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Therapeutics 5 > Exam 1 Med Chem > Flashcards

Exam 1 Med Chem Flashcards

1
Q

Steroids are a broad group of lipids known as

A

isoprenoids or terpenes

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2
Q

Cholesterol is derived from

A

Acetate as well as dietary sources

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3
Q

Where are steroids produced?

A

Adrenal cortex, testes, ovaries, and some peripheral tissues (adipose tissue, the brain)

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4
Q

Steroid hormones only differ in

A

the ring structure and side changes attached. They are all derived from cholesterol.

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5
Q

Common sites where modifications occur to change the specificity of hormones in vivo

A

19, 11, 18, 16, 17. 5

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6
Q

What switch is important for producing estrogens?

A

The switch from hydroxyl to ketone at the C3 position

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7
Q

Stereochemistry of steroids

A

Beta- upward

Downward- alpha

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8
Q

C-17 R group on sterol

A

Aliphatic side chain. Usually contain one or more hydroxyl group

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9
Q

C-17 R group of sex hormones

A

Ketone or hydroxyl group. Usually have 2 carbon side chain.

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10
Q

C-17 R group of cardiac glycoside

A

Lactone ring, usually with O-liked sugars

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11
Q

C-17 R groups for bile acids

A

5-carbon side chain ending in carboxylic acid moiety

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12
Q

C-17 R group for sapogenins

A

Oxacylic (ethereal) ring system.

one or more oxygens in the ring

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13
Q

Glucocorticoids trivial name and site of modification

A

Cortisol (hydrocortisone), corticosterone

C-21 steroids, pregnane-derivative

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14
Q

Mineralocorticoids trivial name and site of modification

A

Trivial name- aldosterone

C-21 steroids, pregnane- derivatives

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15
Q

Androgenic steroids trivial name and site of modification

A

Trivial name- 11-Deoxycorticosterone, dehydroepiandrosterone, testosterone
C-19 steroids, androstane-derivatives

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16
Q

Estrogenic steroids trivial name and site of modification

A

Estradiol

C-18 steroids, estrane derivative

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17
Q

Pregestens trivial name and site of modification

A

Pregnenolone, progesterone

C-21 steroids, pregnane-derivative

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18
Q

C-21 steroids, pregnane derivatives

A

Glucocorticoids, mineralocorticoids, progestens

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19
Q

C-19 steroids, androstane derivatives

A

Androgenic steroids

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20
Q

C-18 steroids, estrange derivatives

A

Estrogenic steroids

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21
Q

What group is required for mineralocorticoid activity and potent glucocorticoid activity?

A

Hydroxyl group

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22
Q

Sex steroid function is conferred by deletion of

A

C20, C21, and introduction of oxygen functional group at C17

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23
Q

Adrenal blood flow

A

Due to the blood flow in the adrenal gland, the cortisol produced in the adrenal cortex will be at its highest concentration in the medullary region.

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24
Q

Cortisol impacts

A

catecholamine release

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25
Q

Zona glomerulosa in the adrenal gland produces predominantly

A

Aldosterone

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26
Q

Zona fasciculata in the adrenal gland produces

A

Predominantly cortisol

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27
Q

Zona reticularis in the adrenal gland produces

A

androgens

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28
Q

In the medulla, cells are of neuronal origin and make primarily

A

catecholamines

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29
Q

What inactivates glucocorticoids and mineralocorticoids?

A

11-keto group (conversion by type II 11bHSD) inactivates glucocorticoids and mineralocorticoids

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30
Q

Why is aldosterone not inactivated by the 11-keto group conversion by type II 11bHSD?

A

Aldosterone is protected against 11bHSD action by the 18 aldehyde group

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31
Q

Sex steroid function is conferred by

A

Deletion of C20, C21

Introduction of oxygen function group at C17

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32
Q

What is produces very early in steroidogenesis?

A

Progesterone

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33
Q

A deficit in an enzyme in steroidogenesis means

A

that you cant get to the end product and precursors build and diffuse into the neighboring cells. The neighboring cells can then turn them into other hormones which leads to the pathologies and phenotypes related to defects and inhibition of steroidogenic enzymes.

