE not work on?

What does this mean?

A

B-2

It can never lower BP

275
Q 
Out of this list of conditions, which ones are acted upon by NE, epi, or both? On what receptors?
Cardiac arrest
Adjunct to local anesthetic
Hypotension
Anaphylaxis
Asthma
A 
Cardiac arrest- both (B-1)
Adjunct to local anesthetic-both (A-1)
Hypotension-both (A-1, B-1)
Anaphylaxis- just epi (B-2)
Asthma-just epi (B-2)
276
Q

What are the two main categories of indirect-acting adrenergic agonists?

A

Releasers and reuptake inhibitors

277
Q

Releasers and reuptake inhibitors

A

two main categories of indirect-acting adrenergic agonists

278
Q

What are the three types of releasers?

What is their drug interaction?

A

Tyramine
Amphetamines
Ephedrine
MAO inhibitors (do not mix!)

279
Q

Tyramine
Amphetamines
Ephedrine
MAO inhibitors (do not mix!)

A

releasers

280
Q

Where is tyramine found?

What increases its bioavailability? What decreases it?

A

Red wine and cheese
MAO inhibition= hypertensive crisis
MAO-A metabolism in gut and liver

281
Q

What is the clinical use of amphetamines?

A

Methyl phenidate in narcolepsy and ADHD

282
Q

What are the two types of reuptake inhibitors?

A

Cocaine and TCAs

283
Q

What is ephedrine used as?

A

Cold medication

284
Q

What are the major uses of A blockers?

A

Hypertension (selective A-1)
Pheochromocytoma (non-selective)
BPH (selective A-1)

285
Q

Hypertension (selective A-1)
Pheochromocytoma (non-selective)
BPH (selective A-1)

A

major uses of A blockers

286
Q

What are two nonselective A-blockers?

What is the difference between them?

A

Phentolamine- competitive inhibitor

Phenoxybenzamine- non-competitive- choice for pheochromocytoma because binds irreversibly

287
Q 
What do all of these have in common?
Prazosin
Doxazosin
Terazosin
Tamsulosin
A

Selective A-1 blockers

288
Q

Selective A-1 blockers

A

Prazosin
Doxazosin
Terazosin
Tamsulosin

289
Q

What are these? What are their clinical uses?
Yohimbine
Mirtazapine

A

Selective A-2 blockers
Yohimbine- postural hypotension and impotence
Mirtazapine- antidepressant

290
Q

What are the main effects of a B-1 blockade?

What are the uses?

A

Decreased HR, SV, CO aka decreased O2 demand (decreased angina, decreased recurrence of MI
Decreased renin release (hypertension management)
Decreased aqueous humor production (decreased IOP, glaucoma)

291
Q

A–>M beta blockers are

A

B-1 selective

292
Q

B-1 selective blockers

A

Acebutolol
Atenolol
Metoprolol

293
Q

P–>Z beta blockers are

A

non-selective

294
Q

Non-selective B blockers

A

Pindolol
Propranolol
Timolol

295
Q

What are the general uses of beta-blockers

A

Angina, hypertension, post MI
Antiarrhythmics (class 2: propranolol, acebutolol, esmolol)
Glaucoma (timolol, betaxolol)
Migraine, thyrotoxicosis, performance anxiety, essential tremor

296
Q

Which drugs have combined A and B-blocking activity?

What are they used for?

A

Labetalol and Carvedilol

CHF

297
Q

Which drug has K channel blockade and B-blocking activity?

A

Sotalol (class 2-antiarrhythmic)

298
Q

Where is histamine released from?

What triggers its release?

A

Mast cells, basophils, and platelets

IgE-mediated allergic reactions, Type 1 hypersensitivity, drugs, venoms, and trauma

299
Q

How can increased histamine production be detected?

A

Increased amounts of its metabolite imidazoleacetic (5HIAA) in the urine

300
Q

Increased amounts of its metabolite imidazoleacetic (5HIAA) in the urine makes its over production detectable

A

histamine

301
Q

What G protein are H1 receptors coupled to?

What are the effects of H1 activation?

A

Gq protein
Increased capillary dilation (via NO)= decrease in BP (leads to shock in anaphylaxis)
Increased capillary permeability= increased edema
Increased bronchiolar sm. m contraction (via IP3 and DAG release)
Increased activation of peripheral nociceptive receptors= increased pain and pruritus (itching)
Decreased AV nodal conduction= bradycardia

302
Q

What receptor activation is this?
Gq protein
Increased capillary dilation (via NO)= decrease in BP (leads to shock in anaphylaxis)
Increased capillary permeability= increased edema
Increased bronchiolar sm. m contraction (via IP3 and DAG release)
Increased activation of peripheral nociceptive receptors= increased pain and pruritus (itching)
Decreased AV nodal conduction= bradycardia

A

H1

303
Q

What G protein is the H2 receptors coupled to?

What are the effects of H2 activation?

