1-Repaglinide A-The only indication for the use of these drugs is as third-line therapy for Type 2 DM who are

r Type 2 DM who are very insulin deficient and prone to

ketosis
2-Acarbose, Miglitol B-Amylin analogue, Used SC as an adjunct to mealtime insulin therapy in patients with Type 1 or Type 2 diabetes who have
problems with postprandial hyperglycemia

ENDOCRINE
3-Insulin C-An Insulin Sensitizer, Highly bound to plasma albumins, Slow onset of activity, Metabolized in the liver, Excreted in bile, May be
administered to patients with renal insufficiency, Cause a shift of triglyceride stores from non-adipose to adipose tissues and from
visceral to subcutaneous fat depots, reduces plasma triglycerides by 10%–15%, raises HDL cholesterol levels, and both increase
LDL cholesterol.
4-Pramlintide D-An insulin Sensitizer, Not bound to serum protein, Not metabolized by liver, Excreted unchanged as the active drug in urine,
Used as first-line therapy in Type 2 (NIDD), particularly in overweight (OBESE) patients, when dietary management and exercise
alone does not result in adequate glycemic control
5-Pioglitazone E-An insulin Secretagouge, Rapid onset of action (Peak = 1 hour) & Short t1/2 = 2-3 hours, Metabolized by hepatic metabolism

MATCHING
(CYP3A4), Less liable to produce hypoglycemia & weight gain and no need for dose adjustment in elderly and in renal
impairment , Given before each meal , Control post- prandial hyperglycemia & HbA1C
6-Tirzepatide F-An insulin Secretagouge, largely (90%–99%) bound to plasma protein , should be administered with caution to patients with
either renal or hepatic insufficiency, Used in Type 2 (NIDD), particularly in NON-OBESE & NON COMPLICATED patients, when
dietary management and exercise alone does not result in adequate glycemic control.
7-Metformin G-Not an insulin Secretagouge, Not an insulin Sensitizer, Its ONLY action is decrease absorption of complex Carbohydrates,
decrease Postprandial hyperglycemia, Decrease bioavailability of Metformin, So concurrent use should be AVOIDED

Qs
8-SC Semaglutide (NOT H-Dual glucose dependent insulinotropic polypeptide (GIP) and glucagon like peptide-1 (GLP-1) receptor agonist, USED BY SC
ORAL) injection in Type 2 DM & Obesity (as it ↓↓ fasting and post-prandial glucose level + ↓↓food intake + ↓↓body weight).
9-Glibenclamide, Glimipride I-GLP-1 agonist, Indicated as an adjunct to diet and exercise to improve glycemic control in adult with type 2 DM, Used in
combination with reduced caloric diet & increased physical activity to reduce excess body weight & maintain long term weight
reduction in adult with obesity or over-weight , Used to reduce risk of Major Adverse Cardiovascular Events (MACE) “CV death,
Non-fatal MI , Non-fatal stroke” in adult with type 2 DM & established CVS disease
10-Glucagon J-Is essential & a true replacement therapy in patients with Insulin Dependent Diabetes (Type 1), Temporary in N.I.D.D. during
STRESS periods , Permanently in N.I.D.D. with renal impairment, Emergency treatment of Diabetic Ketoacidosis & Non-ketotic
Hyperosmolar Diabetic coma.
11-(SGLT2) INHIBITORS K- Use in Hypoglycemia coma , Assess pancreatic β-cell secretory reserve, Heart failure due to over dose β-blockers, Used to
(Canagliflozin, Dapagliflozin, relax intestine in radiology of bowel
Empagliflozin)
12-Teplizumab L-Monoclonal antibody, Approved in USA to delay the onset of stage 3 Type 1 DM in adult and in children aged 8 years or older

1-E, 2-G, 3-J, 4-B, 5-C, 6-H, 7-D, 8-I, 9-F, 10-K, 11-A, 12-L

1-Glucagon A-binds to the  subunit of tyrosine kinase receptors,  Activation of tyrosine kinase activity of  subunit
 Phosphorylation of intracellular proteins  Change in enzyme activity, gene expression and
translocation of Glut-4 transporter  Glucose uptake by adipose tissue & Sk.m.

2-Thiazolidinediones (Glitazones) B-Block ATP-sensitive K+-channel (KATP-Channels) of -Cells of Pancreas  Depolarization  Influx of Ca2+ 1-Insulin A-Causes Hypoglycemia , Weight gain , failure after long use (years) due to exhaustion B-Cells
(Piogltazone, Rosiglitazone)  Excocytosis   Release of Insulin.

