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PLE_PHARMA > ENDOCRINE PHARMACOLOGY > Flashcards

ENDOCRINE PHARMACOLOGY Flashcards

1
Q

All mediate their ultimate effects by regulating the production
by peripheral tissues of other hormones EXCEPT

A

PROLACTIN

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2
Q

Hormones secreted by the Posterior Pituitary are: (2) Take note that both are potent ??

A

Vasopressin
& Oxytocin

VASOCONSTRICTORS

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3
Q

Growth Hormone
(GH,
Somatotropin)

Target organ hormone/mediator?

A

Insulin-like
growth factor-1
(IGF-1)

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4
Q

Thyroidstimulating
hormone
(TSH)

Target organ hormone/mediator?

A

Thyroxine,
Triiodothyronine

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5
Q

Target organ mediator or hormone of Adrenocorticotropi
n
(ACTH)

A

Glucocorticoids,
Mineralocorticoids
, Androgens

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6
Q

MOA: DOPAMINE AGONIST, hence inhibiting prolactin
release from the pituitary gland.
Also slightly inhibits GH release.
Dopaminergic effects on CNS motor control and
behavior

A

BROMOCRIPTINE, PERGOLIDE, CABERGOLINE, QUINAGOLIDE
*All are Preg Cat B

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7
Q

MOA: Activates oxytocin receptors. Stimulates uterine
contraction and labor. Stimulates mammary glands,
lactation and milk let-down.

A

Oxytocin [X], Demoxytocin

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8
Q

Contraindications to oxytocin include

A

fetal distress,
prematurity, abnormal presentation, CPD and
predispositions for uterine rupture

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9
Q

is an oxytocin receptor blocker (not yet FDA
approved since there is concern about increased rates
of infant death)

A

ATOSIBAN

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10
Q

is an agonist of peripheral Oxytocin
receptors

A

CARBETOCIN

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11
Q

MOA: Desmopressin relatively
selective for V2
receptors. Vasopressin V2
receptor agonist which
causes insertion of water
channels in the collecting
duct leading to more water
reabsorption → decrease
the excretion of water; Act
on extra-renal V2 receptors
to increase Factor VIII and
VWF factor

A

DESMOPRESSIN, VASOPRESSIN/ ADH

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12
Q

MOA: Antagonist at V1a, V2
receptors. Increases renal
excretion of water in
conditions associated with
increased vasopressin
(like in SIADH)

A

CONIVAPTAN,
TOLVAPTAN, LIXIVAPTAN

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13
Q

Used for: Central diabetes
insipidus, Hemophilia A,
von Willebrand’s
disease, Esophageal
variceal bleeding, Primary
nocturnal enuresis
(pediatric Px), colon
diverticula

A

DESMOPRESSIN
Vasopressin/ADH

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14
Q

Used in: SIADH, Hyponatremia in
hospitalized patients,
offset fluid retention in
acute heart failure and
SIADH which causes
hyponatremia (dilutional)

A

CONIVAPTAN,
TOLVAPTAN, LIXIVAPTAN

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15
Q

ADH ANTAGONIST THAT IS MORE SELECTIVE FOR V2 RECEPTORS?

A

TOLVAPTAN

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16
Q

MOA: Increases release of IGF-1 in the liver and cartilage.
Stimulates skeletal muscle growth, amino acid transport,
protein synthesis and cell proliferation.

A

SOMATROPIN

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17
Q

Most notable SE of somatropin?

A

Hyperglycemia

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18
Q

Same as somatropin. But no release of IGF-1 because it’s
IGF that you gave already.
RECOMBINANT IGF-1

A

MECASERMIN

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19
Q

Most notable side effect of MECASERMIN?

A

Hypoglycemia,

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20
Q

PEGVISOMANT MOA?

A

Blocks GH receptor

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21
Q

Drug for acromegaly?

A

PEGVISOMANT

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22
Q

MOA? Suppresses the release of growth hormones, glucagon,
insulin, gastrin, IGF-1, serotonin and gastrointestinal
peptides

A

OCTREOTIDE, LANTREOTIDE

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23
Q

Most notable SE of OCTREOTIDE, LANTREOTIDE?

A

biliary sludge and
gallstones

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24
Q

Octreotide is the most widely used somatostatin analog,
(how many times??) more potent than somatostain in GH inhibition

A

45x

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25
Q

All gonadotropin related drugs are Pregnancy Category (?)