A

Gs
Increased gastric acid secretion= increase in GI ulcers
Increased SA nodal rate, positive inotropism and automaticity- cardiac stimulation
Reduces histamine release from mast cells (neg feedback)

304
Q

What receptor activation is this?
Gs
Increased gastric acid secretion= increase in GI ulcers
Increased SA nodal rate, positive inotropism and automaticity- cardiac stimulation
Reduces histamine release from mast cells (neg feedback)

A

H2

305
Q

All of these are active by oral route
All require hepatic metabolism and most cross the placental barrier
Many of them are potent anesthetics because block activation of nociceptors

A

H1 antagonists

306
Q

What are the major antihistamines?
Which ones are 1st generation, which ones 2nd?
What is the difference?

A 
Diphenhydramine-1st
Promethazine-1st
Chlorpheniramine-1st
Meclizine-1st
Cetirizine-2nd
Loratadine-2nd
Fexofenadine-2nd
1st generation antihistamines cause drowsiness- are anti motion sickness, are muscarinic blockers and enter the CNS
2nd generation do not cause drowsiness, are not anti motion sickness, are not antimuscarinics and do not enter CNS
307
Q

Which antihistamine is used for management of chemotherapy-induced vomiting?

A

Diphenhydramine

308
Q

Which anti histamine is the most effective anti-motion sickness drug?

A

Meclizine

309
Q

What are the uses for antihistamines?

A

Allergic reactions (hay fever, rhinitis, urticaria)
Motion sickness, vertigo (M blockers)
Nausea and vomiting with pregnancy (M blockers)
Preoperative sedation (M blockers)
OTC: sleep aids and cold medication (m blockers)
Parkinson disease
Acute EPSs

310
Q

What drugs are used for these conditions?
Allergic reactions (hay fever, rhinitis, urticaria)
Motion sickness, vertigo (M blockers)
Nausea and vomiting with pregnancy (M blockers)
Preoperative sedation (M blockers)
OTC: sleep aids and cold medication (m blockers)
Parkinson disease
Acute EPSs

A

Antihistamines

311
Q

By what mechanism do prostaglandins have a protective role in the stomach?

A

Inhibit proton pump
Improve mucus secretion to cover the lining of the stomach to protect from acid erosion
Enhance bicarb secretion to neutralize the acid

312
Q

What are these mechanisms of?
Inhibit proton pump
Improve mucus secretion to cover the lining of the stomach to protect from acid erosion
Enhance bicarb secretion to neutralize the acid

A

Prostaglandin’s protective role in the stomach

313
Q

What are antacids?

A

Bases floating around in the stomach that neutralize the acids

314
Q

Bases floating around in the stomach that neutralize the acids

A

Antacids

315
Q

What is sucralfate and bismuth subsalicylate?

A

“sticky gel” that coats ulcer crater to protect it from further erosion by acids

316
Q

“sticky gel” that coats ulcer crater to protect it from further erosion by acids

A

sucralfate and bismuth subsalicylate

317
Q

What are examples of H2 antagonists?

Which one is the only one that crosses the BBB?

A 
Cimetidine
Ranitidine
Famotidine
Nizatidine
Only Cimetidine crosses the BBB
318
Q

What is the MOA of H2 antagonists?

A

Suppress secretory responses to food stimulation and nocturnal secretion of gastric acid via their ability to indirectly decrease the activity of the proton pump
Also partially antagonize HCl secretion caused by vagally or gastrin-induced release of histamine from ECL-like cells

319
Q

What drug’s MOA is this?
Suppress secretory responses to food stimulation and nocturnal secretion of gastric acid via their ability to indirectly decrease the activity of the proton pump
Also partially antagonize HCl secretion caused by vagally or gastrin-induced release of histamine from ECL-like cells

A

H2 antagonists

320
Q

What are the uses for H2 antagonists?

A

PUD
GERD
Zollinger-Ellison

321
Q

What drugs are used for these conditions?
PUD
GERD
Zollinger-Ellison

A

H2 antagonists

322
Q

What are the major side effects of Cimetidine?

A

Decrease in androgens= gynecomastia and decreased libido

323
Q

Decrease in androgens= gynecomastia and decreased libido

What are these side effects of?

A

Cimetidine

324
Q

What is the MOA of PPIs?
What is an example of one?
What are their uses?

A 
Irreversible direct inhibitors of the PP (K/H anti port) in the gastric parietal cell
Omeprazole (all -prazoles)
More effective than H2 clockers in PUD
Effective in GERD and Zollinger Ellison
Eradication regimen for H. pylori
325
Q

What is the eradication regimen for H. pylori?

A

PPI
Clarithromycin (macrolide)
Amoxicillin

326
Q

What is Barrett’s? What does it result from? What does this increase the risk of?

A

Metaplastic transformation (squamous cells in lower third of esophagus turn into columnar mucus-producing cells)
From chronic GERD
Increases the risk of developing adenocarcinoma of esophagus

327
Q

What is Misoprostol? What is it also known as? What is its MOA? What are its uses?

A

PGE1 analog- “antidote to aspirin-induced ulcers”
It is cytoprotective. It increases mucus and bicarbonate secretion and decreases HCl secretion.
It is used in NSAID-induced GI ulcers

328
Q

Why is anything with -prost contraindicated in pregnancy?

A

Because it’s a PGE1 analog which can induce contractions= abortion

329
Q

PGE1 analog- “antidote to aspirin-induced ulcers”
It is cytoprotective. It increases mucus and bicarbonate secretion and decreases HCl secretion.
It is used in NSAID-induced GI ulcers

A

Misoprostol

330
Q

What are examples of antacids?