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34
Q

Regulators of aldosterone

A

Extracellular K and Angiotensin II

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35
Q

21-Hydroxylase (CYP21A2) relevance

A

Accounts for 95% of genetic abnormalities in adrenal steroid synthesis.
Converts progesterone to 11-deoxycorticosterone
and
17a-hydroxyprogesterone to 11-deoxycortisol

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36
Q

21-Hydroxylase consequences of deficiency

A

Decreased cortisol and aldosterone. Loss of sodium because of mineralocorticoid deficiency. Virilization because of excess androgen production.

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37
Q

11b-Hydroxylase (CYP11B1) relevance

A

Second most frequent abnormalities in adrenal steroid hormone synthesis
Converts 11-deoxycorticosterone to corticosterone
and
11-deoxycortisol to cortisol

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38
Q

11B-Hydroxylase consequences of deficiency

A

Excess 11-deoxycortisol and 11-deoxycorticosterone. Excess mineralocorticoid activity. Salt and water retention.
Because these are the 2 precursors will activate mineralocorticoid receptor and increase activity, not aldosterone itself

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39
Q

11B-Hydroxysteroid dehydrogenase type II relevance

A 
Inhibited by glycyrrhetinic acid, a compound in authentic licorice 
Converts cortisol (active) into cortisone (inactive) that has less affinity for the mineralocorticoid receptor.
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40
Q

11B-Hydroxysteroid dehydrogenase type II consequences of deficiency

A

Decrease in glucocorticoid inactivation in mineralocorticoid-sensitive cells, leading to excess mineralocorticoid activity.

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41
Q

Progesterone is a precursor for

A

androgens and estrogens

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42
Q

Androstenediol and testosterone are percursors for

A

estrogens, you have to make testosterone to make estrogen

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43
Q

5a reductase activates what?

A

Testosterone into its more active form dihydrotestosterone. It is often expressed in target tissues.

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44
Q

How many steps is progesterone from cholesterol?

A

2

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45
Q

What is the principle corticosteroid in rats?

A

corticosterone

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46
Q

11-B-OHSD inhibitors

A 
Glycerrhetinic acid (licorice)
Bioflavonoids: quercetin, morin, naringenin, gossypol= Cotton seen oil
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47
Q

What do 11-B-OHSD inhibitors lead to?

A

pseudo hyperaldosteronism OR syndrome of apparent mineralocorticoid excess (AME)- the patient will present as if they have high levels of aldosterone, but upon measurement they will have very low levels. This is diagnostic of 11BHSD type II deficiency

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48
Q

How does the 18-aldehyde of aldosterone protect it from 11BHSD type II?

A

It prevents it from acting on the 11-OH by forming a hemiacetal to protect it.

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49
Q

11-B-OHSD inhibitors lead to

A

decreased amounts of inactivation of glucocorticoids in the principal cells. This leads to upregulated ENAC. increased salt and water retention, and HTN

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50
Q

What does the F on fludrocortisone do?

A

Increases its water solubility

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51
Q

Properties of fludrocortisone

A

Has a much higher GR activity so cannot be used orally to correct glucocorticoid activity if they have a normal MR aldosterone level as this would lead to HTN. Topical only when aldosterone levels are normal.
Fludrocortisone is better as an aldosterone rerplacement

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52
Q

Prednisolone properties

A

Increased GR activity
No change in MR activity
More effective as a glucocorticoid replacement when aldosterone levels are normal

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53
Q

Dexamethasone properties

A

Active and stable GR activity
Reduced mineralocorticoid effects
Even better as a glucocorticoid replacement therapeutically than prednisone

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54
Q

Why do we need to have 11-BHSD type II in cells that are responsive to changes in aldosterone?

A

Glucocorticoids can bind to the MR receptor
Glucocorticoids also circulate more than mineralocorticoids, so if we did not activate glucocorticoids, the cells wouldn’t be able to detect small changes in mineralocorticoid concentration. 11-BHSD type II is critical to having appropriate response to aldosterone.