A

X

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26
Q

in women, (?)directs follicle development, whereas (? and?) collaborate in regulating ovarian steroidogenesis

A

FSH

FSH AND LH

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27
Q

in men, (?)regulates spermatogenesis, whereas (?) stimulates
androgen production

A

FSH, LH

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28
Q

Ovulation Induction Protocol??? (3)

A
  • endogenous gonadotropin production is inhibited by
    administration of a GnRH agonist or antagonist
  • follicle development is driven by daily injections of a
    preparation with FSH activity (menotropins, FSH, FSH analog)
  • final stage of oocyte maturation is induced with an injection of
    LH or hCG to mimic the LH surge
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29
Q

Complications of Ovulation Induction?

A
  • multiple pregnancies
  • ovarian hyperstimulation syndrome
    o syndrome of ovarian enlargement, ascites, hypovolemia and
    possibly shock
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30
Q

MOA? FOLLITROPIN ALFA, MENOTROPINS (hMG),
UROFOLLITROPIN, FOLLITROPIN BETA

A

Activates FSH receptors. Mimics effects of endogenous FSH.

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31
Q

CHORIOGONADOTROPIN ALFA,
HUMAN CHORIONIC GONADOTROPIN (hCG),
MENOTROPINS (hMG), LUTROPIN ALFA

A

Activates LH receptors. Mimics endogenous LH.

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32
Q

are mixtures of FSH and LH from
postmenopausal women

A

MENOTROPINS

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33
Q

is a recombinant hCG (recall
my previous note that the B-subunits of LH and hCG are
nearly identical)

A

Choriogonadotropin alfa

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34
Q

Synthesis and Transport of Thyroid Hormones? (4 steps)

A

TRANSPORT

IODINE ORGANIFICATION

COUPLING

PROTEOLYSIS

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35
Q

What happens in IODINE ORGANIFICATION phase of Thyroid Synthesis?

A

o tyrosine residues in thyroglobulin are iodinated to form
monoiodotyrosine (MIT) or diiodotyrosine (DIT)

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35
Q

What happens in TRANSPORT phase of Thyroid Synthesis?

A

o iodide ion is converted to iodine by thyroid peroxidase (TPO)

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36
Q

What happens in IODINE COUPLING phase of Thyroid Synthesis?

A

o 2 molecules of DIT combine to form T4, while 1 molecule each of
MIT and DIT combine to form T3

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37
Q

What happens in PROTEOLYSIS phase of Thyroid Synthesis?

A

o T4 and T3 are released from the thyroid and transported in the
blood by thyroxine-binding globulin (TBG)

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38
Q

o sudden acute exacerbation of all of the symptoms of
thyrotoxicosis, presenting as a life-threatening syndrome

A

THYROID STORM

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39
Q

WOLF-CHAIKOFF VS JOD-BASEDOW

A
  • Wolf-Chaikoff effect: ingestion of iodine causes hypothyroidism
  • Jod-Basedow phenomenon: ingestion of iodine causes
    hyperthyroidism
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40
Q

Which drugs inhibit peripheral
conversion of T4 to T3?

A

Propylthiouracil, Propranolol
Hydrocortison

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41
Q

What drugs can cause druginduced
hyperthyroidism?
(CAM)

A

Clofibrate, Amiodarone, Methadone

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42
Q

TREATMENT of:

hyperthyroidism either through an iodine-induced mechanism in
persons with an underlying thyroid disease or through an
inflammatory mechanism that causes leakage of thyroid hormone

A

TREATMENT: thioamides or corticosteroids

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43
Q

MOA: * block uptake of iodide by the gland through competitive inhibition of
the iodide transport mechanism. Useful in amiodarone-induced hyperT
* potassium perchlorate is rarely used clinically because it is
associated with aplastic anemia

A

ANION INHIBITORS: PERCHLORATE (CLO4–), PERTECHNETATE
(TCO4–), THIOCYANATE (SCN–)

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44
Q

is preferred in the first trimester and should be replaced
by Methimazole (MMI) after this trimester.

A

PTU

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45
Q

is the mainstay of the treatment of postpartum
hyperthyroidism, in particular during lactation

A

METHIMAZOLE

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46
Q

NOTABLE SIDE EFFECT OF PTU?

