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Pharma > Thyroid hormones 18- > Flashcards

Thyroid hormones 18- Flashcards

1
Q

Mechanism of action of thyroid hormones:

A

« T3 and T4 dissociate from Thyroxine-binding globulin (TBG)
and enter cells by diffusion or active transport.
« Inside the cell, T4 deiodinated to T3
» T3 enters the nucleus and attaches to its nuclear receptor
Drug-receptor complex bind to DNA and promotes
transcription of specific genes — mRNA formation— protein
synthesis (production of various enzymes).

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2
Q

Therapeutic Uses of Thyroid Hormones:

A
  1. Replacement therapy in hypothyroidism (levothyroxine)
  2. TSH suppression therapy in thyroid cancer and nontoxic goiter.
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3
Q

Mechanism of Action of Thioamides

A

Thioamides inhibit thyroid hormone synthesis by:-
1.Inhibition of oxidation of iodide to iodine.
2.Inhibition of iodination of tyrosine (organification of iodine).
3. Inhibition of coupling of iodotyrosines to T4 and T3.
4. Propylthiouracil in addition reduces conversion of T4 to T3 in the periphery.

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4
Q

Therapeutic uses of thioamides

A

Used in Treatment of hyperthyroidism:
1. As principal therapy.
2. As adjuvant to 1” to control the disease while waiting its effect.
3. To control the disorder in preparation for surgical treatment.
4. Thyroid storm (PTU inhibits conversion of T4 to T3)
5. In pregnancy:

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5
Q

thioamides used in pregnancy

A

propylthiouracil and methimazole

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6
Q

Mechanism of action of iodide salts and iodine

A
  1. Inhibition of iodide organification
  2. Reduction of the response of thyroid gland to TSH,
  3. Inhibition of proteolysis of thyroglobulin — decrease Release of T3&T4.
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7
Q

Adverse effects of thioamides

A
  1. No-specific: Allergy, most commonly papular rash and GIT upset
  2. Agranulocytosis: the most serious but rare and reversible.
  3. Hepatotoxicity: hepatitis (PTU) & cholestatic jaundice (methimazole)
  4. Immunological reactions: e.g. vasculitis, lymphadenopathy, a lupus-like reaction,
    arthralgia, & polyserositis
  5. Loss of hair, abnormal skin pigmentation
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8
Q

the most serious adverse effect caused by thioamides

A

agranulocytosis

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9
Q

thioamides causes hepatitis

A

propyluracil

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10
Q

thioamides causes cholestatic jaundice

A

(methimazole)

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11
Q

Therapeutic indications of iodine and iodide salts

A
  1. Preparation of the patient for thyroidectomy (8gland size & vascularity).
  2. Thyroid crisis (storm) (inhibit hormone release).
  3. Prophylactic where goiter is endemic. (Added to salt, water and bread).
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12
Q

Adverse effects of iodine and iodide

A
  1. lodism: (dose-dependet, chronic adverse effects) metallic taste, painful salivary glands,
    excess salivation, running eyes & nose, sore throat, cough and diarrhea.
  2. Allergic reactions: angioedema, rash, drug fever and ulceration of mucous membranes.
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13
Q

Mechanism of Action: Radioactive iodine

A
  1. Oral radioactive iodine is rapidly absorbed & concentrated by thyroid gland
  2. It emits Beta rays (cytotoxic) which destroy the gland tissue.
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14
Q

Therapeutic uses: Radioactive iodine

A
  1. Hyperthyroidism in adults over 45 years
  2. Hyperthyroidism in patients not fit for surgery
  3. Recurrence after medical or surgical treatment
  4. Thyroid cancer.
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15
Q

Adverse effects: Radioactive iodine

A
  1. Hypothyroidism (The chief toxic effect).
  2. Thyroid storm (release of thyroid hormone).
  3. Patient may require repeated doses.
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16
Q

Used to control peripheral manifestations of hyperactivity of the sympathetic nervous system (tachycardia, tremors and nervousness) occurring secondary to hyperthyroidism.