What are side effects?

A

Al(OH)3, Mg(OH)2, CaCo3

Side effects: Constipation (Al+3), diarrhea (Mg+2)

331
Q

Al(OH)3, Mg(OH)2, CaCo3

Side effects: Constipation (Al+3), diarrhea (Mg+2)

A

Antacids

332
Q

What do antacids increase the oral absorption of?

Example

A

Weak bases (quinidine-dangerous anti arrhythmic=tachycardia)

333
Q

What do antacids decrease the oral absorption of?

Example

A 
Weak acids (Warfarin- run the risk of thrombotic disorders)
Tetracycline (via chelation)
334
Q

What are all the drugs used for nausea and vomiting? Examples of each

A

5HT3 antagonists: ondansetron (commonly used in cancer chemotherapy), granisetron
DA antagonists: prochlorperazine, metoclopramide
H1 antagonists: diphenhydramine, meclizine, promethazine (M blockers)
Muscarinic blockers: scopolamine
Cannabinoids: dronabinol
NK1-receptor antagonist: aprepitant

335
Q

What are examples of neurokinins? What do they have to do with nausea and vomiting?

A

Substance P and bradykinin

They are inflammatory mediators and pain mediators- pain-induced vomiting

336
Q

Which 5HT3 antagonists are anti-nauseates?

A

ondansetron (commonly used in cancer chemotherapy), granisetron

337
Q

Which DA antagonists are anti-nauseates?

A

prochlorperazine, metoclopramide

338
Q

Which H1 antagonists are anti nauseates?

A

diphenhydramine, meclizine, promethazine (M blockers)

339
Q

Which muscarinic blockers are anti nauseates?

A

Scopolamine

340
Q

Where is serotonin synthesized and stored?
What is it metabolized by?
What is the marker for carcinoid?

A

GI cells, neurons, and platelets
MAO type A
Its metabolite- 5-hydroxyinolacetic acid (5HIAA)

341
Q

Where are 5HT1 receptors found?

A

CNS (usually inhibitory) and smooth muscle (both)

342
Q

What is buspirone?

A

Partial agonist at 5HT1a receptor–>anxiolytic for GAD (generalized anxiety disorder)

343
Q

Partial agonist at 5HT1a receptor–>anxiolytic for GAD (generalized anxiety disorder)

A

buspirone

344
Q

What is sumatriptan?

A

Agonist at 5HT1d receptor in cerebral vessels–>decrease migraine pain by vasoconstricting (contraindicated for people with CV problems)
D=dee worst headache of your life

345
Q

Agonist at 5HT1d receptor in cerebral vessels–>decrease migraine pain by vasoconstricting (contraindicated for people with CV problems)
D=dee worst headache of your life

A

sumatriptan

346
Q

Where are 5HT2 receptors found and what are activation effects?

A

CNS-excitatory

Periphery- vasodilation, contraction of GI, bronchial, and uterine smooth muscle, and platelet aggregation

347
Q

CNS-excitatory

Periphery- vasodilation, contraction of GI, bronchial, and uterine smooth muscle, and platelet aggregation

A

5HT2 receptors

348
Q

What is Olanzapine?

A

Antipsychotic

Antagonist at 5HT2a receptors in the CNS–>decreases symptoms of psychosis

349
Q

Antipsychotic

Antagonist at 5HT2a receptors in the CNS–>decreases symptoms of psychosis

A

Olanzapine

350
Q

What is cyproheptadine?

A

5HT2 antagonist used in carcinoid, other GI tumours, and postgastrectomy, also used for anorexia nervosa
Has marked H1-blocking action: used in seasonal allergies

351
Q

5HT2 antagonist used in carcinoid, other GI tumours, and postgastrectomy, also used for anorexia nervosa
Has marked H1-blocking action: used in seasonal allergies

A

cyproheptadine

352
Q

What is the drug of choice for carcinoid and other GI tumors? How does it work?

A

Octreotide- somatostatin analog

Suppresses actual secretion of serotonin from the GI tumor

353
Q

Where are 5HT3 receptors found? What is their MOA?

A

Area postrema, peripheral sensory and enteric nerves

Activation opens ion channels

354
Q

What is ondansetron? and other -setrons?

A

5HT3 antagonists–>decrease emesis in chemotherapy and radiation and postoperatively

355
Q

5HT3 antagonists–>decrease emesis in chemotherapy and radiation and postoperatively

A

ondansetron and other -setrons

356
Q

What is ergotamine? How does it work in migraines? What are the side effects?

A

Partial agonist at A and 5HT2 receptors in the vasculature and possibly CNS
Also agonists or partial agonists at dopamine receptors
Vasoconstrictive actions decreases pulsation in cerebral vessels may be relevant to acute actions of ergotamine during migraine attack
Used in acute attacks
GI distress, prolonged vasoconstriction–>ischemia and gangrene, abortion near term

357
Q

Partial agonist at A and 5HT2 receptors in the vasculature and possibly CNS
Also agonists or partial agonists at dopamine receptors
Vasoconstrictive actions decreases pulsation in cerebral vessels may be relevant to acute actions of ergotamine during migraine attack
Used in acute attacks
GI distress, prolonged vasoconstriction–>ischemia and gangrene, abortion near term

A

ergotamine

358
Q

What drugs are used for migraine prophylaxis?