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55
Q

Forms of estrogen

A

Estrone, Estradiol, Estriol

56
Q

Estrone (E1)

A

Storage form of E2. The difference between E1 and E2 is an oxidation-reduction reaction.

57
Q

Estradiol (E2)

A

Most active form of estrogen

58
Q

Estriol (E3)

A

Weak activity, acts as an antagonist.
Only really need to consider estriol during pregnancy because the 16-hydroxylase enzyme is in the fetal liver only. Estriol levels go up around 12 weeks of gestation and continue to increase throughout pregnancy and diffuse back into the maternal circulation to protect the mother against the high levels of estradiol during pregnancy.

59
Q

Difference between testosterone and estradiol

A

Aromatase aromatizes the ring of estradiol creating a hydroxyl group and getting rid of 19 carbon

60
Q

Equine estrogens

A

Horses (pregnant mares) excrete a variety of equine estrogens, including equilenin and equilin. These equine estrogens are not synthesized in humans but readily bind to human estrogen receptors. Equine estrogens have an aromatic A ring and therefore lack a 19 methyl group. These substances are excreted in large quantities in equine urine.

61
Q

Antiestrogens

A

SERMS (selective estrogen receptor modulator)
Aminoether derivatives of stillbene (NOT based on cholesterol)
Block TAF1 transcription factor preventing transcription activation.
Clomiphene- fertility
Tamoxifen0 antitumor

62
Q

Synthetic estrogens

A

Ethinyl estradiol and mestranol are both used as oral contraceptives and have increased oral efficacy

63
Q

Progestogens

A

Synthetic progesterone derivatives
Oral contraceptives- desogestrel, norethindrone, norgestrel, ethynodiol
Levonorgestrel (Plan B)- has a 17 alkyl group that slows metabolism and increases T1/2.
Progestogens have modifications to increase T1/2 and abs over progesterone

64
Q

Estrogen and progesterone as pharma target

A

Estradiol ACTIVATES the ER

Tamoxifen BLOCKS inactivation of ER

65
Q

Phytoestrogens

A

Estrogen from plants
Isoflavones with antifertility activity
Coumestrol (some legumes), genistein (soy), daidzen (soy)
Eating a lot of soy can produce diminished reproductive ability because these phytoestrogens have estrogenic activity and slow fertility.

66
Q

Steroid hormone elimination

A

inactivation of steroids involves reductions and conjugation to glucuronides or sulfate to increase their water solubility.
Most are metabolized by the liver and kidneys. 70% of the conjugated steroids are excreted in the urine, 20% leave through the feces, and the rest through the skin
steroids, being cholesterol based, will also recycle through the liver-bile-intestinal pathway

67
Q

Hormones of the pituitary organ

A

Anterior- GH, somatotropin, TSH, ACTH, FSH, LH, prolactin, adorphin
Posterior- oxytocin, ADH

68
Q

Hormones from the thyroid

A

Thyroxin (T4)
Triiodothyronine (T3)
Calcitonin

69
Q

Hormones of the pancreas

A

insulin, glucagon, somatostatin, pancreatic peptide

70
Q

Hormones of the ovaries

A

estrogen, progesterone, inhibin, relaxin

71
Q

Hormones of the testes

A

testosterone, inhibin, mullerian regression factor

72
Q

Hormones of the parathyroid

A

PTH

73
Q

Hormones of the adrenal gland`

A

Cortex: cortisol, aldosterone, androgens

Medulla- epinephrine, norepinephrine`

74
Q

Hypothalamic nuclei

A

2 types of hypothalamic neurons

  • Green (neurohypophysis pathway)
  • Purple- (adenohypophysis pathway)
75
Q

Magnocellular neurons

A

Large cell bodies capable of producing a lot of hormones or neurotransmitters, which is why when its release that the amount is enough ti change the circulating amount of hormone.

76
Q

An important aspect of the hypothalamic and pituitary axis is that the infundibulum or pituitary stalk can be damaged or severed. What occurs when this happens?

