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Therapeutics > Park lecture 4 > Flashcards

Park lecture 4 Flashcards

1
Q

Drug interactions with progestins

A

Other steroids
Anticonvulsants

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2
Q

Why are other steroids contraindicated when taking birth control?

A

Oral contraception will increase blood levels of other steroids

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3
Q

why do anticonvulsants such as phenytoin decrease effectiveness of Oral BC

A

phenytoin induces drug metabolizing enzymes in liver

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4
Q

Use of gut flora with regard to estrogen

A

estrogen needs to go through enterohepatic circulation and gut flora is necessary for that.

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5
Q

relationship between gut flora, enterohepatic circulation and estrogen activity

A

less gut flora= less enterohepatic circulation= estrogenic activity drops

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6
Q

how does tetracycline affect birth control. Why?

A

Tetracycline reduces efficacy of birth control. Tetracycline reduces gut flora.

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7
Q

Plan B is a combination between these two drugs

A

Ethinyl estradiol+norgestrel

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8
Q

progestin only plan B name

A

Levonorgestrel

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9
Q

What are the two parts of adrenal gland?

A

Cortex and medulla

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10
Q

What does medulla produce in adrenal gland

A

Epinephrine and norepinephrine

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11
Q

What does cortex produce in adrenal gland

A

Glucocorticoid, mineralocorticoids and androgens

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12
Q

What are glucocorticoids

A

stress hormones

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13
Q

What is the structural difference between aldosterone and cortisol

A

cortisol has 17-OH

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14
Q

Other name for glucocorticoid

A

cortisol (stress hormones)

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15
Q

Physiological effects of glucocorticoids

A

increase circulating glucose concentrations
potent anti inflammatory effects

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16
Q

Physiological effects of mineralcorticoids (aldosterone)

A

increases Na+ retention. This will lead to an increase in water volume. Leading to an uptick in BP

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17
Q

Difference in where epinephrine and cortisol bind

A

Epinephrine binds glucocorticoid receptor, epinephrine binds B adrenergic receptor

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18
Q

Difference in response time between epinephrine and cortisol (hydrocortisone)

A

Epinephrine has an immediate response whereas cortisol has a long term persistent biologic response

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19
Q

what stimulates the release of ACTH from the pituitary?

A

CRH

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20
Q

what stimulates cortisol release from adrenal gland?

A

ACTH

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21
Q

How is CRH inhibited

A

cortisol has a negative feedback loop that inhibits CRH

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22
Q

Why are the levels of aldosterone not affected with pituitary gland removal?

A

Because liver releases aldosterone precursor (angiotenstinogen)

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23
Q

What are the steps of aldosterone synthesis

A

-Angiotensinogen released from liver
-angiotensinogen is digested by renin and converted to angiotensin 1
-ACE (angiotensin converting enzyme) converts to angiotensin 2
-angiotensin 2 binds to adrenal glands
- adrenal glands release aldosterone

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24
Q

What enzyme converts angiotensin 1 to ang 2

A

ACE

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25
Q

how does losartan lower BP

A

Blocks angiotensin 2 in adrenal gland

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26
Q

glucocorticoids up-regulate enzymes for ___________&____________

A

gluconeogenesis
anti-inflammatory proteins

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27
Q

DNA binding domains of activated dimers bind to specific sequences called

A

GRE( glucocorticoid response element_

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28
Q

rate limiting step for gluconeogenesis in glucocorticoids in catalyzed by

A

PEP carboxylase

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29
Q

What are the cytokines the promote inflammation called

A

Eicosanoids

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30
Q

How does lipocortin II suppress eicosanoid production

A

It suppresses phospholipase A2, which has a critical role in eicosanoid synthesis

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31
Q

What is NFkB

A

NFkB is a promoter that induces a lot of pro-inflammatory genes in immune cells

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32
Q

Effects of glucocorticoids on NFkB.