A

Propranolol
Verapamil
Amitriptyline
Valproic acid

359
Q

What is bromocriptine? How does it work?

A

Agonist of D2 receptor therefore decreases prolactin release

360
Q

What is ergonovine used for?

A

To reduce postpartum bleeding by contracting the uterus

361
Q

What is methysergide?

A

5HT2 antagonist used in carcinoid tumor

362
Q

Cytoprotective in the stomach
Dilate renal vasculature
Contract the uterus
Maintain ductus arteriosus

A

Prostaglandins

363
Q

What does Zileuton do? What is it used in?

A

Inhibits lipoxygenase

Prophylaxis and treatment of asthma

364
Q

What do -lukasts (Zafirlukast) do? What are they used in?

A

Block leukotriene receptors

Treatment and prophylaxis of asthma

365
Q

Inhibits lipoxygenase

Prophylaxis and treatment of asthma

A

Zileuton

366
Q

Block leukotriene receptors

Treatment and prophylaxis of asthma

A

-lukasts

Zafirlukast

367
Q

Chemotactic factor important in inflammation

MOA: inflammatory mediator–>neutrophil chemoattractant; activates PMNs; increases free radical formation–>cell damage

A

LTB4

368
Q

LTB4

A

Chemotactic factor important in inflammation

MOA: inflammatory mediator–>neutrophil chemoattractant; activates PMNs; increases free radical formation–>cell damage

369
Q

Make up slow-reacting substance of anaphylaxis (SRS-A)

Cause anaphylaxis and bronchoconstriction (role in asthma)

A

LTA4, LTC4, and LTD4

370
Q

LTA4, LTC4, and LTD4

A

Make up slow-reacting substance of anaphylaxis (SRS-A)

Cause anaphylaxis and bronchoconstriction (role in asthma)

371
Q

Constitutive, Expressed in most tissues including platelets and stomach
Acts to synthesize thromboxane and cytoprotective prostaglandin, respectively

A

COX-1

372
Q

COX-1

A

Constitutive, Expressed in most tissues including platelets and stomach
Acts to synthesize thromboxane and cytoprotective prostaglandin, respectively

373
Q

Inducible, expressed in the brain and kidney and at sites of inflammation

A

COX-2

374
Q

COX-2

A

Inducible, expressed in the brain and kidney and at sites of inflammation

375
Q

What is misoprostol? What is it used for?

A

A PGE1 analog

Used in the treatment of NSAID-induced ulcers (protective action on gastric mucosa)

376
Q

A PGE1 analog

Used in the treatment of NSAID-induced ulcers (protective action on gastric mucosa)

A

Misoprostol

377
Q

What is Alprostadil? What is it used for?

A

PGE1
Maintains patency of ductus arterioles
Vasodilation; used in male impotence

378
Q

PGE1
Maintains patency of ductus arterioles
Vasodilation; used in male impotence

A

Alprostadil

379
Q

What is used to close a patent ductus arteriosus?

A

Indomethacin (most powerful NSAID)

380
Q

PGE2 and PGF2-A are known mainly for

A

contraction of uterus and abortion

381
Q

contraction of uterus and abortion

A

PGE2 and PGF2-A are known mainly for

382
Q

What is the MOA of PGE2?

Example of a drug and what it is used for

A

MOA: uterine smooth muscle contraction

Dinoprostone; can be used for cervical ripening and as an abortifacient

383
Q

MOA: uterine smooth muscle contraction

Dinoprostone; can be used for cervical ripening and as an abortifacient

A

PGE2

384
Q

What is the MOA of PGF2-A?

Two examples of drugs and their uses

A

Uterine and bronchiolar smooth muscle contraction
Carboprost: abortifacient
Latanoprost: for treatment of glaucoma (reduced IOP)

385
Q

Uterine and bronchiolar smooth muscle contraction
Carboprost: abortifacient
Latanoprost: for treatment of glaucoma (reduced IOP)

A

PGF2-A

386
Q

How does Latanoprost work in glaucoma? What is a common side effect?

A

It vasodilates the canals of Schlemm, thereby improving outflow of aqueous humour (reducing IOP)
Causes dark pigmentation of the iris

387
Q

It vasodilates the canals of Schlemm, thereby improving outflow of aqueous humour (reducing IOP)
Causes dark pigmentation of the iris

A

Latanoprost

388
Q

Platelet stabilizer and vasodilator
Drug: epoprestenol
Uses: pulmonary hypertension
What prostaglandin is it and where is it found?

A

PGI2 (prostacyclin) found in endothelial cells

389
Q

What does PGI2 do? Example drug? What is it used for?

A

Platelet stabilizer and vasodilator
Drug: epoprestenol
Uses: pulmonary hypertension

390
Q

Which prostaglandins both increase in primary dysmenorrhea? What helps in primary dysmenorrhea?

A

PGE2 and PGF-A

NSAID because block their synthesis

391
Q

Platelet aggregator

Inhibition of their synthesis underlies protective role of aspirin post MI

A

TXA2 (thromboxane)

392
Q

TXA2 (thromboxane)

A

Platelet aggregator

Inhibition of their synthesis underlies protective role of aspirin post MI

393
Q

What is the prototypical NSAID?

