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OU PDA > Exam 3 II > Flashcards

Exam 3 II Flashcards

1
Q

Steroid start from which structure?

A

CPPP

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2
Q

adrenal cortex

A

produce glucocorticoids and mineralocorticoids

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3
Q

testis

A

produce androgens

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4
Q

ovaries

A

produce estrogens and progestagens

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5
Q

Cortico-steroids

A
  • aka Adrenocorticoids
  • Glucocorticoids
  • Mineralocorticoids
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6
Q

anabolic steroids

A
  • synthetic

- example of androgen

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7
Q

estrane

A

18 carbon steroidal unit

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8
Q

androstane

A

19 carbon steroidal unit

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9
Q

pregnane

A

21 carbon steroidal unit

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10
Q

cholestane

A

27 carbon steroidal unit

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11
Q

cholane

A

24 carbon steroidal unit

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12
Q

configurational isomers

A
  • there are 8 possible variations
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13
Q

What are the common configurational isomers?

A
  • trans-trans-trans
  • cis-trans-trans
  • cis-trans-cis
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14
Q

What structural feature denotes a steroid as a delta?

A

if there is a double bond between between 4/5 or 5/6

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15
Q

What does the statins inhibit and why?

A
  • inhibits HMG-CoA reductase

- because it converts HMG-CoA to mevalonic acid which goes on to cholesterol synthesis

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16
Q

glucocorticoids and examples

A
  • affect intermediary metabolism
  • inhibit inflammation
  • ex. cortisol, cortisone
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17
Q

mineralocorticoids and example

A
  • salt retention

- aldosterone

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18
Q

pathologic conditions related to adrenal cortex

A
  • Cushing’s disease
  • Addison’s disease
  • Conn’s syndrome
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19
Q

What structural feature denotes glucocorticoids?

A
  • OH at C17 in the alpha configuration
  • OH at C11
  • double bond at C4/5
  • carbonyl at C3
  • beta-Ketol at C17
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20
Q

What is the structural difference between glucocorticoids and mineralocorticoids?

A

mineralocorticoids doesn’t contain OH at C17

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21
Q

What is important about the C11 OH in mineralocorticoids and glucocorticoids?

A

it is the site of which these compounds attach themselves to the receptors

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22
Q

What are problems with natural corticoids?

A
  • rare availability of cortisol
  • not resistant to first pass metabolism
  • side effects
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23
Q

What are the products of first pass metabolism of cortisol?

A
  • C11 OH -> keto group =O
  • C3 =O -> alpha OH
  • double bond C4/5 gone
  • C17 OH -> keto =O
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24
Q

Why does alpha OH at C3 destroys activity?

A

no steroid in body has alpha OH at C3, it’s all beta

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25
Q

What are the two categories of adrenocorticoid drugs?

A
  • cortisol

- prednisolone

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26
Q

What are characteristics of cortisol esters?

A
  • more stable

- slow absorption

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27
Q

What are characteristics of cortisol cypionate esters?

A
  • more lipophilic

- slow absorption in oral administration

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28
Q

What are characteristics of cortisol salt forms?

A
  • water soluble
  • IV or IM
  • fast hydrolysis
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29
Q

What is the difference between cortisol and prednisolone?

A

prednisolone has a double bond at C1/2

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30
Q

What are the purpose of modifications of prednisolone?

A

add substituents to C16 to protect OH and side chains on C17 from being metabolized

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31
Q

It is common to see F as a substituent on C9 in prednisolone. Why is this?

A
  • it’s small enough to replace H and not change structural feature
  • it enhances activity (lec 4-20 @ 4:40)
  • helps stabilize OH group at C11
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32
Q

What is the advantage of forming an acetonide and tying two -OH groups?

A

stabilizing compound and giving it a longer half life

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33
Q

How does the double bond at C1/2 increase potency?