A

AGRAnuLOCYTOSIS

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47
Q

are teratogens (causes
Aplasia Cutis Congenita) in the 1st trimester

A

Methimazole and Carbimazole

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48
Q

is the other name of Methimazole

A

THIAMAZOLE

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49
Q

Drug of choice for nonpregnant hyperthyroid Px
because of longer DOA (24h) and increased potency

A

METHIMAZOLE

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50
Q

Notable side effect of MEHITAMZOLE, CARBIMAZOLE?

A

AGRANULOCYTOSIS, ALTERERD SENSE OF SMELL AND TASTE

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51
Q

Administered orally sodium 131I, it is concentrated by the
thyroid and incorporated into storage follicles

A

Radioactive Iodine (I131) [X]

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52
Q

Notable SE of RADIOACTIVE IODINE

A

Permanent Hypothyroidism

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53
Q

Permanent cure of thyrotoxicosis without surgery

A

RADIOACTIVE IODINE

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54
Q

Preparation for thyroidectomy to reduce the size and
vascularity of the thyroid gland, Radiation prophylaxis.

A

POTASSIUM IODIDE [D], LUGOL’S SOLUTION /
Potassium Iodide Saturated Solution (KISS)

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55
Q

NOTABLE SE OF POTASSIUM IODIDE [D], LUGOL’S SOLUTION /
Potassium Iodide Saturated Solution (KISS)

A

ANGIOEDEMA

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56
Q
  • Blocks beta-receptors (control HR and other cardiac
    abnormalities of severe thyrotoxicosis).
  • Inhibits peripheral conversion of T4 into T 3 (Only
    Propranolol)
A

PROPRANOLOL, ESMOLOL, METOPROLOL, ATENOLOL

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57
Q

o medical emergency representing the end state of untreated
hypothyroidism

A

MYXEDEMA COMA

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58
Q

Treatment of MYXEDEMA COMA?

A

o intravenous loading dose of levothyroxine (300–400 mcg),
followed by 50–100 mcg daily

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59
Q

MOA: Thyroid receptor agonist

A

LEVOTHYROXINE (T4) [A],
LIOTHYRONINE (T3) [A], LIOTRIX [A]

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60
Q

4 B’s of thyroid hormone

A

Brain maturation, Bone
growth, Beta-adrenergic effects, and increase in Basal metabolic rate

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61
Q

regulate sodium and potassium reabsorption in the collecting
tubules of the kidney

A

MINERALOCORTICOIDS

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62
Q

CONVERTS CHOLESTEROL TO PREGNENOLONE

A

DESMOLASE

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63
Q

GLUCORTICOIDS:

Low Potency (1)
Medium Potency (2)
High Potency (2)

A

Low potency: Hydrocortisone (cortisol)
Medium potency:
Fluticasone, Mometasone
High-potency:
Desoximetasone, Clobetasol

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64
Q

is the prototype glucocorticoid

A

Hydrocortisone (cortisol)

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65
Q

is the glucocorticoid with the highest
anti-inflammatory potency.

A

BETAMETHOSONE

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66
Q

is the mineralocorticoid with the
highest salt-retaining potency

A

Fludrocortisone

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67
Q

Behavioral changes secondary to steroid use is termed

A

Roid Rage

68
Q

MOA: Inhibits Desmolase, blocking conversion of cholesterol
to pregnenolone. Reduces synthesis of all hormonally
active steroids.
Uses Breast cancer, Cushing

A

AMINO-glutethimide

69
Q
  • Abused by body builders to lower circulating levels of
    cortisol in the body and prevent muscle loss
A

Amino-glutethimide [D]

70
Q

MOA: Inhibits cholesterol side-chain cleavage, cytochrome
P450 enzymes and other enzymes necessary for
synthesis of all steroids

A

KETOCONAZOLE

71
Q

MOA: Blocks conversion of 11-deoxycortisol to cortisol via
inhibition of 11B-hydroxylase

A

METYRAPONE

72
Q

MOA: Competitive inhibitor at the GC receptor as well as
progesterone receptor

Also used as an approved abortifacient for medical
abortion (usually together with misoprostol)

A

MIFEPRISTONE

73
Q

MOA: Strong agonist of
mineralocorticoid receptors and
moderate activation of
glucocorticoid receptors.
Increases Na reabsorption,
K and H excretion

A

FLUDROCORTISONE [C],
DEOXYCORTICOSTERONE

74
Q

Blocks Aldosterone
receptors
(mineralocorticoid
receptor antagonist)