A

Aspirin (ASA)

394
Q

Causes irreversible inhibition of COX
Covalent bond via acetylation of a serine hydroxyl group near the active site
Actions are dose-dependent

A

Aspirin

395
Q

Actions of aspirin

A

Causes irreversible inhibition of COX
Covalent bond via acetylation of a serine hydroxyl group near the active site
Actions are dose-dependent

396
Q

What are the low-dose actions of aspirin (~80mg/day)

A

Antiplatelet aggregation

The basis for post MI prophylaxis and to reduce the risk of recurrent TIAs

397
Q

Antiplatelet aggregation
The basis for post MI prophylaxis and to reduce the risk of recurrent TIAs
are the actions of?

A

low dose aspirin (~80mg/day)

398
Q

What are the moderate dose actions of aspirin? (~325mg)

A

Analgesia and antipyresis

399
Q

Analgesia and antipyresis

are the actions of?

A

Moderate dose aspirin (~325mg)

400
Q

What are the high dose actions of aspirin? (~3-5 g/day)

A

Antiinflammatory

401
Q

Antiinflammatory

are the actions of?

A

High dose aspirin (3-5 grams/day)

402
Q

How to low to moderate doses of aspirin work in uric acid elimination?
How do high doses work in uric acid elimination?

A

Aspirin=weak acid= competes with other acids for secretion
Low to moderate doses: decrease tubular secretion–>hyperuricemia (cannot use it for gout!)
High doses: decrease tubular reabsorption–>uricosuria

403
Q

What happens to the acid-base and electrolyte balance at high doses of aspirin?

A

Mild uncoupling of oxidative phosphorylation–> increased respiration–>decreased pCO2–>respiratory alkalosis–>renal compensation–>increased HCO3 elimination–>compensated respiratory alkalosis (pH=normal, decreased pCO2, decreased HCO3)

404
Q

What happens to the acid-base and electrolyte balance at toxic doses of aspirin?

A

Inhibits respiratory center–>decreased respiration–>increased pCO2–>respiratory acidosis (decreased pH, decreased HCO3, normalization of pCO2) plus inhibition of Krebs cycle and severe uncoupling of oxidative phosphorylation (decreased ATP) –>metabolic acidosis, hyperthermia, and hypokalemia

405
Q

What are the side effects of aspirin toxicity?

A

GI irritation: gastritis, ulcers, bleeding
Salicylism: tinnitus, vertigo, decreased hearing
Bronchoconstriction: exacerbation of asthma
Hypersensitivity, especially the “triad” of asthma, nasal polyps, rhinitis
Reye syndrome: encephalopathy
Increased bleeding time (anti platelet)
Chronic use: associated with renal dysfunction

406
Q

What are these side effects of?
GI irritation: gastritis, ulcers, bleeding
Salicylism: tinnitus, vertigo, decreased hearing
Bronchoconstriction: exacerbation of asthma
Hypersensitivity, especially the “triad” of asthma, nasal polyps, rhinitis
Reye syndrome: encephalopathy
Increased bleeding time (anti platelet)
Chronic use: associated with renal dysfunction

A

Aspirin toxicity

407
Q

What are aspirin drug interactions?

A

Ethanol (increases GI bleeding)
OSUs and warfarin (increases their effects)
Uricosurics (decreases their effect)

408
Q

Other NSAIDS

A 
I-SINK
Ibuprofen
Sulindac
Indomethacin (most potent)
Naprox
Ketorolac (used for post-op pain)
409
Q 
I-SINK
Ibuprofen
Sulindac
Indomethacin (most potent)
Naprox
Ketorolac (used for post-op pain)
A

Other NSAIDS

410
Q

Ketorolac<ASA

in terms of what?

A

Analgesia

411
Q

How do other NSAIDs compare to aspirin in analgesic effects?

A

Ketorolac>ibuprofen/naproxen>ASA

412
Q

How do other NSAIDs compare to aspirin in GI irritation?

A

All < ASA

413
Q

All NSAIDs < ASA

in terms of what?

A

GI irritation

414
Q

Which NSAID has no renal side effects?

A

Sulindac

415
Q

What are the specific toxicities of indomethacin?

A

Thrombocytopenia
Agranulocytosis
and > CNS effects

416
Q

Thrombocytopenia
Agranulocytosis
and > CNS effects
are toxicities of what drug?

A

Indomethacin

417
Q

What are the specific toxicities of Sulindac?

A

Stevens-Johnson syndrome

Hematotoxicity

418
Q

Stevens-Johnson syndrome
Hematotoxicity
are toxicities of what drug?

A

Sulindac

419
Q

What are the primary differences between nonselective COX inhibitors and the selective COX 2 inhibitors?

A

Selective COX-2 inhibitors have less GI toxicity and less antiplatelet action

420
Q

What is the MOA of acetaminophen?

A

No COX inhibition in peripheral tissues and lacks significant anti-inflammatory effects
Equivalent analgesic and antipyretic activity to ASA due to inhibition of COX in CNS

421
Q

Where is acetaminophen mainly metabolized?
What is the minor pathway and what does it result in? What is it inactivated by?
What happens in acetaminophen OD? Why?