A

beta blockers

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17
Q

moa of betablocker as antithyroid agent

A
  • Used to control peripheral manifestations of hyperactivity of the sympathetic nervous system (tachycardia, tremors and nervousness) occurring secondary to hyperthyroidism.
  • Propranolol also prevents peripheral conversion of T4 into the more active T3.
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18
Q

Control Of Release of Aldosterone:

A

1) Renin-Angiotensin System activation by hypovolemia & hyponatremia.
2) Hyperkalemia.

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18
Q

1ry hyperaldosteronism:

A

Adenoma in Zona glomerulosa “Conn’sgdisease”.

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19
Q

what is escape phenomenon

A

Prolonged hypervolemia — decrease Sensitivity of distal convoluted tubules (D.C.T.) to the effect of Aldosterone — No Na& Water retention BUT still K excretion.

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20
Q

useful in hyperaldosteronism

A

Spironolactone

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21
Q

2ry hyperaldosteronism:

A

Occurs in chronic heart
failure, liver cirrhosis & Nephrotic syndrome.

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22
Q

Mineralocorticoid preparations:

A

A) Des-Oxy-Corticosterone (D.O.C.)
B) Fludrocortisone Acetate

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23
Q

Pure mineralocorticoid with NO glucocorticoids activity.

A

Desoxycorticosterone

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24
Q

Used to replace mineralocorticoid activity in Addison’s disease.

A

Desoxycorticosterone
Fludrocortisone Acetate

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25
Q

mineralocorticoid with glucocorticoid action

A

Fludrocortisone Acetate

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26
Q

cortisol Bound to …………

A

plasma proteins mainly to Corticosteroids-Binding-Globulin (CBG = Transcortin) & albumin.

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27
Q

effect of CS on ACTH

A

Suppresses release of corticotropin releasing hormone (C.R.H.) from hypothalamus & Suppresses release of A.C.T.H. from Anterior pituitar

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28
Q

effect of CS on calcium

A

decrease absorption of calcemia causing hypocalcemia

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29
Q

effect of CS on gastric

A

increase HCl worsen peptic ulcer

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30
Q

effect of CS on eye

A

cataract and increase in intraocular pressure

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31
Q

Pharmacological Actions Of Cortisol

A

1) Negative Feedback effect (A.C.T.H)
2) Organic Metabolism:
3) CNS: EUphoria & DEpression
4) Cataract & increase in intraocular pressure (IOP)
5) 5) Gastric: increase HCl and worsen peptic ulcer
6) Anti-Inflammatory Effect:
7) Anti — Vitamin D
8) Anti-Allergic & Immunosuppressant:
9) Blood
10) Anti-Stress & Anti-Shock effect:
11) Delays Wound Healing:
12) Uricosuric effect:

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31
Q

effect of CS on blood

A

a. Stimulates erythropoiesis & increases release of RBCs from bone marrow:
= In Cushing’s disease (Hypercortisolemia) — Polycythemia.
= |n Addison’s disease (Hypocortisolemia) — Anemia.
b. Increases circulating P.M.N.L. by their migration from the circulation.
c. Increases number of platelets.
d. T Coagulability of blood.
e. Decreases lymphocytes — Lymphopenea (Catabolic effect on lymphoid tissues).
f. Decreases eosinophils = Eosinopenea.

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32
Q

Therapeutic Uses of Glucocorticoids

A

A) Replacement therapy in adrenocortical insufficiency (Addison’s disease):
a) Acute Addisonian Crisis: cortisol
b) Chronic Addison’s Disease: cortisone acetate/ mineral: DOCA and fludrocortisone acetate
B) Supplementary & Suppressive therapy
1) Anti-Inflammatory: treat inflammation in:
a.Encephalitis, cerebral edema & Intra-cranial pressure.
b.Rheumatic carditis.
¢. Chronic active hepatitis.
d.Nephritis & nephritic syndrome.
e.Arthritis: Rheumatic, Rheumatoid, Gouty & Osteoarthritis.
2) Allergic diseases: in the skin, eye & bronchial asthma.
3) Immunosuppressive in :
a) Auto-immune diseases:
- Collagen disease: Polyarthritis & systemic lupus erythematosis.
- Blood diseases: Hemolytic & aplastic anemia, thrombocytopenia
- Inflammatory bowel syndrome e.g. ulcerative colitis.
b) Suppress tissue & organ rejection.
4) Suppress lymphoid tissues— Treat lymphoma & leukemia.
5) Suppress A.C.T.H. in adreno-genital syndrome.
6) Suppress hypertrophic scars & keloid formation.
7) Shock & Stress conditions.
8) Hypervitaminosis D & Hypercalcemia.