3-Glucagon-like peptide-1 (GLP-1) analogs C-The primary effect is to reduce hepatic glucose production by activating the enzyme AMP-dependent 2-Thiazolidinediones (Glitazones) B-Causes Anorexia, nausea, vomiting, abdominal discomfort, and diarrhea, Lactic Acidosis , Long use
(Exenatide, Liraglutide, Semaglutide, Albiglutide) protein kinase (AMPK). (Piogltazone, Rosiglitazone) decrease absorption of Vitamin B-12

4-Sulfonylurea (Glibenclamide, Glimipride) D-They bind to specific nuclear receptor (Peroxisome-Prolifrator-Activator-Receptor-Gamma = PPAR-γ) in 3-Glucagon-like peptide-1 (GLP-1) analogs C-The most common are weight gain and edema, Increased incidence of heart failure after use of these
insulin-sensitive tissues e.g. adipose, skeletal muscles & liver. These receptors modulate the expression of (Exenatide, Liraglutide, Semaglutide, Albiglutide) drugs for several years , Increase incidence of osteoporosis and fracture of long bones , Hepatotoxicity
genes involved in synthesis of cellular molecules important for lipid and glucose metabolism, tissues liver function should be monitored intermittently during treatment
differentiation and insulin signaling
4-Saxagliptin D-Causes Flatulence, diarrhea & hypoglycemia with sulfonylurea, May increase liver transaminases that is
5-Di-Peptidyl Peptidase-4 inhibitors E-Inhibit -Glucosidase on brush border of intestinal mucosa   Absorption of complex reversed on stoppage, Oral glucose (not sucrose) is given in hypoglycemia, as they impair digestion and
(Sitagliptin, Vildagliptin, Saxagliptin, Alogliptin) Carbohydrates  Postprandial hyperglycemia absorption of sucrose

6-Tirzepatide F-Subcutaneous , Synthetic analogs of Glucagon like Peptide-1 → Bind to GLP-1 receptors → reduce 5-(SGLT2) INHIBITORS E-Risk of hypoglycemia when used with sulfonylurea, Nausea is common (about 40% of patients),
postprandial glucose elevation and glucagon levels, delay gastric emptying,  insulin release & and (Canagliflozin, Dapagliflozin, Empagliflozin) anorexia, vomiting & headache, Pancreatitis, renal impairment and acute renal injury may occur,
suppress appetite Delayed gastric emptying may decrease absorption of some oral drugs, Has to be injected
7-Pramlintide G-Inhibit Di-Peptidyl Peptidase 4 (DPP-4) enzyme leading to prolongation of the action of endogenously 6-Teplizumab F-May increase Risk of heart failure, Infrequent pancreatitis
released GLP-1 and GIP
7-Metformin G-Increased incidence of genital infections and urinary tract infections , Dehydration & Hypotension, Low
8-Metformin H-Subcutaneous , Synthetic amylin analogue which reduces glucagon secretion and delays gastric incidence of hypoglycemia , Decrease mineral bone density & increase risk of fractures
emptying and decreases appetite, and reduces postprandial glucose elevation
9-Alpha-Glucosidase Inhibitors I-Inhibit glucose absorption from the proximal convoluted tubule through inhibition of specific 8-Alpha-Glucosidase Inhibitors H-Premedicate with NSAID or Acetaminophen , Anti-histamine & Anti-emetic for the first 5 days of dosing
(Acarbose, Miglitol) transporter result in glucose excretion of only 30–50% of the amount filtered causing glycosuria and (Acarbose, Miglitol)
lowers glucose levels in patients with type 2 diabetes.
9-Sulfonylurea (Glibenclamide, Glimipride I-Hypoglycemia, Hypersensitivity reactions: either local at injection site (usually subside spontaneously) or
10-Insulin J-Dual glucose dependent insulinotropic polypeptide (GIP) and glucagon like peptide-1 (GLP-1) receptor generalized , Subcutaneous Lipodystrophy , Hypokalemia, Somogyi Effect (Rebound morning
agonist hyperglycemia ), Weight gain, Resistance
11-SODIUM GLUCOSE COTRANSPORTER 2 K- Specific membrane receptors   Adenylate cyclase   cAMP,  Glycogenolysis &
(SGLT2) INHIBITORS Gluconeogenesis ,  Lipolysis & Catabolic, Counter regulatory to insulin, +ve Ino & +ve Chrono , Smooth
(Canagliflozin, Dapagliflozin, Empagliflozin) muscle relaxation. 1-I, 2-C, 3-E, 4-F, 5-G, 6-H, 7-B, 8-D, 9-A
12-Teplizumab L- Humanized Monoclonal antibody that target CD3 antigen, Deactivation of pancreatic B-Cell auto-
reactive T lymphocyte leading to increase in the proportion of regulatory T-cell, BY IV INFUSION