A

Glucocorticoids bind NFkB receptors and prevent the binding of NFkB

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33
Q

Glucocorticoid physiological effect on liver

A

increase gluconeogenesis
increase glycogen storage

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34
Q

Physiological effect of glucocorticoid on muscle

A

promotes protein degradation

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35
Q

Why does glucocorticoid promote degradation of protein?

A

degrade protein to use for amino acid as an energy source

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36
Q

Physiological effect of glucocorticoid on protein synthesis and sensitivity to insulin

A

Decreases protein synthesis and decreases sensitivity to insulin

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37
Q

Physiological effect of glucocorticoid on adipose tissue

A

Promotes lipolysis and decreases sensitivity to insulin

38
Q

Physiological effect of glucocorticoids on immune system

A

Blocks synthesis on cytokines (immunosuppresor) and inhibitor of eicosanoids (anti-inflammatory)

39
Q

what is adrenal insufficiency (hypo-adrenalism)

A

Decrease in secretion of steroid hormone by adrenal cortex

40
Q

What is (primary) addisons disease caused by

A

destruction of cortex by tuberculosis or atrophy.

41
Q

symptoms of hypoadrenalism

A

low bp, hyper pigmentation, anorexia, anemia, vomiting

42
Q

cessation of long term systemic glucocorticoid therapy can lead to

A

addisonian symotoms

43
Q

Name the 3 types of adnreal insufficiency and what organ they affect.

A

Primary- adrenal defect
secondary- pituitary defect
tertiary- hypothalamic defect

44
Q

What hormone levels are affected by primary adrenal insufficiency? why?

A

Both cortisol and aldosterone levels go down.

45
Q

How are the CRH and ACTH levels in primary adrenal insufficiency?

A

Both are high

46
Q

What happens to the size of the adrenal gland in primary insufficiency? why? What do we call this?

A

cortisol levels low so ACTH continuously stimulates the adrenal gland, causing it to get bigger, this is called congenital hyperplasia

47
Q

What hormone levels are affected by secondary adrenal insufficiency? why?

A

pituitary can not make ACTH, Leads to low cortisol. Aldosterone is not affected.

48
Q

CRH levels in secondary adrenal insufficiency?

A

High because of the lack of negative feedback from cortisol

49
Q

Which hormones will be low in tertiary adrenal insufficiency?

A

All of them except aldosterone.

50
Q

only defect where aldosterone is affected?

A

primary (adrenal)

51
Q

Which hormone goes down in all of the defects

A

cortisol

52
Q

Which defect is the only one to not cause a decrease in ACTH

A

Primary

53
Q

Which defect is the only one to cause a decrease in CRH

A

Tertiary

54
Q

What is the similarity between pituitary cushings disease and ectopic cushings disease

A

Both cause an increase in ACTH

55
Q

what is the difference between pituitary cushings disease and ectopic cushings disease

A

both lead to increased production of ACTH, but pituitary cushings is due to pituitary carcinoma while ectopic cushings is due to non-pituitary carcinoma

56
Q

symptoms of cushings disease

A

increased protein catabolism (easy bruising, delayed wound healing)
osteoporosis
opportunistic infections (anti-inflammatory caused by cortisol levels)

57
Q

long term therapeutic use of systemic glucocorticoids can lead to

A

Cushings syndrome

58
Q

what happens to the hormone levels in adrenal cushings

A

Increase in cortisol levels. This leads to a negative feedback loop and decreases ACTH and CRH

59
Q

What happens to hormone levels in pituitary cushings syndrome

A

ACTH levels go up, leading to increase in cortisol, leading to negative feed back of CRH, decreasing it.

60
Q

what happens to hormone levels in ectopic cushings disease

A

Ectopic ACTH is high, leadning to an increase in cortisol. This will lead to negative feedback of CRH, leadning to PITUITARY ACTH to be low

61
Q

In synthetic glucocorticoid activity, addition of 9a-F to hydrocortisone will have this effect

A

strong miceralcorticoid and glucocorticoid activity. This will lead to intense Na+ retention. leading to edema

62
Q

use of 9a- F

A

mineralcorticoid replacement therapy

63
Q

what is the structural modification in the synthetic glucocorticoids prednisone/prednisolone?