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33
Q

Adverse Effects of Glucocorticoids:

A

Abrupt withdrawal after long use — Acute Addisonian Crisis.
Moon face & Buffalo hump
Hyperglycemia — Worsens Diabetes mellitus
Osteoporosis
Hypocalcemia
Delays healing of wounds.
Hypokalemia — Worsens Digitalis toxicity
Na retention: Edema and Hypertension — May lead to HF
weight gain
Immunosuppressant — increase Susceptibility to infection,
Mask manifestations of bacterial & viral infections
Peptic ulceration.
Cataract & increases intra-ocular pressure — Glaucoma.
Teratogenicity
Thromboembolic manifestations.

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34
Q

Contraindications Of Glucocorticoids:

A

1- Abrupt withdrawal: acute adrenal insufficiency syndrome.
2- Cushing’s disease.
3- Diabetes mellitus.
4- Osteoporosis.
5- Repeated intra-articular injections.
6- Hypertension & Heart failure.
7- Digitalis toxicity.
8- Uncontrolled infection.
9- Peptic ulcer.
10- Thromboembolic diseases.
11- Psychological disturbances.
12- During pregnancy.
13- Glaucoma.

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35
Q

Short acting glucocorticoid

A

Hydrocortisone (cortisol) & cortisone:

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36
Q

The only glucocorticoid that has no effect on the fetus in pregnancy

A

Prednisone

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36
Q

Intermediate & long acting CS

A

Prednisone (intermediate), dexamethasone (long acting)

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37
Q

CS has no mineralcorticoid action

A

dexamethasone

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38
Q

a somatostatin analogue inhibits ACTH and growth hormone secretion and reduces the circulating levels of cortisol in patients with ACTH-producing pituitary
tumors and is also used in the treatment of acromegaly.

A

Pasireotide

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39
Q

Pasireotide uses

A

inhibits ACTH and growth hormone secretion
used in treatment of acromegaly

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40
Q

long-acting dopamine D2 receptor agonist used primarily to treat hyperprolactinemia, also inhibit ACTH release

A

Cabergoline

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41
Q

Antihistamine (H1-blocker) + Anti-serotonin. }
Suppresses release of A.C.T.H.

A

Cyproheptadine

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42
Q

Ketoconazole

A

a. Anti-fungal.
b. Inhibits adrenal steroid hormone synthesis when used in larger doses
c. Useful in Cushing’s disease.

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43
Q

Inhibits 11-B-Hydroxylase enzyme selectively -decrease Synthesis of BOTH Aldosterone & Cortisol »increase ACTH

A

Metyrapone (Mitopirone):

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44
Q

Test the function of anterior pituitary to secrete A.C.T.H

A

Metyrapone (Mitopirone):

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45
Q

a- Destruction of adrenocortical cells.
b- Useful in Cushing’s disease & Inoperable adrenocortical carcinoma.

A

Mitotane

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46
Q

It causes a reduction in the synthesis of all hormonally active steroids. Because it inhibits conversion of Cholesterol — Pregnenolone (First step in steroidogenesis).

A

Aminoglutethimide

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47
Q

It can be used with metyrapone or ketoconazole to reduce steroid secretion in patients with Cushing’s syndrome due to adrenocortical cancer who do not
respond to mitotane.

A

Aminoglutethimide

48
Q

Aminoglutethimide uses

A

a- It causes a reduction in the synthesis of all hormonally active steroids. Because it inhibits conversion of Cholesterol — Pregnenolone (First step in steroidogenesis).
b- It can be used with metyrapone or ketoconazole to reduce steroid secretion in patients with Cushing’s syndrome due to adrenocortical cancer who do not respond to mitotane.