A

Liver
via P450, a reactive metabolite
Glutathione
Hepatotoxicity.The finite stores of GSH are depleted. When this happens, the reactive metabolite reacts with hepatocytes= nausea, vomiting, abdominal pain, and ultimately liver failure due to centrilobular necrosis.

422
Q

How do you manage acetaminophen OD-induced hepatotoxicity ? When should you do this?

A

With N-acetylcysteine (supplies -SH groups)

Preferably within first 12 hours

423
Q

What are examples of DMARDs? What are they used for?

A 
Hydroxychloroquine
Methotrexate
Sulfalazine
Glucocorticoids
Gold salts
Penicilamine
Leflunomide
Etanercept
Inflixamib
Anakinra

RA

424
Q 
Hydroxychloroquine
Methotrexate
Sulfalazine
Glucocorticoids
Gold salts
Penicilamine
Leflunomide
Etanercept
Inflixamib
Anakinra

What are these?

A

DMARDs

425
Q

What is the mechanism of hydroxychloroquine? What are its side effects?

A

MOA: Stabilizes lysosomes and decreases chemotaxis

Side effects: GI distress and visual dysfunction (cinchonism)
hemolysis in G6PD deficiency

426
Q

MOA: Stabilizes lysosomes and decreases chemotaxis

Side effects: GI distress and visual dysfunction (cinchonism)
hemolysis in G6PD deficiency

A

hydroxychloroquine

427
Q

What is the MOA of methotrexate? What are its side effects?

A

MOA: cytotoxic to lymphocytes

Side effects: Hematotoxicity

428
Q

MOA: cytotoxic to lymphocytes

Side effects: Hematotoxicity

A

methotrexate

429
Q

What is the MOA of sulfalazine? Side effects?

A

MOA: it is broken down by colonic bacteria in 5-ASA (antiinflammatory-possibly inhibits COX- with benefits in UC) and sulfapyridine which decreases B cell function
Side effects: Hemolysis in G6PD deficiency

430
Q

MOA: it is broken down by colonic bacteria in 5-ASA (antiinflammatory-possibly inhibits COX- with benefits in UC) and sulfapyridine which decreases B cell function
Side effects: Hemolysis in G6PD deficiency

A

sulfalazine

431
Q

What is the MOA of glucocorticoids? Side effects?

A

MOA: Decreases LTs, ILs, and platelet activating factor (PAF)
Side effects: ACTH suppression, cushingoid state, osteoporosis, GI distress, glaucoma

432
Q

MOA: Decreases LTs, ILs, and platelet activating factor (PAF)
Side effects: ACTH suppression, cushingoid state, osteoporosis, GI distress, glaucoma

A

glucocorticoids

433
Q

What is the MOA of gold salts? Side effects?

A

MOA: Decrease lysosomal and macrophage functions

Side effects: Dermatitis, hematotoxicity, nephrotoxicity

434
Q

MOA: Decrease lysosomal and macrophage functions

Side effects: Dermatitis, hematotoxicity, nephrotoxicity

A

gold salts

435
Q

What is the MOA of penicillamine? Side effects?

Other use?

A

MOA: suppresses T cells and circulating rheumatoid factor
Side effects: Proteinuria, hematotoxicity, and autoimmune disease

**Also used in Wilson’s disease (liver cirrhosis and CNS damage bc of Cu accumulation) because it is a chelator of Cu

436
Q

MOA: suppresses T cells and circulating rheumatoid factor
Side effects: Proteinuria, hematotoxicity, and autoimmune disease

**Also used in Wilson’s disease (liver cirrhosis and CNS damage bc of Cu accumulation) because it is a chelator of Cu

A

Penicillamine

437
Q

What is the MOA of leflunomide? Side effects?

A

MOA: inhibits dihydro-orotic acid dehydrogenase (DHOD) –> decreased UMP–>decreased ribonucleotides–>arrests lymphocytes in G1
Side effects: Alopecia (baldness), rash, diarrhea, hepatotoxicity

438
Q

MOA: inhibits dihydro-orotic acid dehydrogenase (DHOD) –> decreased UMP–>decreased ribonucleotides–>arrests lymphocytes in G1
Side effects: Alopecia (baldness), rash, diarrhea, hepatotoxicity

A

leflunomide

439
Q

What is the MOA of etanercept? Side effects?

What is another use?

A

MOA: Binds TNF; is a recombinant form of TNF receptor
Side effects: Infections
Also used in Crohn’s

440
Q

MOA: Binds TNF; is a recombinant form of TNF receptor

Side effects: Infections

A

etanercept

441
Q

What is the MOA of inflixamib? Side effects?

What is another use?

A

MOA: Monoclonal antibody to TNF
Side effects: infections

Also used in Crohn’s

442
Q

MOA: Monoclonal antibody to TNF

Side effects: infections

A

inflixamib

443
Q

What is the MOA of anakinra? Side effects?

What is another use?

A

MOA: IL-1 receptor antagonist
Side effects: infections
Also used in Crohn’s

444
Q

MOA: IL-1 receptor antagonist
Side effects: infections
Also used in Crohn’s

A

anakinra

445
Q

____ are used to treat the symptoms of RA, _____ are used to treat the disease

A

NSAIDS

DMARDs

446
Q

Which drug is recommended for mild arthritis?