A

SPIRONOLACTONE

75
Q

When given continuously:
antifertility (suppresses
gonadal function)
When given pulsatile:
promotes gonadal function

A

GNRH AGONISTS

END WITH -RELINS (EXCEPT
LEUPROLIDE)

76
Q

Suppresses the LH surge
to prevent premature
ovulation in assisted fertility

A

GNRH ANTAGONISTS

END WITH -RELIX
(RELIX KA LANG –

77
Q

Used inPalliative therapy of hormone-responsive tumors
(breast or prostate CA), central precocious puberty,
controlled ovarian stimulation, male infertility,
endometriosis, apoplexy and blindness (if given to a
patient with a GnRH-secreting pituitary tumor)

A

LEUPROLIDE, GONADORELIN, GOSERELIN,
HISTRELIN, NAFARELIN, TRIPTORELIN

78
Q

is a synthetic human GnRH

A

Gonadorelin

79
Q

MOA: Blocks GnRH receptors.
Reduces endogenous production of LH and FSH

A

GANIRELIX, CETRORELIX, ABARELIX, DEGARELIX

80
Q

Endogenous hormone that is involved in pubertal changes,
controlling ovulation, preparing the female reproductive tract
for fertilization, acts on lipid and bone metabolism

A

ESTROGEN

81
Q

Most potent naturally-occurring estrogen is

A

17B-estradiol >
estrone > estriol

82
Q

Principal source of estrogen in pre menoupausal? in post menopausal?

A

Principal source in pre-menopausal: ovaries
o Principal source in post-menopausal: adipose tissue

83
Q

is a mixture of conjugated estrogen used in
HRT

A

PREMARIN

“PREMARIN is from PREgnant MARe’s urine”

84
Q

what carcinoma is seen in daughters of
mothers who took DES

A

Clear cell vaginal adenocarcinoma

85
Q

is a synthetic steroid with weak estrogenic,
progestogenic and androgenic activity, and hence is an
agonist of the estrogen, progesterone and androgen
receptor. It is primarily used in menopausal hormone
therapy, postmenopausal osteoporosis and endometriosis.

A

TIBOLONE

86
Q

Give 3 absolute contraindications of oral contraceptives

A

● Women age >35 years who smoke > 15 cigarettes per day
● Known ischemic heart disease or multiple risk factors for
cardiovascular disease (older age, smoking, diabetes, and
hypertension)
● Past thromboembolic event, stroke or known thrombogenic
mutations
● Complicated valvular heart disease
● Complicated solid organ transplantation
● Hypertension (systolic >160 mmHg or diastolic >100 mmHg)
● Systemic lupus erythematous (positive or unknown
antiphospholipid antibodies
● Cirrhosis, hepatic adenoma or hepatoma
● Pregnancy and early postpartum (<21 days)
● undiagnosed abnormal uterine bleeding

87
Q

Give 3 relative contraindications of oral contraceptives

A

● Hypertension (adequately controlled or systolic 140-159 or
diastolic 90-99)
● Women receiving anticonvulsant drug therapy
● Women following bariatric surgery (malabsorptive procedure)

88
Q

MOA of Combination Hormonal Contraceptives

A

MOA of Combination Hormonal Contraceptives
* inhibition of ovulation (the primary action)
* effects on the cervical mucus glands, uterine tubes, and endometrium
that decrease the likelihood of fertilization and implantation

89
Q

Differences between monophasic vs biphasic/triphasic oral contraceptives

A

● MONOPHASIC
o combination estrogen-progestin tablets that are taken in
constant dosage throughout the menstrual cycle
● BIPHASIC or TRIPHASIC
o combination preparations in which the progestin or estrogen
dosage, or both, changes during the month
o more closely mimics hormonal changes in menstrual cycle

90
Q

what oral contraceptives are recommended for breastfeeding moms since they do not
affect lactation

A

Progestin only prepartions

91
Q

What oral contraception is used for postcoital contraceptive?

A

LEVONORGESTREL,
ETHINYL ESTRADIOL + LEVONORGESTREL

92
Q

emergency contraception should be taken until when?

A

Must be taken within 72 hours of unprotected sexual
intercourse (not effective once implantation has occurred)

93
Q

MOA: Estrogen antagonist actions in breast tissue and CNS.
Estrogen agonist effects in uterus, liver and bone.