49
Q

Natural estrogens:

A

Estradiol

50
Q

Semisynthetic estrogens

A

Ethinyl estradiol:Highly potent,
Mestranol: long duartion

51
Q

Synthetic estrogens:

A

Diethylstilbestrol

52
Q

Therapeutic uses of estrogens

A
  1. Contraception with progestogens.
  2. Postmenopausal hormonal therapy (HT):For menopausal symptoms” hot flushes & vaginal atrophy”
  3. Replacement therapy:. in
    1ry hypogonadism (ovarian failure).
    Premature menopause
    Surgical menopause
53
Q

to decrease risk of endometrial carcinoma.

A

add progestogen with estrogens

53
Q

Adverse Effects of estrogens

A

1) Nausea and Breast tenderness (most common)
2) Thromboembolic events & myocardial infarction. Estrogens enhance the coagulability of blood by increasing levels of factors II, VII, IX and X resulting in high incidence of thromboembolic disease.
3) Salt & water retention leading to edema & hypertension which causes increased weight gain
4) Increased blood sugar levels
5) Risk of breast cancer.
6) Risk of endometrial carcinoma: add progesterone to decrease risk

54
Q

Contraindications of estogens

A

1) Carcinomas of endometrium
2) History of thromboembolic disorders.

55
Q

Therapeutic uses of progestins

A
  1. Oral contraception: alone or with estrogen: main use.
  2. Functional uterine bleeding.
  3. Dysmenorrhea.
  4. Amenorrhea: artificial cycle: estrogen for 25 days supplemented with progesterone 15th to 25th day .Menstruation occurs on withdrawal.
  5. Endometriosis.
56
Q

Hydroxyprogesterone caproate: route

A

IM,

56
Q

used in Endometriosis

A

Progesterone

57
Q

progestins given IM

A

Progesterone
Hydroxyprogesterone caproate

58
Q

progestin given orally

A

Medroxyprogesterone acetate:
Norethindrone:
Norgestrel:

59
Q

Adverse Effects of progestins

A

Weak androgenic actions of some of the progestogens derived from testosterone.
Edema
Psychic depression.
Increase Cholesterol: atherosclerosis

60
Q

Selective Estrogen Receptor Modulators (SERMs)

A
  • SERMs are a class of estrogen-related compounds that display selective agonism or antagonism for estrogen receptors depending on the tissue type.
  • This category includes tamoxifen, raloxifene, clomiphene citrate.
60
Q

Tamoxifen uses

A

1- treatment of metastatic Breast Cancer
2- adjuvant therapy after mastectomy or radiation

61
Q

treatment of metastatic Breast Cancer

A

Tamoxifen

62
Q

adjuvant therapy after mastectomy or radiation

A

Tamoxifen

63
Q

Tamoxifen

A

Anti-Estrogens: Selective Estrogen Receptor Modulators (SERMs)

64
Q

Raloxifene: uses

A
  • Effective for prevention & treatment of osteoporosis
  • Reduction in risk of breast cancer
65
Q

Clomiphene Citrate:

A

Used as Ovulation-inducing agent

65
Q

Used as Ovulation-inducing agent

A

Clomiphene Citrate:

66
Q

anti insulin Effective for prevention & treatment of osteoporosis

A

Raloxifene

66
Q

Raloxifene

A

Anti-Estrogens: Selective Estrogen Receptor Modulators (SERMs)

67
Q

Clomiphene Citrate:

A

Anti-Estrogens: Selective Estrogen Receptor Modulators (SERMs)

68
Q

Aromatase Inhibitors (Als): moa

A

Decrease the production of estrogen.

68
Q

Estrogen Synthesis Inhibitors:

A

Aromatase Inhibitors (Als):

69
Q

They are of 2 types: of aromatase inhibitors

A
  • Steroidal Als: which binds permanently to aromatase enzyme (suicide inhibition), example:
    exemestane
  • Non-steroidal Als: which bind reversibly to aromatase, example: letrezole
  • Can be used in treatment of breast cancer & induction of ovulation.
  • Itis devoid from the androgenic side effect of steroidal Als.
70
Q

Steroidal Als:

A

exemestane

71
Q

Non-steroidal Als:

A

letrezole

72
Q

هt blocks ER in hypothalamus preventing the usual negative feedback effect of estrogen on GnRH
leading to increased FSH-> marked stimulation and enlargement of ovaries & increase estrogen
secretion & induction of ovulation.