A

the chair-conformation is flatter and can sit at the receptor site better

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34
Q

Function of adrenocorticoid antagonists

A
  • compete for binding site

- inhibit biosynthesis of adrenocorticoids

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35
Q

ring A in estrogen

A

benzene

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36
Q

aromatase

A
  • gives estrogen compounds their benzene ring

- rate limiting step

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37
Q

metabolism of estrogen

A
  • OH group added to C2 or C4
  • COMT methylates that OH group
  • activity in lost
  • OH on C17 can be glucuronidated
  • t1/2 of 20min
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38
Q

Why is the distance between two -OH in estrogen important?

A

it is 8.55 Å and the receptor is 8.55 Å in size

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39
Q

What are structural features of estrogen?

A
  • aromatic A ring
  • phenol at C3
  • beta OH at C17
  • 8.55 Å between -OH groups
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40
Q

Modifications of estrogen to increase half life

A
  • ether at C3
  • ester at C3 or C17
  • add ethlyne at C17
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41
Q

Function of estrogen antagonists

A
  • compete for binding site

- inhibit biosynthesis of estrogens

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42
Q

ER-alpha

A

female reproductive tract and mammary gland

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43
Q

ER-beta

A
  • vascular endothelial cells

- CV and bone tissue

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44
Q

What can aromatase inhibitors be used for?

A
  • control reproductive functions

- treatment of estrogen-dependent breast cancers

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45
Q

progesterone

A

serves as precursor to:

  • androgen
  • estrogen
  • adrenocorticoids
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46
Q

What are structural features of progesterone?

A
  • 21 C skeleton
  • double bond at C4/5
  • ketone at C3
  • O functionality a C3 and 20
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47
Q

formation of HCG

A
  • lose double bond of progesterone at C4/5
  • C3 is glucronidated
    => HCG
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48
Q

metabolism of progesterone

A
  • reduction of -OH at C3
  • double bond at C4/5 metabolized
  • rapid metabolism: t1/2 of 5-10min
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49
Q

How can we modify progesterone to increase half life?

A
  • add -OH to C17
  • add methyl group to C6
  • double bond at C6/7
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50
Q

What happens if you block 5alpha-reductase?

A

stops synthesis of testosterone

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51
Q

Side effects of testosterone

A

it can have both anabolic and androgenic activity

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52
Q

Functions of antiandrogens

A
  • block receptors

- inhibits synthesis of androgens

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53
Q

Which enzymes can you inhibit to inhibit production of androgen?

A
  • 17a-hydroxylase/17,20-lyase

- 5a-reductase

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54
Q

Which location in the human body is there presence of prostaglandins?

A
  • reproductive tract
  • seminal vesicles
  • menstrual fluid
  • umbilical cord
  • placenta
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55
Q

Where else can you find prostaglandins?

A

Gorgonian Coral / Sea Whip Coral

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56
Q

What is the starting material for prostaglandins?

A

from a 20 carbon fatty acid (arachidonic acid)

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57
Q

structural features of prostanoic acid

A
  • 20C fatty acid
  • 7C chain attached to C8 in alpha
  • 8C chain attached to C12 in beta
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58
Q

How are prostaglandins named?

A
  • 3 letters
  • PG”X”(subnumber + alpha/beta)
  • 3rd letter denotes a functionality group
  • subnumber denotes the amount of double bonds in the C8/12 chain
  • alpha / beta denotes orientation of -OH at C9 (only for F series)
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59
Q

There is a double bond in prostaglandins that is always at the same location. Where is this location?

A

at C13/14

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60
Q

Why is the consequence of C13=C14 in prostaglandins?

A
  • allylic structure
  • allylic OH at C15
  • weak
  • degraded fast
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61
Q

eicosanoids

A

bioactive oxidative metabolites of 20 x carbon fatty acids

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62
Q

Eicosanoids are precursors to what?

A
  • prostaglandins
  • thromboxane
  • leukotriene
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63
Q

phospholipase A2

A
  • produce arachidonic acid

- anti-inflammatory drugs are PLA2 inhibitors

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64
Q

COX

A
  • take arachidonic acid to further produce PG

- target of NSAIDs

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65
Q

metabolism of PG

A
  • oxidize C15-OH into =O
  • reduction of C13=C14
  • beta-oxidation: cutting off 2C from C1 twice
  • omega oxidation: C20 from methyl to carboxyl
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66
Q

How can you protect the allylic -OH in PG?