1-K, 2-D, 3-F, 4-B, 5-G, 6-J, 7-H, 8-C, 9-E, 10-A, 11-I, 12-L
1-Dicoumarol (Warfarin) A-Displace sulfonylureas causing Hypoglycemia 1-Teriparatide A-Its action mediated by action of Adenyl Cyclase enzyme in bone and kidney resulting in increased
formation of cyclic AMP, which is responsible for resorption of Ca from bone, and increase
2-Phenobarbitone, Phenytoin & Rifampicin B-Displaced by sulfonylurea causing bleeding , Decrease excretion of chlorpropamide
phosphate excretion by kidney.
3-B-Blockers (Propranolol) C-HME inducers increase Metabolism of Sulfonylureas
2-Abaloparatide B-It is a recombinant segment of human parathyroid hormone, administered once-daily by
4-Alcohol D-HME inhibitors decrease Metabolism of Sulfonylureas subcutaneous injection , Stimulate osteoblastic activity over osteoclastic activity leading tp Bone
formation.
5-MAO-I, Allopurinol, Cimetidine & Chloramphenicol E-Augment hypoglycemia & decrease compensatory hepatic glycogenolysis, Mask
sympathetic manifestation of hypoglycemia leading to Silent coma. 3-Bisphosphonates C-A synthetic peptide analogue of human parathyroid hormone related protein

6-Thiazides, Corticosteroids & Contraceptives F-Decrease the action of sulfonylureas 4-Denosumab D-The main site of action is GIT, Increases calcium & phosphate absorption , Regulate bone
resorption and bone formation depending on the level of calcium in Blood, Weak increase of calcium
7-Aspirin, Phenylbutazone & sulfa G-Causes hypoglycemia , enhancing hypoglycemia of sulfonylurea & phosphate reabsorption from kidney .
5-Calcitonin E-Polypeptide hormone produced and secreted by parafollicular cells of the thyroid gland in
1-B, 2-C, 3-E, 4-G, 5-D, 6-F, 7-A response to high calcium, inhibits osteoclastic activity so, it decreases bone resorption,
inhibits calcium and phosphate reabsorption by the kidney tubules

1-Methimazole A-Thyroid hormone, Stable and low cost, Long t 1/2 (7days), Given once daily, Less risk of 6-Romoszumab F-Decrease osteoclastic bone resorption through decrease in osteoclastic activation/ formation,
Increase on osteoclastic apoptosis, Inhibition of cholesterol biosynthetic pathway important for
cardiotoxicity
osteoclast function.
2-Propylthiouracil B-Thyroid hormone, Stable but higher cost, Shorter t 1/2 (24h), Multiple daily doses, Greater risk 7-Thiazide G-Monoclonal antibody that target RANKL and block osteoclast activation
of cardiotoxicity
3-Radioactive iodine (I131) C-Prodrug, inhibit thyroid hormone synthesis 8-Estrogen H-Monoclonal antibody (IgG2) that binds sclerostin leading to its inhibition which result in increase
bone formation and to lesser extent decrease bone resorption.
4-Liothyronine (T3) D-Active metabolite of ad rug , inhibit thyroid hormone synthesis
9-Glucocorticoids I-Prevent resorbing effect of P.T.H. in early menopause
5-Hydrocortisone E-Thioamides inhibit thyroid hormone synthesis and reduces conversion of T4 to T3 in the
periphery 10-Fluoride J-Diuretic, Decrease renal Ca excretion
6-Beta blockers (Propranolol) F-Inhibit thyroid hormone release by Inhibition of proteolysis of thyroglobulin , decrease the size and
vascularity of hyperplastic thyroid gland, reduce the response of thyroid gland to TSH 11-Vit.D (Calcitriol) K-Supplement with Ca known to decrease the frequency of fracture but if given IN EXCESS, it
increase frequency of fractures
7-Levothyroxine (L-T4) G-It emits Beta rays (cytotoxic) which destroy the gland tissue
12-Parathyroid hormone L-Decrease Ca absorption and Increase bone resorption
8-Iodide salts and iodine (Potassium iodide, Lugol,s H-Not used as sole therapy , Used to control peripheral manifestations of hyperactivity of the
iodine) sympathetic nervous system occurring secondary to hyperthyroidism, prevents peripheral
1-B, 2-C, 3-F, 4-G, 5-E, 6-H, 7-J, 8-I, 9-L, 10-K, 11-D, 12-A
conversion of T4 into the more active T3.
9-Carbimazole I-Used in Myxedema coma if the patient has associated adrenal or pituitary insufficiency.