A

Severed- the patient would lose both the regulation of anterior and posterior pituitary hormones. However, over time, via angiogenesis and revascularization, the vascular network can regenerate, thus restoring the ANTERIOR pituitary hormone regulation to some degree but since the posterior pituitary system involves these neuronal axons, if those axons are severed, they don’t repair so readily so the patient may never have restoration in terms of the POSTERIOR pituitary hormones

77
Q

Posterior pituitary hormone nuclei

A

Axons go down through the pituitary stalk or infindibulum into the posterior pituitary. Posterior pituitary hormones are produced in the hypothalamic cell bodies and go by axonal trafficking down to the terminus. When these neurons are stimulated they stimulate the release of the hormone into circulation.
Neuropophysis

78
Q

Anterior pituitary hormone nuclei

A

Parocellular neurons terminate at the bottom of the hypothalamic region or the median eminence. They’re releasing hormone into the portal circulation (hypothalamo-hypophyseal portal vessels). These hormones travel directly to the anterior pituitary where they work on cells within the anterior pituitary to secrete a 2nd level of hormone which goes into circulation.

79
Q

Posterior lobe of the hypothalamic-pituitary pathway produces which hormones?

A

ADH/vasopressin and oxytocin

Different hypothalamic nuclei produce the 2 different hormones

80
Q

Pars intermedia

A

Area between the anterior and posterior pituitary.

Makes melanocyte-stimulating hormone and regulates melanin

81
Q

Oxytocin goes into

A

Uterine muscles, mammary glands

82
Q

ADH goes into

A

Kidney tubules

83
Q

Whatdoes gonadotropin-releasing hormone at the hypothalamic nuceli trigger the release of?

A

FSH and LH at the anterior pituitary

84
Q

What do FSH and LH do?

A

Germ cell development
Female- ovum
Male- sperm

Secrete hormones
Female- estradiol, progesterone
Male- testosterone

85
Q

What stimulates the release of growth hormone?

A

GHRH (growth hormone releasing hormone)

86
Q

What inhibits the release of growth hormone?

A

Somatostatin

87
Q

What does growth hormone do?

A

Secretes insulin-like growth factor 1 (IGF-1) which is critical
Protein synthesis, carbohydrate and lipid metabolism

88
Q

TSH is triggered by

A

Thyrotropin releasing hormone (TRH)

89
Q

What does TSH do?

A

Secretes thyroxine, triiodothyronine in the thyroid

90
Q

Prolactin is inhibited by

A

Dopamine

91
Q

What does prolactin do?

A

Breast development and milk production (in male may facilitate reproductive function)

92
Q

ACTH is triggered by

A

CRH (corticotropin releasing hormone)

93
Q

What does ACTH do?

A

In the adrenal cortex it secretes cortisol.

Activates the 1st step in conversion in steroidogenesis which eventually leads to cortisol.

94
Q

What is growth hormone stimulated by?

A

GH-releasing hormone, ADH, GABA, Ghrelin, NE, DA, serotonin, estrogen, sleep, stress, exercise
Decreased glucose concentration
Fasting/starvation
Hormones of puberty (estrogen, testosterone)
alpha-adrenergic agonists (clonidine)
Beta-adrenergic antagonists (propranolol)
DA agonists (bromocriptine)
GABA agonists (muscimol)

95
Q

What is prolactin inhibited by?

A

DA
GABA
DA agonists (bromocriptine, pergolide, cabergoline)

96
Q

What is growth hormone inhibited by?

A

Somatostatin, elevated IGF-1, growth hormone, progesterone, glucocorticoids, postprandial hyperglycemia, elevated free fatty acids
DA antagonists (phenothiazines)
alpha adrenergic antagonists (phentolamine)
beta-adrenergic agonists (isoproterenol)
Serontonin antagonists (methysergide)
Pregnancy

96
Q

What is ACTH stimulated by?

A

CRH

97
Q

What is the physiologic effect of growth hormone?