A

add methyl group to C15

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67
Q

Why do you get GI side effects from taking non-selective NSADs?

A

because COX1 is involved in protecting GI mucosa

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68
Q

COX1 and COX2 are similar in structure. How do you target COX2?

A
  • active site of COX 2 is much larger

- have a drug that fits in that pocket but not COX1 pocket

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69
Q

salicylic acid

A
  • natural product from willow bark

- non-selective COX inhibitor

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70
Q

function of serotonin

A
  • regulate smooth muscle: CV and GI

- enhance platelet aggregation

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71
Q

What is the precursor to serotonin?

A

tryptophan

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72
Q

What is the rate limiting step in producing serotonin?

A
  • TPH (tryptophan hydroxylase)

- never saturated

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73
Q

With respect to products of trp, how is depression diagnosed?

A

higher ratio of kynurenine : serotonin

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74
Q

VMAT

A

transports serotonin into vesicle

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75
Q

SERT

A

re-uptakes serotonin back into nerve ending

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76
Q

What is the primary site for serotonin synthesis?

A

Enterochromaffin cells

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77
Q

What is the fate of serotonin after its reuptake into nerve endings?

A
  • stored via VMAT

- degraded by MAO

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78
Q

What can be used as marker for serotonin-producing tumor?

A

5HIAA levels which is a break down product of serotonin

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79
Q

serotonin receptors

A
  • 5HT1: Gi
  • 5HT2: Gq
  • 5HT3: ligand-gated ion channel
  • 5HT4-7: Gs, Gi
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80
Q

What stimulates release of serotonin?

A
  • mechanical stretching
  • glucose
  • efferent vagal stimulation
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81
Q

serotonin effects on GI

A
  • stimulate peristalsis
  • enhance peristalsis effects
  • N/V/D
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82
Q

serotonin role in clot formation

A

enhance aggregation response

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83
Q

serotonin role in immune system

A
  • bind to serotonin receptors on immune cells

- induce release of cytokines

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84
Q

serotonin role in CV system

A
  • induce vasoconstriction
  • amplify vasoconstriction effects of other NT
  • vagus nerve activation (opposite of previous, this causes hypotension)
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85
Q

What are the autacoids?

A
  • histamine
  • bradykinin
  • kallidin
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86
Q

What are autocoids?

A
  • molecule that our body secretes that has local and short action
  • synthesized in same tissue that they act upon
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87
Q

storage of histamine

A
  • granules of mast cells
  • bound to heparin in mast cells
  • basophils in blood
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88
Q

Where is histamine synthesized?

A
  • granules in skin
  • gastric mucosa
  • hematopoietic cells
  • neurons
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89
Q

How is histamine metabolized?

A
  • MAO

- oxidative deamination

90
Q

role of histamine

A
  • mediate inflammation
  • increase gastric acid secretion
  • NT in nervous system
91
Q

What happens to antibodies (IgE) after they are released by plasma cells?

A
  • they bind to FceRI receptor on mast cells

- this primes the mast cells

92
Q

How does crosslinking trigger release of histamine?

A

crosslinking -> conformational change -> increase intracellular Ca -> release of histamine

93
Q

What is the role of histamine in CNS?

A
  • sleep-wake cycle
  • appetite
  • immunity
  • learning and memory
94
Q

What does histamine cause in the periphery?

A
  • epidermis: itch

- dermis: pain & itching

95
Q

What is another way histamine can be released other than in the allergic reaction?

A

histamine displaced from its bound form

96
Q

What are symptoms of “red-man syndrome”?

A
  • pruritus
  • erythema
  • hypotension
  • flushing in face, neck, upper body
97
Q

Histamine receptor are what kind of receptors?

A

GPCRs

98
Q

What are the different types of histamine receptors?