A

Clomiphene citrate:

73
Q

t is useful in restoring regular menstrual cycle and starting ovulation in about 50% of women with polycystic ovary syndrome.

A

Metformin

74
Q

The drug inhibits estrogen synthesis =increases GnRH release =increases FSH release
=induction of ovulation

A

Aromatase Inhibitors

75
Q

Treatment of infertility due to ovulatory failure:

A

Clomiphene citrate
Human Menopausal Gonadotrophins
Metformin
Aromatase Inhibitors (e.g. Letrezole)

75
Q

inhibits the activity of progesterone.

A

Mifepristone

76
Q

Mifepristone moa

A

inhibits the activity of progesterone.

77
Q

it is used as postcoital contraceptive

A

Mifepristone

77
Q

It binds to progesterone receptors with no progesterone activity (progesterone
antagonist).

A

Mifepristone

77
Q

Used in treatment of endometriosis & fibrocystic disease of breast.

A

Danazol

78
Q

Danazol adverse effects

A

Adverse effects:
1) Androgenic: acne, hirsutism & Deepening of voice
2) Weight gain
3) Decrease breast size
4) Libido changes

79
Q

Danazol moa

A

Inhibits the mid-cycle surge of LH and FSH, but with no effect on basal level.
Inhibits steroid synthesis in the ovary : reduces ovarian function leading to atrophic changes in the endometrium.

80
Q

Anti-Progestogens

A

Mifepristone
Danazol

81
Q

androgen uses

A

Replacement therapy in male 1ry hypogonadism due to deficiency of androgens or 2ry
hypogonadism due to failure of pituitary.

81
Q

Preparations of androgen

A

Preparations
= Natural androsterone and testosterone (more active).
They are rapidly metabolized in liver, so ineffective orally.
= Synthetic:
Testosterone propionate sublingual, .M. or S.C.
Methy! testosterone sublingual.

81
Q

Adverse effects of androgen

A

1) Cholestatic jaundice (with testosterone), undesirable sexual activity,
2) masculinization in females, hirsutism ,salt retention,
3) precocious puberty and premature closure of epiphyseal plates in children.

82
Q

contraindication of androgen

A

cancer prostate.

83
Q

Inhibits conversion of testosterone into di-hydro-testosterone by inhibiting 5areductase, so it blocks action of androgen on tissues requiring dihydrotestosterone (prostate
and hair follicles). It is given orally to reduce benign prostatic hyperplasia (BPH).

A

Finasteride

84
Q

compete with testosterone for receptors: Used in
hypersexuality in males and in hirsutism, and in cancer prostate.

A

Flutamide, Cyproterone

84
Q

competitive inhibitor of aldosterone, also competes with di-hydrotestosterone for the androgen receptors in target tissues. It also reduces 17a-hydroxylase
activity, lowering plasma levels of testosterone and androstenedione. It is used in dosages
of 50-200 mg/day in treatment of hirsutism in women and appears to be as effective as
finasteride, flutamide or cyproterone.

A

Spironolactone

84
Q

Mechanism of action of contraceptive

A
  1. Estrogen inhibits the release of FSH and so suppresses the development of the ovarian follicle.
  2. The progestogen inhibits the release of LH and thus prevents ovulation and it also increases viscosity of cervical mucus so impair penetration of sperms
  3. They both alter the endometrium in such a way as to discourage implantation.
85
Q

mechanism of action: Progestin only contraceptives:

A

1) Increases viscosity of cervical mucus so impair penetration of sperms.
2) Hinder implantation through effect on endometrium & on motility and secretions of the fallopian tubes

85
Q

Oral progestogens:

A

Minipill

86
Q

= Does not inhibit ovulation
= Does not inhibit the cycle
= Does not inhibit lactation
Mechanism of contraception: thick cervical mucus & endometrial changes

A

Minipill

87
Q

long acting contraception

A

depot therapy):

87
Q

depot therapy Side effects

A

Menstrual iregularities are very common; infertility persists for many months after stop.