A

Stimulate IGF-1 prodcution and IGF-1 and GH promote growth in all body tissues

98
Q

Prolactin is stimulated by

A

TRH, VIP, estrogen, serotonin, histamin, endogenous opioids, pregnancy and nursing
DA antagonists (phenothiazines, haloperidol, methyldopa)
Opiates
Estrogens
H2RAs
MAOi

100
Q

What is ACTH inhibited by?

A

Elevated cortisol

101
Q

What are the physiologic effects of ACTH?

A

Glucocorticoid effects

Pigmentation

102
Q

What is ADH stimulated by?

A

Hyperosmolality and volume depletion

103
Q

What is ADH inhibited by

A

hypervolemia, hypoosmolality

104
Q

What is the physiologic effect of ADH

A

Acts on renal collecting ducts to prevent diuresis

105
Q

What are the 3 effects of the nursing reflex?

A
  1. ) Nursing stimulates mechanoreceptors in the nipples leading to inhibition of DA release and increased prolactin levels. Prolactin release stimulates milk production.
  2. ) Neuronal pathway terminates on hypothalamic nuclei that are producing oxytocin which stimulates those neurons to release oxytocin which helps in terms of milk expression by leading to contraction of the myomammary epithelial
  3. ) Suckling causes a decrease in gonadotropin releasing hormone which causes a delay in going back to regular menstrual cycle while nursing which lengthens the time before a female returns to normal reproductive cycle.
106
Q

What happens in the nursing reflex?

A
  1. ) Stimulus from suckling travels from breast to the hypothalamus
  2. ) DA release is inhibited.
  3. ) Oxytocin release is stimualted.
  4. ) GnRH production is decreased which inhibits the ovarian cycle.
107
Q

What does oxytocin do?

A

Released via posterior pituitary and goes into circulation where it acts to increase intracellular Ca and increase smooth muscle contraction.
Oxytocin enhances the expression of milk to help in feeding the neonate.

108
Q

What are the effects of prolactin?

Lactation

A

Increases milk yield
Promotes gene expression of milk proteins
Stimulates biosynthesis of lactose
Induces lipoprotein lipase in the breast
Stimulates reabsorption of Na from milk

109
Q

What is the effect of prolactin? Reproduction

A

Hyperprolactinemia inhibits gonadotropin secretion
In nonlactating individuals, hyperprolactinemia induces galactorrhea, amenorrhea, and impotence
During lactation, inhibits follicular growth and aromatase levels (keep estrogen levels low)

110
Q

What is the effect of prolactin? Water and electrolyte homeostasis

A

Milk production is regulated by loss of fluid and electrolytes.
Stimulates intestinal absorption of sodium
Stimulates renal 25 (OH) vitamin D which is the rate limiting step in forming vit D3
Increases intestinal Ca and phosphate abs

111
Q

Growth hormone secretion

A

GHRH is released from hypothalamic nuclei and will bind to somatotrophs in the anterior pituitary via GHRH receptor which is Gas-coupled causing increased CAMP, activation of protein kinase A which affects plasma membrane Ca channels, and increased Ca, and vesicular fusion and release of growth hormones.

112
Q

Why is growth hormone secretion inhibited during pregnancy?

A

You want mobilized nutrients from the mother to be going to grow the fetus, not growing the mother

113
Q

Somatomedins (IGF) effect on GH

A

Inhibits in the anterior pituitary

Stimulates in the hypothalamus

114
Q

Growth hormone release

A

Short-loop feedback

Amplitude of release is significantly higher at night because mobilized energy can be used for growth during sleep.