1-D, 2-E, 3-G, 4-B, 5-I, 6-H, 7-A, 8-F, 9-C

1-Methimazole A-Thyroid hormone, Its absorption decreased by Food, antacids, Ca products, iron 1-Alendronate, Risedronate A-Used systemically Hypocalcemia (Rickets - Osteomalacia- in renal disease), Topically in psoriasis to
decrease cellular proliferation
2-Potassium iodide B-Thioamide causes Hepatotoxicity, Used in 1st trimester of pregnancy but contraindicated in the
remainder of the pregnancy due to associated liver failure . 2-Denosumab B-Used in hypercalcemia & osteoporosis and Paget’s disease, A special property is the relief of pain
associated with osteoporotic fracture. Therefore, may be beneficial in patients who have recently
3-Radioactive iodine (I131) C-Thioamide, Causes cholestatic jaundice , Contraindicated in 1st trimester of pregnancy due to
associated embryopathy but used in the remainder of the pregnancy . suffered a vertebral fracture, Given by SC or NASAL SPRAY.
3-Ibandronate, Zoledronic acid C-Hormonal replacement therapy in POST-MENOPAUSAL osteoporosis but it may enhance breast
4-Propylthiouracil D-Causes Dose-dependet, chronic adverse effects like metallic taste, painful salivary glands, excess
cancer
salivation, running eyes & nose, sore throat, cough and diarrhea, Its effect starts in 1-2 days and is
maximum in 10 - 14 days, then benefit declines even with continuous administration (compensatory 4-Abaloparatide D-Hormonal replacement therapy in POST-MENOPAUSAL osteoporosis with NO breast or uterine
↑ in TSH). cancer
5-Levothyroxine (L-T4) (NOT Liothyronine T3) E-Causes Hypothyroidism (The chief toxic effect), Thyroid storm (release of thyroid hormone), 5-Selective Estrogen Receptor Modulator E-A recombinant segment of human parathyroid hormone, Anabolic agent given SC , used in steroid
Patient may require repeated doses, Contraindicated in pregnancy , Lactation and Young age. induced osteoporosis and Post-menopausal women with osteoporosis, RESERVED for patient
at high risk of fracture.
1-C, 2-D, 3-E, 4-B, 5-A
6-Vit.D F-A synthetic peptide analogue of human parathyroid hormone related protein, Used to reduce the
risk of vertebral and non-vertebral fractures in post-menopausal women with osteoporosis.
1-Thioamides A-Used as Replacement therapy in hypothyroidism, TSH suppression therapy in thyroid cancer and
nontoxic goiter 7-Calcitonin G-Monoclonal antibody that target RANKL and block osteoclast activation, Used by SC injection in
treatment of Post-menopausal osteoporosis in women at high risk of fracture, Should be
2-Iodide salts and iodine (Potassium iodide, Lugol,s B-THE PRINICIPLE THERAPY of hyperthyroidism, As adjuvant to I131 to control the disease while
iodine) waiting its effect, To control the disorder in preparation for surgical treatment, Thyroid storm (Inhibit reserved for women INTOLERENT OR UNRESPONSIVE to other osteoporosis agents
hormone synthesis) 8-Estrogen H-Monoclonal antibody (IgG2) that binds sclerostin leading to its inhibition , Used by SC injection in
3-B-blocker (Propranolol) C-Used as Prophylactic where goiter is endemic, Preparation of the patient for thyroidectomy , treatment of Post-menopausal osteoporosis in women at high risk of fracture
Thyroid crisis (storm) (inhibit hormone release).
9-Teriparatide I-ORAL bisphosphonate, Approved for treatment and prevention of osteoporosis.
4-Hydrocortisone D-Used in Hyperthyroidism in adults over 45 years, Hyperthyroidism in patients not fit for surgery,
Recurrence after medical or surgical treatment , Thyroid cancer 10-Romoszumab J-INTRAVENOUS bisphosphonate, For patient intolerable to ORAL preparations, Approved for
treatment and prevention of osteoporosis
5-Radioactive iodine (I131) E-Not used as sole therapy , Used to control peripheral manifestations of hyperactivity of the
sympathetic nervous system occurring secondary to hyperthyroidism, prevents peripheral
conversion of T4 into the more active T3. 1-I, 2-G, 3-J, 4-F, 5-D, 6-A, 7-B, 8-C, 9-E, 10-H

6-Levothyroxine (L-T4) F-Used in Myxedema coma if the patient has associated adrenal or pituitary insufficiency.