88
Q

Minipill Disadvantages

A

1) Break-through bleeding is common
2) Irregular menstrual cycles.
3) Less effective than the combined method. Missing a dose: conception.

89
Q

Subcutaneous implants SE

A

Subcutaneous implants:

89
Q

Mechanism of action of large dose of estrogens:

A

-Large dose of estrogen (postcoital pills): Increase motility of oviduct & endometrial changes and
decreased fertilization & implantation
-Withdrawal of large dose of estrogens : Withdrawal bleeding then expel fertilized ovum

90
Q

Disadvantage of large dose of estrogens

A

Nausea and vomiting occur frequently.

91
Q

Contra-indications of oral contraceptives:

A

History of thromboembolic disease or varicose veins.
Breast Cancer
Liver disease.
Diabetes
Cardiovascular diseases e.g. hypertension, coronary heart disease
Uterine fibromyomata (may increase).
Migraine.
Women over 35 years.
Undiagnosed vaginal bleeding.

92
Q

Oral contraceptives antagonize the effect of:

A
  1. Oral anticoagulants: oral contraceptives increased level of blood clotting factors.
  2. Some antihypertensive: oral contraceptives may increase Bl. pr.
  3. Antihypercholesterolemic drugs: oral contraceptives increase level of blood cholesterol & triglycerides.
93
Q

Adverse effects of oral contraceptives:

A

The most common adverse effects:
1) Headache, and nausea
2) Fluid retention > Weight gain & Increased blood pressure may also occur
3) Breast fullness & mastalgia.
4) Progestins may be associated with: depression, changes in libido, hirsutism, and acne. Also,
Break-through bleeding (common with progestogens alone or low dose combination method).
Severe adverse effects:Although rare
1) Thromboembolism, myocardial infarction, and stroke (most common among women who are
over 35 years and smoke).
2) Increased incidence of cervical cancer and breast cancer
3) cholecystitis, gall stones & jaundice

94
Q

Oral contraceptives effect may be reduced

A

Enzyme inducers: phenytoin, phenobarbitone, rifampicin
Mineral oil: decrease intestinal absorptionof oral steroids.
Tobacco smokingand antifibrinolytics increase the incidence of thromboembolism.

94
Q

GnRH Analogues uses

A

1 - Cancer prostate
2 - Uterine fibroids
3 - Endometriosis
4 - Precocious puberty

95
Q

Growth hormone-inhibiting hormone (Somatostatin): uses

A

1- Bleeding esophageal varices (IV infusion of octreotide)
2- Diarrhea and flushing associated with carcinoid tumors.
3- Acromegaly

96
Q

used in Acromegaly

A

Growth hormone-inhibiting hormone (Somatostatin):

96
Q

promotes growth in Pituitary dwarfism (GH deficiency), as replacement therapy prior to epiphyseal closure.

A

Growth hormone (GH):

97
Q

Gonadotropins: uses

A

used in the treatment of infertility.

98
Q

Hyperprolactinemia is treated with

A

D2 receptor agonists, such as Cabergoline and Bromocriptine.

98
Q

treat diabetes insipidus.

A

vasopressin

99
Q

drugs increase secretion of prolactin

A

drugs that act as dopamine antagonists (e.g metoclopramide & antipsychotics such as risperidone) and drugs decreasing dopamine (reserpine, a-methyl dopa) can
increase the secretion of prolactin

100
Q

vasopressin uses

A

The major use of vasopressin is to treat diabetes insipidus.
- Also_used in the management of:
- Cardiac arrest
- In controlling bleeding due to esophageal varices.

101
Q

An analog of vasopressin and is preferred for the treatment of diabetes insipidus and
nocturnal enuresis

A

Desmopressin

101
Q

Oxytocin uses

A
  1. Induction of labor in uterine inertia (1.V)
  2. Control of postpartum hemorrhage (1.M)
  3. Impaired milk ejection (nasal spray)

Pharma (7 decks)

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