A

H1, H2, H3, H4

99
Q

H1 role and examples of drugs that target them

A
  • acute allergic reaction

- cetirizine

100
Q

H2 role and examples of drugs that target them

A
  • gastric acid secretion
  • cimetidine
  • rantidine
101
Q

H3 role and examples of drugs that target them

A
  • NT modulation
  • thioperamide
  • clobenpropit
  • tiprolisant
102
Q

H4 role and examples of drugs that target them

A
  • immune modulator

- thioperamide

103
Q

Where are H1 located?

A
  • smooth muscle
  • endothelium
  • brain
104
Q

Where are H2 located?

A
  • gastric mucosa
  • cardiac muscle
  • mast cells
  • brain
105
Q

Where are H3 located?

A
  • presynaptic auto / hetero receptors
  • brain
  • myenteric plexus
106
Q

Where are H4 located?

A
  • eosinophils
  • neutrophils
  • CD4 t cells
107
Q

H1 G protein mechanism

A
  • coupled to Gaq
  • phosphlipase C -> IP3 and DAG
  • increase Ca
108
Q

H2 G protein mechanism

A
  • couples to Gas

- increase cAMP

109
Q

H3 G protein mechanism

A
  • coupled to Gai

- decrease cAMP

110
Q

H4 G protein mechanism

A
  • couple to Gai
  • decrease cAMP
  • increase Ca
111
Q

What are the effects of H1 histamine receptor?

A
  • ↑ Ca -> eNOS -> NO -> vascular smooth muscle -> ↑cGMP -> ↓ Ca -> relax smooth muscle
  • ↑ Ca -> endothelial cells contract -> exudate
  • ↑ attention & vigilance
  • ↓ appetite
112
Q

What are the effects of H2 histamine receptor?

A
  • increases gastric acid secretion via parietal cell
  • increase working memory
  • ↑ cAMP -> activate protein kinase -> ↓ Ca -> relax smooth muscle
113
Q

What are the effects of H3 histamine receptor?

A
  • regulates release of its own and other’s receptors

- ↓ cAMP -> ↓ Ca2 -> ↓ NT

114
Q

What are the effects of H4 histamine receptor?

A
  • induce chemotaxis
  • secrete cytokines
  • regulate neuropathic pain and pruritus
115
Q

What would histamine agonists be used for?

A
  • provocative tests for bronchial hyper-reactivity

- positive control for triple response

116
Q

triple response

A
  • localized red spot
  • flare
  • wheal
117
Q

examples of first generation antihistamines

A
  • diphenhydramine
  • chlorpheniramine
  • hydroxyzine
  • doxylamine
118
Q

What is the target of first generation antihistamines?

A

H1 receptor

119
Q

side effects of first generation antihistamines

A
  • dry mouth / nose
  • dilated pupils
  • decreased motility
  • sedation
120
Q

What are the antihistamines used to treat motion sickness and how does it work?

A
  • promethazine
  • dimenhydrinate
  • has anti-muscarinic activity -> decrease motility
121
Q

examples of second generation antihistamine

A
  • loratadine
  • cetirizine
  • fexofenadine
122
Q

characteristics of second generation antihistamine

A
  • they are metabolites of first generation
  • longer duration
  • less sedating
123
Q

examples of third generation antihistamine

A
  • desloratadine

- levocetirizine

124
Q

characteristics of third generation antihistamine

A
  • long acting

- not associated with sedation or cardiotoxicity

125
Q

H3 inverse agonist

A
  • Pitolisant

- reduce sleep cycles in patients with narcolepsy

126
Q

types of kinin

A
  • bradyknin

- kallidin

127
Q

properties of kinin

A
  • potent vasodilator

- released when there is some sort of tissue damage, infection, inflammation

128
Q

bradykinin

A
  • predominant kinin in plasma
  • made from HMW kininogen
  • bind to bradykinin B2 receptor
  • metabolite bind to B1 receptor
129
Q

kallidin

A
  • predominant kinin in tissue
  • made from LMW kininogen
  • can be a precursor to bradykinin
  • bind to bradykinin B2 receptor
  • metabolite bind to B1 receptor
130
Q