A

An extra double bond between C1 and C2

64
Q

How will this extra double bond between C1 and C2 affect the activity of prednisone/prednisolone

A

Will lead to better and tighter binding of glucocorticoid and reduced mineralcorticoid activity

65
Q

methylprednisolone structural mpdification?

A

Addition of 6a group

66
Q

What effect does addition of 6a group have on glucocorticoid activity

A

reduced mineralcorticoid activity

67
Q

Difference and similarity between triamcinolone and fludrocortisone

A

Both have F but triamcinolone has a double bond between C1 and C2 and also a 16 OH to it.

68
Q

Effect of 16-OH on triamcinolone

A

reduces mineralcorticoid activity
increases hydrophilicity
lowers oral bioavailability

69
Q

dexamethasone and betamethasone structural modification from prednisone

A

16-a- methyl group added. (They are enantiomers of each other)

70
Q

difference in structure between dexamethasone and triamcinalone

A

Triamcinalone has a 16-oh, whereas dexamethasone has a 16 methyl group

71
Q

16-a-methyl substituent on prednisolone effect

A

increases lipophilicity (leads to increased receptor binding, leading to a stronger effect)
reduced mineralcorticoid activity
increases oral bioavailability

72
Q

effect of long ester groups in 21 C position

A

It will be a pro drug that can be activated by esterases
increased lipophilicity and prolonged action

73
Q

most potent synthetic glucocorticoid is

A

dexamethasone

74
Q

glucocorticoid effect on acute bronchioconstriction, why?

A

No effect. Will not stop an acute asthma attack as it is happening. Takes hours/days for full effect, more long term

75
Q

how are glucocorticoids more long term in terms of action in asthma

A

inhibit eicosanoids
decrease vascular permeability
modify cytokine and chemokine production

76
Q

Inhaled glucocorticoid desired properties

A

high potency
minimal systemic effects
prolonged action
low oral bioavailability
short half life

77
Q

how to make inhaled glucocorticoids prolonged?

A

lipophilicity

78
Q

explain triamcinalone acetonide chemical tweaks for inhalation

A

Acetonide group on 16 and 17 OH leads to better bioavailability

79
Q

Why does acetonide on 16 and 17 Oh groups in triamcinalone acetonide do?

A

Makes it resistant to hydrolysis, leading to better bioavailability

80
Q

flunisolide chemical and structural properties

A

has acetonide covering 16 and 17 OH and has a 6-a Fluorine
Has a short half life (rapidly metabolized by liver, minimal side effects)

81
Q

budensonide having butyl acetal group on 16,17 leads to

A

faster topical uptake and low oral bioavailability

82
Q

mometasone furoate structural and chemical features

A

Has 21 Cl instead of 21 OH.
low oral bioavailability
rapid onset of action and highly potent
negligible systemic effect (rapid metabolism)

83
Q

fluticasone propionate inactivated by

A

hydrolysis of thioesters

84
Q

fluticasone propionate structural and chemical features

A

has S-F bond on 21 C
highly potent but poor solubility (forms microcrystals)

85
Q

Desired properties of topical glucocorticoids

A

High lipophilicity
minimal systemic effects
prolonged action

86
Q

adverse effects of glucocorticoids in terms of crossover activity

A

crossover mineralcorticoid activity

87
Q

adverse effects of glucocorticoids in metabolism

A

Increased glucose production (may unmask diabetes)
osteoporosis (glucocorticoids inhibit osteoblasts)
premature epiphyseal closure

88
Q

adverse effets of glucocorticoids on face shape and GI

A

cushings like effects, round face, hump back and peptic ulcers

89
Q

___________ are usually potent topical glucocorticoids

A

halogenated analogues

90
Q

recognize structures of topical and inhaled glucocorticoids

A
91
Q

Substitution of chlorine atom for 17-OH does what

A

Enhances anti-inflammatory effects

92
Q

_________and _______ have better potency for topical applications due to high lipophilicity

A

Ester and acetonides

Therapeutics (46 decks)

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