1-B, 2-C, 3-E, 4-F, 5-D, 6-A

1-Parathyroid hormone A-Cause Esophagitis and esophageal ulcer , Should be administered with 1 liter of water and patient 1-Gonadotropin releasing A-GnRH Analogues , Given continuously to inhibit gonadotropins release , reduced production of androgens and estrogens, USED in
hormone Cancer prostate, Uterine fibroids , Endometriosis, Precocious puberty, given I.V., S.C. or nasal spray
should stay in upright position for at least 30 minutes after taking it, CONTRAINDICATED IN
Renal impairment and Peptic ulcer 2-Reserpine, α-methyl dopa B-Synthetic analog of somatostatin, Its half-life is longer than that of the natural compound, USED in Bleeding esophageal varices (IV
infusion ), Diarrhea and flushing associated with carcinoid tumors, Acromegaly
2-Calcitonin B-It causes Increased risk of infections, 2ry malignancies, hypocalcemia and dermatological
reactions. 3-Growth hormone-inhibiting C-A recombinant human growth hormone, It increases growth via stimulating the production of somatomedins, It stimulates protein
hormone (Somatostatin) synthesis and lipolysis, USED to promotes growth in Pituitary dwarfism (GH deficiency), as replacement therapy prior to epiphyseal
3-Vit.D C-It Increases blood Ca and Mg level , Decrease urinary Ca level, Reduce blood phosphate level , closure.
Increase urinary phosphate level
4-Prolactin D-Gonadotropins, has FSH & LH activity, USED in treatment of infertility, given by SC or IM injections.

-Chronic elevation of its level will deplete bone stores of Ca, However, intermittent exposure to it 5-Syntocinon E-Gonadotropins, has LH activity, USED in treatment of infertility, given by SC or IM injections.
will activate osteoblasts more than osteoclasts. 6-Human menopausal F-Dopamine antagonists , increase the secretion of prolactin (Hyperprolactinemia), associated with galactorrhea and hypogonadism
gonadotropin (hMG) (amenorrhea-galactorrhea syndrome).
4-Denosumab D-It Decreases blood Ca level, Increases urinary Ca level, Decreases blood phosphate level, Increases
urinary phosphate level 7-Vasopressin G-Drugs decreasing dopamine level (decrease release), increase the secretion of prolactin (Hyperprolactinemia), associated with
galactorrhea and hypogonadism (amenorrhea-galactorrhea syndrome).
5-Oral Bisphosphonate E-It Increases blood Ca level, Decreases urinary Ca level, Increases blood phosphate level, Decreases
(Alendronate, Risedronate ONLY) urinary phosphate level. 8-Somatotropin H-D2 receptor agonists, Used in treatment of Hyperprolactinemia

9-Octreotide I-Has both antidiuretic and vasopressor effects, it binds to the V2 receptor to increase water permeability
-If calcium level is normal → it acts on osteoblasts (bone hardening). and reabsorption in the collecting tubules, Causes vasoconstriction through V1 receptor, USED in the management of diabetes
-If calcium level is low → it acts on osteoclasts → increases bone resorption → increases insipidus, Cardiac arrest and In controlling bleeding due to esophageal varices, given by (SC / IM / IV)
Ca++ level in blood
10-Metoclopramide, J-An analog of Vasopressin Long acting, Mainly antiduretic through V2 receptor, minimal activity at the V1 receptor , largely free of
Risperidone vasopressor effects, preferred for the treatment of diabetes insipidus and nocturnal enuresis, given by (intranasal, IV infusion,
1-C, 2-D, 3-E, 4-B, 5-A oral).

11-Human chorionic K-Synthetic derivative of oxytocin, USED in induction of labor in uterine inertia (by I.V route) , control of postpartum hemorrhage
gonadotropin (hCG) (by I.M route), Impaired milk ejection (by nasal spray)
1-Ergosterol (D2) A-It is synthesized Vit.D preparation and used for secondary hyperparathyroidism due to renal
12-Desmopressin L-Endogenous hormone secreted in the hypothalamus, D-cells of pancreas and in the gut, It binds to receptors in the pituitary that
failure, requires hepatic activation to active metabolite, NOT effective in patient with liver
suppress GH and thyroid-stimulating hormone release, It also inhibits the release of insulin, glucagon, and gastrin
disease
13-Leuprolide, Nafarelin M-Endogenous hormone, Pulsatile secretion of it from the hypothalamus is essential for the release of the follicle-stimulating
2-Cholecalciferol (D3) B-The Most active form of Vit.D, DOESN’T require hepatic activation
hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, However, continuous administration of it inhibits
3-Alfacalcidol (One-alpha =1α-hydroxycholecalcifrol) C-Vit.D from plant origin FSH & LH release through down-regulation of its receptors on the pituitary.
4-Calcitriol (1, 25-dihydroxycholecalcifrol) D-Vit.D from animal source and can be synthesized in the skin from 7- dehydrocholesterol by 14-Cabergoline,Bromocriptine. N-Endogenous hormone, Stimulates milk production , Its secretion is inhibited by dopamine acting at D2 receptors
exposure to ultraviolet rays
15-Oxytocin O-Endogenous hormone, Stimulates the contraction of pregnant uterus and is reflexly released from pituitary following suckling to
contract myo-epithelium of breast
1-C, 2-D, 3-A, 4-B
1-M, 2-G, 3-L, 4-N, 5-K, 6-D, 7-I, 8-C, 9-B, 10-F, 11-E, 12-J, 13-A, 14-H, 15-O