A

TAMOXIFEN

94
Q

Given for breast cancer patients who are ER+ PR+

A

TAMOXIFEN [D], TOREMIFENE [D]

95
Q

MOA: Estrogen antagonist actions in breast tissue, uterus and
CNS. Estrogen agonist effects in liver and bone.
Increases bone mineral density.

A

RALOXIFENE

96
Q

RALOXIFENE

A
97
Q

Acts as antagonist to estrogen receptors in the pituitary →
inhibit negative feedback mechanism by estrogen → leads
to pituitary stimulation causing ↑ LH and FSH

A

CLOMIPHENE

98
Q

is the enzyme which converts Testosterone to
Estrogen(Estradiol)

A

AROMATASE

99
Q

Effective against breast cancers that have become
resistant to tamoxifen

A

ANASTROZOLE [X], LETROZOLE, EXEMESTANE

100
Q

is an IRREVERSIBLE Aromatase inhibitor

A

Exemestane

101
Q

MOA: Weak cytochrome P450 inhibitor and partial agonist of
progestin and androgen receptors

A

DANAZOL

102
Q

Pharmacologic antagonist of glucocorticoid and
progesterone receptors
Uses: Medical abortion, Cushing’s syndrome

A

MIFEPRISTONE

103
Q

Complication: failure to induce complete abortion
􀀀sepsis d/t unusual organisms (Clostridium sordelli)

what abortifacient has this complication?

A

MIFEPRISTONE

104
Q

Active form of testosterone?

A

DIHYDROTESTOSTERONE

105
Q

Give 2 clinical uses of testosterone?

A
  • Replacement therapy in hypogonadism
  • Stimulate RBC production in certain anemias
  • Promote weight gain in patients with wasting syndromes (e.g.
    AIDS patients)
  • performance enhancement in athletes
    o exploited illicitly to increase muscle bulk and strength
  • Effects of androgen: secondary sexual characteristics, fertility
    and libido, male pattern baldness, increases muscle mass,
    increased RBC production, decreased urea nitrogen excretion,
    maintains normal bone density
106
Q

MOA: Competitive antagonist at androgen receptor

A

Flutamide [D], Bicalutamide, Nilutamide

107
Q

MOA: Antagonist at androgen receptor. Marked progestational
effect that suppresses the feedback enhancement of LH
and FSH.

A

CYPROTERONE [X], CYPROTERONE ACETATE

108
Q

Inhibits 5á-reductase enzyme that converts testosterone
to dihydrotestosterone

A

FINASTERIDE [X], DUTASTERIDE

109
Q

is the most potent form of
testosterone, essential in the development of male
secondary sexual characteristics.

A

Dihydrotestosterone

110
Q

Can be given to counteract flare effect in GnRH agonist
treatment

A

FINASTERIDE [X], DUTASTERIDE

111
Q

Giving this drug aids in the management of
smooth muscle hypertrophy in the prostate

A

5-alpha reductase

112
Q

In treating advanced prostate cancer with leuprolide, what can be
given to prevent the initial increase in testosterone?

A

Finasteride

113
Q

chronic disorder of carbohydrate, fat, and protein metabolism
due to a relative or absolute deficiency in insulin secretory
response

A

DIABETES MELLITUS

114
Q

o progressive disorder characterized by increasing insulin
resistance and diminishing insulin secretory capacity
o frequently associated with obesity and is much more
common than type 1 diabetes
o usually has its onset in adulthood

A

TYPE 2 DIABETES

115
Q

Difference in Type 1 and Type 2 in terms of C-peptide

A

Type 1 DM: no C-peptide. Type 2: have C-peptide

116
Q
  • cleavage of proinsulin and cross-linking result in formation of ??? and ???
A

of insulin and a residual C-peptide

117
Q

C-Peptide is used to? (2)

A

o differentiate type 1 and type 2 DM
o rule out factitious hypoglycemia

118
Q

MOA: binds to a tyrosine kinase receptor, which phosphorylates itself
and a variety of intracellular proteins when activated by the
hormone
* activation of phoshphatidylinositol-3 kinase pathway and MAP
kinase pathway

A

INSULIN

119
Q

is also capable of inducing entry of K+ (potassium) into cells

A

Insulin

Rapid acting insulin has “amino acids” in their name. Lis (lysine) Pro
(Proline). Etc. Because to make them rapid acting, binaliktad yung
positions ng mga amino acid na ito para maging rapid acting.
Glargine sounds like LARGE! Tunog Long yung effect
DeteMIR ends with MIR for Myristic Acid. A fatty acid added to the
structure to make it long acting