B2 receptor

A
  • vasodilation

- acute pain

131
Q

B1 receptor

A
  • vasodilation

- chronic pain

132
Q

ACE

A

aka kininase II that breaks down bradykinin to inactive metabolites

133
Q

C1-INH

A

inhibit proteases of kallikrein-kinin

134
Q

C1-INH deficiency

A
  • increases amount of bradykinin
  • leads to vasodilation
  • angioedema
135
Q

HAE

A

hereditary angioedema

136
Q

What are mechanisms of drugs used to treat HAE?

A
  • selective B2 receptor antagonist
  • C1 esterase inhibitor
  • kallikrein inhibitor
137
Q

example of selective B2 receptor antagonist

A

Icabitant (HOE-140/Firazyr – FDA–approved in 2011)

138
Q

example of C1 esterase inhibitor

A
  • Cinryze (FDA-approved 2008)

- Berinert (FDA-approved 2009)

139
Q

example of kallikrein inhibitor

A

Ecallantide (Kalbitor – FDA–approved 2009)

140
Q

Which PG are the most biologically important?

A
  • PGE
  • PGF
  • PGI
  • thromboxane
141
Q

What are the types of PG receptors?

A
  • EP
  • FP
  • IP
  • DP
  • TP
142
Q

What kind of receptors are PG receptors?

A

GPCRs

143
Q

What are the fates of arachidonic acid?

A
  • leukotriene

- PG

144
Q

Why are there GI side effects when taking NSAIDs?

A
  • NSAIDs prevent production of PG

- PG has a cytoprotextive effect on GI

145
Q

corticosteroid mechanism of action

A

inhibit phospholipase A

146
Q

PG effect on CV system

A
  • dilation of arterioles, pre-cap, sphincters, post-cap venules
  • increase CO
  • increase HR
147
Q

PG effect on ductus arteriousus

A

maintaining opening of duct. art.

148
Q

PG effect on blood platelets

A

inhibit platelet aggregation

149
Q

PG effect on smooth muscle

A
  • bronchial relax
  • uterine: during pregnancy, body becomes more sensitive to PG
  • intestinal contract
150
Q

PG effect on gastric secretions

A
  • inhibit gastric secretion and pepsin content
  • increase mucus secretion
  • cytoprotective effect on GI
151
Q

PG effect on peripheral nervous system

A
  • cause pain / irritation

- sensitize nerve endings

152
Q

PG effect on inflammatory / immune response

A

potentiate pain-producing effects of other autocoids

153
Q

PG effect on reproductive system

A

amniotic fluid elevated during labor

154
Q

What can happen if NSAIDs are taken during pregnancy?

A

it may prolong pregnancy and labor

155
Q

therapeutic applications of PG

A
  • induce abortion
  • labor inducion
  • dysmenorrhea (painful uterine bleeding)
  • impotence
  • platelet aggregation
  • open angel glaucoma
  • GI ulcers
  • pulm. HTN
  • patent duct. art.
156
Q

dinoprostone

A
  • brand name Cervidil
  • PGE2
  • used for therapeutic abortion
157
Q

alprostadil

A
  • brand name Caverject
  • used for ED
  • used to prevent platelet aggregation -> improve harvest and storage of blood platelets
  • used to maintain duct. art.
158
Q

epoprostenol

A
  • brand name: Flolan

- used for pulmonary HTN

159
Q

misoprostol

A
  • brand name: Cytotec

- used as cytoprotective agent

160
Q

latanoprost

A
  • brand name: Xalatan

- used for open angle glaucoma

161
Q

glucocorticoid effect on carbohydrate and protein

A
  • catabolize protein from muscle and bone
  • decreased growth
  • osteoporosis
  • elevated levels of glucose
162
Q

glucocorticoid effect on calcium

A
  • decrease Ca absorption from intestine

- destroy protein matrix of bone

163
Q

glucocorticoid effect on lipid

A

fat redistribution

164
Q

glucocorticoid effect on immunological activity

A
  • decrease eosinophils, lympocytes, neutrophils, basophils
  • decreased function of lymphocytes and macrophages
  • atrophy of lymphoid tissue
165
Q

glucocorticoid effect on inflammatory activities

A
  • inhibit PLA2

- decrease PG, leukotrienes, thromboxanes

166
Q

glucocorticoid effect on CNS system

A
  • depression
  • irritability
  • psychotic episodes
  • altered EEG
167
Q

What happens to adrenal gland when on chronic glucocorticoid?