1-Hydrocortisone (cortisol) A-Rarely used clinically steroid hormone synthesized and secreted from Zona glomerulosa, Its release controlled by 1-Norgestrel A-Natural estrogens, steroids, undergo first- pass metabolism and so when taken orally have low bioavailability.
Renin-Angiotensin System activation by hypovolemia & hyponatremia and Hyperkalemia 2-Mifepristone B-Semisynthetic estrogens , Steroidal synthetic, Highly potent, taken orally
2-Prednisone B-Aldosterone Antagonist , useful as K+-Retaining diuretic especially in cases of hyper-aldosteronism. 3-Clomiphene Citrate C-Semisynthetic estrogens , Steroidal synthetic, Fat soluble, stored in adipose tissue,long duration, rapidly oxidized
3-Dexamethasone C-Pure mineralocorticoid with NO glucocorticoids activity, 1/100 activity of aldosterone, Used to replace 4-Misoprostol D-Synthetic estrogens, Non-steroidal, Effective orally
mineralocorticoid activity in Addison’s disease, NOT effective orally due to extensive hepatic first pass metabolism
5-Exemestane E-Natural Progestogen, Rapidly Metabolized , Given by IM injection
4-Pasireotide D-Synthetic mineralocorticoid, Mineralocorticoid (125 X Cortisol) & Glucocorticoid (10 X Cortisol) activities, Useful
orally (0.1 – 0.3 mg) to replace mineralocorticoid activity in Addison’s disease 6-Danazol F-Synthetic progestin preparation, Derivatives of progesterone, Given Orally or IM

5-Cyproheptadine E-Active , Short acting , Equal glucocorticoid (anti-inflammatory) & mineralocorticoid (salt-retaining) activities 7-Raloxifene G-Synthetic progestin preparation, Derivatives of nortestosterone (androgenic precursor), Given Orally

6-Prednisolone F-Pro-drug, Short acting , Equal glucocorticoid (anti-inflammatory) & mineralocorticoid (salt-retaining) activities 8-Letrezole H-Synthetic progestin preparation, Derivatives of nortestosterone (androgenic precursor), Given Orally or SC IMPLANT

7-Cabergoline, Bromocriptine G-Pro-drug, Intermediate acting, Mainly glucocorticoid with Less mineralocorticoid activities, The only glucocorticoid 9-Medroxyprogesterone I-Selective Estrogen Receptor Modulator, Used in treatment of metastatic Breast Cancer and as adjuvant therapy after mastectomy
acetate or radiation BUT may INCREASE RISK OF ENDOMETRIAL CANCER, Increase risk of DVT & pulmonary embolism and causes hot
that has no effect on the fetus in pregnancy
flush
8-Metyrapone (Mitopirone) H-Active, Intermediate acting, Mainly glucocorticoid with Less mineralocorticoid activities
10-Progesterone, J-Selective Estrogen Receptor Modulator, Effective for prevention & treatment of osteoporosis and Reduction in risk of breast cancer,
9-Cortisone I-Long acting, Only glucocorticoid with ABSENT mineralocorticoid activities. Hydroxyprogesterone NO EFFECT ON ENDOMETRIUM BUT it increases risk of venous thromboembolism and doesn't relieve Post-Menopausal hot
caproate flushes
10-Mitotane J-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 11-Ethinyl estradiol K-Estrogen Receptor Modulators at estrogen receptors, Used as Ovulation-inducing agent