120
Q

WHAT STRATEGY:

most physiologic strategy because it copies the body’s
normal production of insulin as closely as possible
o long-acting insulin (BASAL) + short-acting insulin with every
meal (BOLUS)

A

BASAL BOLUS

121
Q

WHAT STRATEGY:

o fixed amounts of long-acting insulin to be given routinely
o amount of short-acting insulin varied depending on preprandial
CBG

A

SLIDING INSULIN SCALE

122
Q

period in type 1 DM when exogenous insulin requirements
decrease due to an increase in the endogenous production of
insulin
* initiation of insulin therapy causes activation of residual
pancreatic beta cells

A

ON INSULIN: HONEYMOON PERIOD

123
Q

Rapid Acting Insulin? (3)

A

Lispro, Aspart, Glulisine

124
Q

Short Acting Insulin (1)

A

Regular Insulin

125
Q

Intermediate Acting Insulin

A

NPH, Lente

126
Q

Long acting insulin (1)

A

Ultralente

127
Q

Ultra-Long Acting Insulin (3)

A

Glargine, Detemir, Lantus

128
Q

Who are at Risk for Insulin-related Hypoglycemia (4)

A

Advanced renal
disease, elderly, children <7 y/o

129
Q

1st generation Sulfonylureas (3)

A

Chlorpropamide, Tolbutamide, Tolazamide

130
Q

What generation of sulfonylureas: High propensity to cause hypoglycemia especially
among elderly patients that’s why it is seldom used

A

First Generation

Chlorpropamide, Tolbutamide, Tolazamide

131
Q

Has the lowest risk of developing hypoglycemia since they
have short duration of action

A

Meglitinide

132
Q

Used in diabetics with sulfa allergies
taken for post-prandial
hyperglycemi

A

Meglitinide

133
Q

MOA: * reduces postprandial and fasting glucose levels
* activates AMP-stimulated protein kinase leading to inhibition
hepatic and renal gluconeogenesis

A

BIGUANIDES

134
Q

FIRST LINE: T2DM, also DM Prevention
PCOS, DOC for OBESE Diabetic

A

METFORMIN

135
Q

Worse SE of Metformin

A

Worse SE: lactic acidosis
(especially in renally and hepatically impaired patients,
hence contraindicated), Vit B12 malabsorption, weight loss

136
Q

(2) antidiabetic drug that bypass the insulin receptor.
Both of these medications act via gene expression to sensitize tissue
receptor to insulin

A

Metformin and its cousin Thiazolidinediones bypass the insulin receptor.
Both of these medications act via gene expression to sensitize tissue
receptor to insulin

137
Q

MOA: increase target tissue sensitivity to insulin by activating the
peroxisome proliferator-activated receptor-gamma nuclear
receptor (PPAR-Ɣ receptor)

A

THIAZOLIDINEDIONES

138
Q

THIAZOLIDINEDIONE that reduces mortality and macrovascular
events (myocardial infarction and stroke)

A

Pioglitazone

139
Q

MOA: Inhibits intestinal α-glucosidases → reduce conversion
of starch and disaccharides to monosaccharides →
reduce post prandial hyperglycemia

A

Acarbose, Miglitol, Voglibose

ALPHA-GLUCOSIDASE INHIBITOR

140
Q

MOA: Activates amylin receptors. Reduce post-meal glucose
excursions Suppresses glucagon release. Delays gastric
emptying. Stimulates CNS to reduce appetite (anorectic
effect).

A

AMYLIN ANALOG: PRAMLINTIDE

141
Q

Most notable SE of exenatide, liraglutide? (GLP-1 AGONIST)

A

Acute pancreatitis

142
Q

What GLP 1 Agonist has possible thyroid ca risk?

A

Liraglutide

143
Q

Sitagliptin, Saxagliptin, Linagliptin,
Vildagliptin, Teneligliptin DRUG CLASS?

A

DPP-4 INHIBITORS

Inhibits dipeptidyl peptidase-4 (DPP-4) that degrades GLP-1
and other incretins → raises circulating GLP-1 levels.

144
Q

Exenatide, Liraglutide,
Lixisenatide, Semaglutide, Dulaglutide DRUG CLASS?

A

GLP-1 AGONIST

Activates GLP-1 receptors → reduction of post-meal glucose
excursions.