A
  • decreased ACTH

- leads to atrophy of adrenal gland

168
Q

How do you combat against adrenal atrophy (due to glucocorticoid)?

A
  • taper off glucocorticoid
  • administer ACTH
  • alternate day therapy
169
Q

effect of mineralcorticoid

A
  • Na and water retention
  • K and H loss
  • act on distal tubules and collecting ducts
170
Q

examples of mineralcorticoid

A
  • aldosterone
  • fludrocortisone
  • DOC (Desoxycorticostirone)
171
Q

protein binding of glucocorticoids

A
  • bound to CBG (corticosteroid binding globulin)

- aka transcortin

172
Q

How can you explain dexamethasone’s increased potency?

A
  • because CBG has low affinity for synthetic compounds

- more in the free / active form

173
Q

symptoms of drug induced Cushing’s syndrome

A
  • elevated glucose
  • depress immune system
  • peptic ulver
  • myopathy
  • psychosis
  • osteoporosis / fractures
174
Q

therapeutic uses of adrenal steroids

A
  • adrenal insufficiency (Addison’s)
  • Congenital Adrenal Hyperplasia
  • arthritis
  • allergic reactions
  • ocular inflammation
175
Q

What is one thing to note before treating ocular inflammation with adrenal steroids?

A
  • make sure that it’s not associated with infection
  • if it is infected and treated with a. steroids, pain will go away but infection will stay
  • a. steroids will enhance infection
176
Q

Contraindications and precautions for adrenal steroids

A
  • agitation
  • ulcer
  • diabetes
  • osteoporosis
  • HTN
  • infections
177
Q

adrenal steroid inhibitors

A
  • aminoglutethimide

- spironolactone

178
Q

aminoglutethimide

A
  • brand name: Cytadren
  • inhibits synthesis of glucocorticoid steroid
  • treat Cushing’s
  • prevent production of estrogen in breast cancer pt
179
Q

spironolactone

A
  • brand name: Aldactone
  • mineralocorticoid receptor antagonist
  • structurally similar to aldosterone and sits on the receptor and prevent activity
  • used as diuretic
  • similar structure to testosterone; inhibits test. synthesis
  • treat hirsuitism
180
Q

Where does spermatogenesis occur?

A
  • Seminiferous Tubule

- Sertoli Cells

181
Q

Where is testosterone produced?

A

Leydig cells

182
Q

Which hormone stimulates anterior pituitary?

A
  • GnRH

- puberty stimulates hypothalamus to release GnRH

183
Q

5a-reductase

A

testosterone -> dihydrotestosterone (a more active metabolite)

184
Q

What are the androgenic effects of puberty?

A
  • growth of genital glands
  • voice change
  • body hair
  • skin thickness
185
Q

What are the anabolic effects of puberty?

A
  • positive N balance
  • protein synthesis
  • body growth (weight, muscle, bone, etc)
  • closure of epihysis
186
Q

characteristics of testosterone

A
  • metabolized in liver
  • ester forms have better efficacy
  • 98% is bound to SHBG (mainly) and albumin
187
Q

Explain the signal transduction of testosterone

A
  • in target tissue, testosterone is converted to active metabolite by 5a-reductase
  • goes into nucleus to bind to receptor
  • transcription -> biological activity
188
Q

Target tissues convert testosterone into its active metabolite. All but which tissues do not do this?