11-Aminoglutethimide 12-Tamoxifen L-Steroidal aromatase Inhibitor, binds permanently to aromatase enzyme (suicide inhibition), Inhibits estrogen synthesis, Has
K-Long-acting dopamine D2 receptor agonist used primarily to treat hyperprolactinemia, also inhibits ACTH
androgenic side effect
secretion from corticotroph tumors (off-label use).
13-Norethindrone M-Non-steroidal aromatase Inhibitor, bind reversibly to aromatase, Inhibits estrogen synthesis, Can be used in treatment of breast
12-Ketoconazole L-Antihistamine (H1-blocker) + Anti-serotonin, Suppresses release of A.C.T.H.
cancer & induction of ovulation, devoid from the androgenic side effect of Steroidal aromatase Inhibitor
13-Spironolactone M-Anti-fungal, Inhibits adrenal steroid hormone synthesis when used in larger doses, Useful in Cushing’s disease. 14-Mestranol N-Inhibits the activity of progesterone, binds to progesterone receptors with no progesterone activity (progesterone antagonist), also
14-Desoxycorticosterone Acetate N-Inhibits 11--Hydroxylase enzyme selectively , inhibit Synthesis of BOTH Aldosterone & Cortisol increasing binds to glucocorticoid receptors, very effective in terminating early pregnancy, used as postcoital contraceptive
Desoxycorticosterone Trimethyl ACTH, Used in Cushing’s disease and Test the function of anterior pituitary to secrete A.C.T.H 15-Diethylstilbestrol O-Prostaglandin analog , administered orally or intravaginally, induce uterine contractions
Acetate
16-Estradiol P-Weak androgen, anti-progestin and anti-estrogenic effects, Inhibits the mid-cycle surge of LH and FSH, but with no effect on basal
15-Fludrocortisone Acetate O-Destruction of adrenocortical cells, Useful in Cushing’s disease & Inoperable adrenocortical carcinoma.
level, Inhibits steroid synthesis in the ovary : reduces ovarian function leading to atrophic changes in the endometrium,
16-Aldosterone P-It causes a reduction in the synthesis of all hormonally active steroids, it inhibits conversion of Cholesterol into Used in treatment of endometriosis & fibrocystic disease of breast.
Pregnenolone (First step in steroidogenesis), Used in patients with Cushing’s syndrome due to adrenocortical 1-H, 2-N, 3-K, 4-O, 5-L, 6-P, 7-J, 8-M, 9-F, 10-E, 11-B, 12-I, 13-G, 14-C, 15-D, 16-A
cancer

1-E, 2-G, 3-I, 4-J, 5-L, 6-H, 7-K, 8-N, 9-F, 10-O, 11-P, 12-M, 13-B, 14-C, 15-D, 16-A
1-Letrezole A-Non-steroidal compound used to induce ovulation, blocks Estrogen Receptors in hypothalamus preventing the usual negative
feedback effect of estrogen on GnRH leading to increased FSH, it may cause Ovarian enlargement Multiple Ovulation &
multiple pregnancies

2-Dihydrotestosterone B-It has FSH and LH activities , Its use must be followed by human chorionic gonadotrophin with LH activity only for induction of
ovulation
3-Testosterone propionate , C-It lowers insulin, androgen and cholesterol levels, It is useful in restoring regular menstrual cycle and starting ovulationin about
Methyl testosterone 50% of women with polycystic ovary syndrome

4-Flutamide, Cyproterone D-Aromatase inhibitor, inhibits estrogen synthesis leading to increase in GnRH release and FSH release inducing ovulation, Better to
be given with small dose of FSH
5-Nandrolone, E-Natural androgens, rapidly metabolized in liver, so ineffective orally
Methandrostenolone
6-Human Menopausal F-Synthetic androgens, given by sublingual, I.M. or S.C.
Gonadotrophins
7-Spironolactone G-Anabolic Steroids, used in osteoporosis, general wasting, acute renal failure and aplastic anemia, Cause In children Precocious
puberty & In women virilization (Acne, hirsutim, voice change)
8-Androsterone , Testosterone H-Inhibits conversion of testosterone into di-hydro-testosterone by inhibiting 5α-reductase, so it blocks action of androgen on tissues
requiring dihydrotestosterone (prostate and hair follicles). It is given orally to reduce benign prostatic hyperplasia (BPH).

9-Metformin I-Compete with testosterone for receptors, Used in hypersexuality in males and in hirsutism, and in cancer prostate

10-Clomiphene citrate J-A competitive inhibitor of aldosterone, also competes with di-hydro-testosterone for the androgen receptors in target tissues. It
also reduces 17α-hydroxylase activity, lowering plasma levels of testosterone and androstenedione. It is used in treatment of
hirsutism in women

11-Finasteride K-Active metabolite of Testosterone , results from the action of reductase enzyme on Testosterone, ALL tissues require this active
metabolite EXCEPT skeletal muscles doesn’t require this active form.