145
Q

Empagliflozin, Dapagliflozin, Canagliflozin DRUG CLASS?

A

SGLT-2 INHIBITOR

146
Q

MOA of SGLT-2 INHIBITOR?

A

NA-GLUCOSE CO-TRANSPORTER 2 (SGLT 2)
INHIBITOR → inhibits reabsorption of glucose in the
kidneys back to the blood → excretion of glucose out in
the urine.

147
Q

Most notable SE of SGLT-2 INHIBITOR

A

strong smell of urine

148
Q

An appetite suppressant which is an
amphetamine derivative. Side effects will be
similar with amphetamine

A

PHENTERMINE
[X]

149
Q

MOA: Inhibits gastrointestinal and pancreatic lipases. Reduces
absorption of fats

A

ORLISTAT (XENICAL)

150
Q

Net effect
on serum calcium/phosphate
levels of PTH?

A

Serum calcium
increased,
serum phosphate
decreased

151
Q

Net effect
on serum calcium/phosphate
levels of Active Vitamin D Metabolites (Calcitriol)

A

Serum calcium and
phosphate both increased

152
Q

MOA: Interacts selectively with estrogen receptors leading to
inhibition of bone resorption w/o stimulating breast or
endometrial hyperplasia

A

SERM: RALOXIFENE [X]

153
Q

WHAT HORMONE?

Inhibits calcium excretion, promotes phosphate excretion and
stimulates the production of active vitamin D metabolites
* Promotes bone turnover by increasing the activity of both
osteoblasts and osteoclasts

A

PARATHYROID HORMONE

154
Q

At high doses, net effect of elevated PTH

A

is increased bone
resorption via osteoclast activation, hypercalcemia, and
hyperphosphatemia

155
Q

Stimulus for the release of PTH

A

decreased free ionized calcium

156
Q

MOA: Acts through PTH receptors to produce a net increase
in bone formation, stimulates bone turnover

A

TERIPARITIDE (RECOMBINANT PTH )
Acts through PTH receptors to produce a net increase
in bone formation, stimulates bone turnover
This is a key difference between endogenous PTH and
Teriparatide: PTH has net bone resorption, Teriparatide
has net bone formation (‘wag malito!)

157
Q

Commonly added to dairy products and other food
products
* Given topically for psoriasis; given with calcium
supplements for osteoporosis

A

ERGOCALCIFEROL, CHOLECALCIFEROL

158
Q

is a prodrug that is converted in the
liver to 1,25-dihydroxyvitaminD

A

DOXERCALCIFEROL

159
Q

are analogs of calcitriol
and are used topically for psoriasis and are being
investigated

A

Paricalcitol, Calcipotriene

160
Q
  • Peptide hormone secreted by parafollicular C cells in the thyroid gland
  • decreases serum calcium and phosphate by inhibiting bone
    resorption and inhibiting renal excretion of these minerals
  • bone formation is not impaired initially, but ultimately it is reduced
A

CALCITONIN

161
Q

MOA: Acts through calcitonin receptors to inhibit bone
resorption

USES: Paget’s disease of bone, Hypercalcemia, Osteoporosis,
Tumor marker for thyroid cancer

A

Calcitonin, Salcatonin

MNEMONIC: Calcitonin means CALCium INside the bone

162
Q

MOA: Suppresses the activity of osteoclasts in part via
inhibition of Farnesyl Pyrophosphate synthesis.
Inhibits bone resorption and secondarily, bone formation
by acting on the basic hydroxyapatite crystal structure

A

BISPHOSPHONATES: Alendronate, Etidronate, Ibandronate, Pamidronate, Risedronate,
Tiludronate, Zoledronic Acid (Prototype)

163
Q

notable SE of Bisphosphonates?

A

Esophagitis, Osteonecrosis of the
jaw,

164
Q

MOA: Binds to dietary phosphate and prevents its absorption

A

Sevelamer

165
Q

MOA: Binds to RANKL and prevents it from stimulating
osteoclast differentiation and function → inhibits bone
resorption

A

DENOSUMAB

ANTI RANKL MONOCLONAL ANTIBODY

166
Q

MOA: Activated calcium-sensing receptor → Inhibits PTH
secretion

A

CINACALCET

“Sinakal siya! Patay!, Cinacal siya, PTHay

167
Q
A

PLE_PHARMA (16 decks)

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