A
  • hypothalamus

- pituitary

189
Q

testosterone propionate

A
  • brand name: Testex

- natural androgen

190
Q

methyltestosterone

A
  • brand name: Virilron

- orally active androgen

191
Q

How can you modify testosterone to reduce metabolism?

A

alkylate -OH at C17

192
Q

oxandrolone

A
  • brand name: Oxandrin
  • anabolic steroid
  • ratio of anabolic : androgenic = about 10:1
193
Q

What are approved uses for anabolic steroids?

A
  • burn
  • chronic illness
  • atrophy due to chemotherapy
194
Q

Adverse effects of androgens

A
  • jaundice
  • edema
  • testicular atrophy
  • prostate hypertrophy -> prostate cancer
  • feminizing effects for males
195
Q

Mechanism of action of anti-androgens

A
  • inhibit synthesis (GnRH)
  • inhibit formation into active metabolite
  • androgen-receptor antagonist
196
Q

GnRH inhibitor

A

Leuprolide

197
Q

5α- reductase Inhibitor

A

finasteride

198
Q

flutamide

A
  • brand name: Eulexin
  • non-steroidal receptor inhibitor
  • inhibits androgen to receptor in nucleus
  • used in prostate cancer
  • most effective when used in combination with Leuprolide
199
Q

What are other functions of estrogen?

A

protective effect in bone and CV system

200
Q

progesterone

A
  • needed for complete sexual development

- menstrual regulation

201
Q

conjugated estrogen

A
  • brand name: Premarin
  • sulfated esters of estrone
  • can be taken orally
202
Q

ethinyl estradiol

A
  • brand name: Estinyl

- has a C17 substituent that protects itself from FPM

203
Q

diethylstilbesterol

A
  • brand name: Stilphostrol
  • orally active and not destroyed b y FPM
  • not steroid in structure; has similar -OH ends like steroid though
204
Q

side effects of ovarian steroids

A
  • nausea
  • fluid retention
  • stroke
  • thromboembolism
  • chloasma
  • breast cancer
205
Q

teamoxifen

A
  • brand name: Nolvadex
  • similar to estrogen in structure - alters transcription
  • low dose: estrogenic activity
  • high dose: anti-estrogenic activity
206
Q

raloxifene

A
  • brand name: Evista
  • selective ER-beta
  • treat / prevent PM osteoporosis
207
Q

anastrozole

A
  • brand name: Arimidex
  • inhibit aromatase
  • used in advanced breast cancer
208
Q

progesterone acetate

A
  • brand name: Cyclin
  • natural
  • poor GI absorption
209
Q

norethindrone

A
  • brand name: Norlutin
  • good oral activity
  • substituents to prevent being metabolized
210
Q

RU-486

A
  • brand name: Mifefpristone
  • competitive antagonist of progesterone
  • used for medical abortion
211
Q

How can we control membrane penetration of histamine?

A
  • ionize it

- mast cells have pH of 5.6 and keeps histamine in its cation form

212
Q

What are the mechanisms by which histamine is metabolized?

A
  • N-methylation

- oxidation

213
Q

structure of 1st generation anti-histamine

A
  • two aromatic groups

- tertiary aliphatic amine

214
Q

characteristics of 1st generation histamine

A
  • highly lipophilic
  • sedative
  • anti-musc, anti-a-adrenergic, anti-serotonin
215
Q

What are the classifications of first generation anti-histamines?

A
  • Ethylenediamines
  • Ethanolamine Ethers
  • Alkyl Amines
  • Piperazines
  • Tricyclic H1 Antihistamines
216
Q

Ethylenediamines

A

early version of anti-histamines

217
Q

Ethanolamine Ethers

A
  • Diphenylhydramine
  • Dramamine (motion sickness)
  • Doxylamine (sleep)
  • anti-cholinergic effects
218
Q

Alkyl Amines

A
  • longer duration

- decreased sedative effects

219
Q

Piperazines

A
  • teratogenic effects is rodents

- cetirizine

220
Q

characteristics of second generation antihistamines

A
  • increased H1 selectivity
  • limited CNS entry
  • long-acting

OU PDA (8 decks)

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