Which for moderate to severe?

A

Hydroxychloroquine

Methotrexate

447
Q

What is gout?

A

An increase in body stores of uric acid.

Acute attacks involve joint inflammation and precipitation of uric acid crystals

448
Q

An increase in body stores of uric acid.

Acute attacks involve joint inflammation and precipitation of uric acid crystals

A

Gout

449
Q

What are the three treatment strategies for gout?

A
  1. Reducing inflammation with Colchicine, NSAIDs, or glucocorticoids
  2. Accelerating renal excretion of uric acid with uricosuric drugs
  3. Reducing conversion of purines to uric acid by inhibiting XO
450
Q
  1. Reducing inflammation with Colchicine, NSAIDs, or glucocorticoids
  2. Accelerating renal excretion of uric acid with uricosuric drugs
  3. Reducing conversion of purines to uric acid by inhibiting XO
A

treatment strategies for gout

451
Q

What is the MOA of colchicine?

What are its acute and chronic side effects?

A

MOA: binds to tubulin–> decreased mictrotubular polymerization; decreased LTB4 and decreased leukocyte and granulocyte migration
Acute side effects: diarrhea and GI pain
Chronic side effects: hematuria, alopecia, myelosuppression, gastritis, and peripheral neuropathy

452
Q

MOA: binds to tubulin–> decreased mictrotubular polymerization; decreased LTB4 and decreased leukocyte and granulocyte migration
Acute side effects: diarrhea and GI pain
Chronic side effects: hematuria, alopecia, myelosuppression, gastritis, and peripheral neuropathy

A

colchicine

453
Q

What is alloxanthine?

A

A suicide inhibitor: metabolite inhibits its own formation
It is the metabolite of allopurinol. Allopurinol is metabolized by xanthine oxidase into alloxanthine, and then alloxanthine inhibits xanthine oxidase

454
Q

What are the drugs allopurinol and probenecid used for?

A

Prophylaxis of chronic gout

455
Q

What is the action of allopurinol?

A

It is a prodrug converted by xanthine oxidase, forming alloxanthine, which inhibits the enzyme= decreased purine metabolism= decreased uric acid

456
Q

What does xanthine oxidase do?

A

Metabolizes purines to uric acid

457
Q

Metabolizes purines to uric acid

A

xanthine oxidase

458
Q

What are the drug interactions of allopurinol?

Describe this drug interaction

A

With 6-mercaptopurine (6-MP) (anti cancer)
6-MP is inactivated by xanthine oxidase. Allopurinol inhibits this. So you get a buildup of active anti-cancer drug- can cause tremendous toxicity from the bone marrow= suppressing effect
OR, if careful about it, allows you to decrease the dose of 6-MP by 2/3 with the same effect

459
Q

What is the action of probenecid?

Side effects?

A

MOA: Inhibits proximal tubule pumps that reabsorb and secrete - so inhibits proximal tubule reabsorption of urate (ineffective if GFR <50mL/min)
Also inhibits secretion of many acidic drugs (cephalosporins, fluroquinolones, penicillins)
Side effects: Crystallization if high excretion of uric acid
ASA may decrease effects by competing with urate for excretion= hyperuricemia

460
Q

MOA: Inhibits proximal tubule pumps that reabsorb and secrete - so inhibits proximal tubule reabsorption of urate (ineffective if GFR

A

probenecid

461
Q

What are the effects of glucocorticoids?

A

Decreased leukocyte migration (decrease in integrins)
Increased lysosomal membrane stability= decreased phagocytosis (decreased fusion of lysosomes and endosomes)
Decreased capillary permeability
Inhibit PLA2 (via lipocortin expression)= decreased PGs and LTs
Decreased expression of COX 2
Decreased PAF (thrombosis and inflammatory responses)
Decreased interleukins (mediators of stimulation of lymphocytes)

462
Q

Decreased leukocyte migration (decrease in integrins)
Increased lysosomal membrane stability= decreased phagocytosis (decreased fusion of lysosomes and endosomes)
Decreased capillary permeability
Inhibit PLA2 (via lipocortin expression)= decreased PGs and LTs
Decreased expression of COX 2
Decreased PAF (thrombosis and inflammatory responses)
Decreased interleukins (mediators of stimulation of lymphocytes)
Are the effects of what?

A

Glucocorticoids

463
Q

What do integrins do? How do glucocorticoids affects them?