115
Q

Growth hormone/ IGF-1 actions

A

In the adipose tissue:

  • Decreased glucose uptake
  • Increase lipolysis

Chondrocytes

  • Increased AA uptake
  • Increased protein synthesis
  • Increased DNA and RNA synthesis
  • Increased chondroitin sulfate
  • Increased collagen
  • Increased cell size and number

Muscle

  • Increased glucose and AA uptake
  • Increased protein synthesis
116
Q

GH at high levels can activate

A

PRL receptors

But, PRL does not activate GH receptor

117
Q

Bell-shaped response curve of GH

A

In case of saturation due to excess GH, the receptors cannot dimerize and can’t have an active receptor.
Must maintain optimal GH level

118
Q

Actions of glucocorticoids

A 
Increase gluconeogenesis
Increase proteolysis
Increased lipolysis
Decrease glucose utilziation
decrease insulin sensitivity
Inhibit inflammatory response
Suppress immune response
119
Q

Actions of mienralocorticoids

A

Increase Na reabsorption
increase K secretion
Increase H secretion

120
Q

Inhibitory factors of cortisol release

A

Opioids

Somatostatin

121
Q

Stimulatory factors of cortisol release

A 
Sleep-wake transition
Stress
Hypoglycemia
ADH
alpha adrenergic agonists
Beta adrenergic antagonists
Serotonin
122
Q

Diurnal secretion of cortisol

A

Highest during the day

123
Q

CRH and ACTH signaling

A

CRH acts on its receptor at the level of corticotrophes in the anterior pituitary. Gas-linked producing a release of ACTH which goes into circulation. ACTH also via Gas-coupled receptor then activates cholesterol demolase starting the process of steroidogenesis within the adrenal cortex.

124
Q

Regulation of CRH-ACTH- adrenocortical axis

A

IL-1B has a positive effect on teh release of cortisol. Cortisol is going to have a neg feedback on the monocytes and neutrophils. So in this way, there is a negative feedback loop on cortisol via the immune system. It is this reason that after trauma surgery glucocorticoids are oten administered as a means to diminish the immune response to avoid multi-organ failure or transplant rejection. Unfortunately, the high levels overwhelm 11BHSD in the kidney and leads to salt and water retention (edema/puffiness)

125
Q

Actions of glucocorticoids: metabolism

A

Degrade muscle protein and increase nitrogen excretion
Increase gluconeogenesis and plasma glucose
Increase hepatic glycogen synthesis
Decrease glucose utilization (anti-insulin)
Redistribute fat

126
Q

Actions of glucocorticoids: hemodynamic

A

Maintain vascular integrity
Maintain fluid volume
Maintain responsiveness to catecholamine pressor effects

127
Q

Actions of glucocorticoids: immune function

A

Increase anti-inflammatory cytokine production
Impairs cell-related immunity
Increases neutrophil, platelet, RBC counts
Inhibits bradykinin and serotonin inflammatory effects

128
Q

Why do people gain obesity in cushings syndrome?

A

Cortisol inhibits glucose uptake in adipose tissues and muscle cells. Cortisol will increase gluconeogenesis in the liver which will increase hepatocyte release of glucose that will result in a hyperglycemic effect. This leads to hyperinsulinemia that stimualtes lipogenesis in adipose tissues and inhibits lipolysis in adipose tissue. In this case, the addition of body fat is due to the hyperinsulinemia that is a secondary consequence of hypercortisolemia

129
Q

Cortisol inhibits

A

ACTH secretion

130
Q

ACTH stimulates

A

Steroidogenesis and has trophic effects on the adrenal cortex

131
Q

Prolonged ACTH exposures causes

A

adrenal cortex hyperplasia, if genetic congenital adrenal hyperplasia (CAH)

132
Q

Congenital adrenal hyperplasia (CAH)

A

Overproduction of androgens
Lack of sex hormones
Intersex development
Mineralocorticoid excess (HTN/hypokalemic alkalosis) if you can make aldosterone.
Mineralocorticoid deficits (salt wasting) if you cant make aldosterone
Adrenal insufficiency

133
Q

The total absence of aldosterone is

A

lethal

134
Q

A deficit in __________means we cant get aldosterone or cortisol

A

21-beta-hydroxylase

135
Q

What is the rate limiting step of the renin-angiotensin-aldosterone system?

A

Renin release at the level of the kidney

136
Q

Angiotensin II is necessary to activate

A

Aldosterone synthase which gives us aldosterone

137
Q

ACEi can be used to knock down aldosterone production by

A

Decreasing angiotensin II

Therapeutics 5 (6 decks)

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