A

Integrins are required for sticking of WBCs to endothelial wall (part of the immunoglobulin family).
Glucocorticoids decrease integrins which in turn decrease leukocyte migration. So someone on glucocorticoids= leukocytosis (increased WBC count)

464
Q

Side effects of glucocorticoids

A

Suppression of ACTH: cortical atrophy, malaise, arthralgia, and fever- may result in a shock state with abrupt withdrawal
Iatrogenic (drug-induced) cushingoid syndrome= fat deposition, muscle weakness/atrophy, bruising, acne
Hyperglycemia due to increased gluconeogenesis (corticosteroids induce PEPCK-control enzyme of gluconeogenesis)= increased insulin demand and other adverse effects (caution in diabetic patients)
Osteoporosis: vertebral fractures- aseptic hip necrosis (because of increased osteoclast activity)
Increased GI acid and pepsin release= ulcers, GI bleeding (due to lack of PG) (bc of proteolysis and thinning of tissues= can have perforation)
Electrolyte imbalance: Na/water retention= edema and hypertension, hypokalemic alkalosis, hypocalcemia (caution with hypertensive patients)
Decreased skeletal growth in children
Decreased wound healing, increased infections (thrush from C. albicans)
Increased glaucoma, increased cataracts (via increased sorbitol) Sorbitol does osmotic damage to lens
Increased mental dysfunction

465
Q

Suppression of ACTH: cortical atrophy, malaise, arthralgia, and fever- may result in a shock state with abrupt withdrawal
Iatrogenic (drug-induced) cushingoid syndrome= fat deposition, muscle weakness/atrophy, bruising, acne
Hyperglycemia due to increased gluconeogenesis (corticosteroids induce PEPCK-control enzyme of gluconeogenesis)= increased insulin demand and other adverse effects (caution in diabetic patients)
Osteoporosis: vertebral fractures- aseptic hip necrosis (because of increased osteoclast activity)
Increased GI acid and pepsin release= ulcers, GI bleeding (due to lack of PG) (bc of proteolysis and thinning of tissues= can have perforation)
Electrolyte imbalance: Na/water retention= edema and hypertension, hypokalemic alkalosis, hypocalcemia (caution with hypertensive patients)
Decreased skeletal growth in children
Decreased wound healing, increased infections (thrush from C. albicans)
Increased glaucoma, increased cataracts (via increased sorbitol) Sorbitol does osmotic damage to lens
Increased mental dysfunction

A

Side effects of glucocorticoids

466
Q

What cells cause damage in asthma?
What is the main damage-causing agent?
How does the respiratory tract react?
What happens in the upper airways?

A 
Eosinophils
Cationic protein in their membrane "MBP"- major basic protein, is what causes damage along the respiratory tract. Causes bronchial hyper reactivity (particularly bronchospasm )
With chronic inflammation and damage= hypertrophy and hyperplasia- thickening of bronchiolar wall
Increase in goblet cells= mucus secretion
467
Q

What induces bronchoconstriction?

A

Acetylcholine
Adenosine
Leukotrienes

468
Q

Acetylcholine
Adenosine
Leukotrienes

A

Inducers of bronchoconstriction

469
Q

What inhibits acetylcholine (and thus inhibits bronchoconstriction)?

A

Ipratropium

470
Q

What does Ipratropium do ?

A

Inhibits Acetylcholine and thus bronchoconstriction

471
Q

What inhibits adenosine and thus bronchoconstriction?

A

Theophylline

472
Q

What does theophylline do?

A

Inhibits adenosine and thus bronchoconstriction

473
Q

What inhibits leukotrienes (and thus bronchoconstriction) and how?

A

-lukasts (zafirlukast) by blocking LTC4 and LTD4 receptors

Zileuton by blocking the synthesis of LTC4 and LTD4 by blocking lipoxygenase

474
Q

What drugs are widely used for relief of acute bronchoconstriction and in prophylaxis of exercise-induced asthma?

A

B-2 selective agonists (albuterol, metaproterenol, terbutaline)

475
Q

These drugs used via inhalation cause bronchodilation in acute asthma, especially COPD patients, and they may be safer than B agonists in patients with CV disease

A

Ipratropium and other M blockers

476
Q

What are the drugs of choice in bronchospasm caused by B blockers?

A

Ipratropium and other M blockers

477
Q

What are the two ways in which theophylline bronchodilates?

A
  1. Via inhibition of phosphodiesterase (PDE)= increase in cAMP
  2. Antagonism of adenosine (a bronchoconstrictor)
478
Q

What works in these ways to cause bronchodilation?

  1. Via inhibition of phosphodiesterase (PDE)= increase in cAMP
  2. Antagonism of adenosine (a bronchoconstrictor)
A

Theophylline

479
Q

What is theophylline toxicity increased by?

A

Erythromycin
Cimetidine
Fluoroquinolones

480
Q

Erythromycin
Cimetidine
Fluoroquinolones

A

Increase theophylline’s toxicity

481
Q

How do Cromolyn and Nedocromil work in asthma?

MOA and prophylaxis:

A

MOA: Prevent degranulation of pulmonary mast cells and decrease release of histamine, PAF and LTC4 from inflammatory cells
Prophylaxis: decrease symptoms and bronchial hyperactivity (BHR), especially responses to allergens

482
Q

MOA: Prevent degranulation of pulmonary mast cells and decrease release of histamine, PAF and LTC4 from inflammatory cells
Prophylaxis: decrease symptoms and bronchial hyperactivity (BHR), especially responses to allergens

A

How Cromolyn and Nedocromil work in asthma

483
Q

What role to beclomethasone and flunisolide play in asthma?

A

They are surface-active drugs used via inhalation for both acute attacks and for prophylaxis

484
Q

They are surface-active drugs used via inhalation for both acute attacks and for prophylaxis of asthma

A

beclomethasone and flunisolide

Pharmacology (2 decks)

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