1-D, 2-K, 3-F, 4-I, 5-G, 6-B, 7-J, 8-E, 9-C, 10-A, 11-H
 ENDOCRINE EXPLAIN WHY Qs
1-Thiazides & Diazoxide inhibit release of insulin / Contraindicated in Diabetic patients 8-Hypoglycemia is the most common adverse effect of insulin

Thiazides & Diazoxide ------> Open K--channels-----> Hyperpolarization-------> Inhibit Release. Due to:
2-Insulin causes Hypokalemia. / Used in Hyperkalemia due to renal failure/ it is essential to True Hyper-insulinism:
- Too much or bad timing of insulin.
monitor K level when treating DKA with insulin.
Relative Hyper- insulinism:
Because it ↑ potassium uptake into cells -----> HYPOKALEMIA. -Too little food intake or missing meal.
- Too much muscular exercise
3-Insulin NOT essential (But NOT Contraindicated) in patients with N.l.D.D.(Non-Insulin
Dependent DM = Type 2 DM). 9-Rebound morning hyperglycemia can occur following insulin- induced hypoglycemia during
night.
Because patients with type 2 DM still have a FUNCTIONING B-cells that can produce insulin, the
major problem in this type is INSULIN RESISTANCE so these patients can be managed with Diet
Due to excess release of counter-regulating hormones (Glucagon, Catecholamines, Etc.). and this
control, life style change & oral hypoglycemic, so insulin is not essential in this condition, BUT if
is Avoided by reducing the evening dose of insulin.
the previous lines of treatment FAILED to control DM -----> INSULIN IS GIVEN.
10-Insulin causes weight gain
4-Insulin is essential & a true replacement therapy in patients with l.D.D.(Insulin Dependent
DM= Type 1 DM).
Because:
- It is ANABOLIC: ↑ amino acids uptake by Muscle, ↓ protein catabolism, ↑ protein synthesis.
Because these patients have a COMPLETELY DESTROYED B-CELLS due to AUTOIMMUNE DISEASE
-It ++ Lipogenesis by ++ of lipoprotein lipase & inhibit Lipolysis by inhibition of Triglyceride lipase.
OR VIRAL INFECTION that destroys the B-cells of pancreas, So, NO INSULIN IS PRODUCED.
11-Sulfonylurea is used in Type 2 DM not Type 1 DM.
5-Insulin is used in STRESS periods ( e.g.Infection,Operation & Pregnancy) in patients with type
2 DM NOT oral hypoglycemics.
Because it is SECRETAGOUGE needs a FUNCTIONING B-cells (about 30 % functioning B-cells), in
Type 1 DM ----> B-cells are completely destroyed.
Because in stress condition -----> HYPERGLYCEMIA is MARKED -----> so it needs a large amount of
1- They depend on the presence of endogenous insulin (about 30% functioning B-cells):
insulin to be produced to overcome this marked elevation, in these patient of type 2 DM the B-
a- They Block ATP-sensitive K+-channel (KATP-Channels) of B-Cells of Pancreas →Depolarization
cells of pancreas do its best to produce insulin to lower this hyperglycemia which is NOT
→ Influx of Ca++ → Exocytosis →↑Release of Insulin.
ENOUGH , so if u give ORAL HYPOGLYCEMICS it won't add any extra effect because the B-cells
b- Sensitize B-Cells to effect of Glucose →↑Release of insulin.
become EXHAUSTED & can't produce more insulin , so in these condition INSULIN IS USED.
c- Inhibit release of catecholamines (Anti-insulins) →↑Release of insulin.
2- ↓release of Glucagon (Directly or through ↑Insulin & Somatostatin).
Additional reason, IN PREGNANCY ----> Oral hypoglycemics are teratogenic + cause fetal
3- Extra-pancreatic effect →↑ No. & sensitivity of insulin receptors →Potentiate peripheral
hypoglycemia, so insulin is used.
actions of Insulin e.g. Anti-lipolytic & Anti glycogenolytic effects.
6-In insulin therapy, frequent change site of injection is recommended
12-Sulfonylurea is used in NON-OBESE type 2 DM
In order to avoid occurrence of Subcutaneous Lipodystrophy ------> Lipo-hypertrophy or Lipo-
Because it
atrophy.
-↑ Insulin release which ANABOLIC.
-STIMULATEs APPETITE
7-Insulin resistance can occur with insulin therapy.
13-Sulfonylurea shows many drugs interactions
Due to high activity of insulinase enzyme or over production of Insulin antibodies.
Because it is:
-highly bound to plasma proteins.
-Metabolized in liver so affected by HME inhibitors & inducers.
14-Sulfonylurea is contraindicated in pregnancy & lactation. 22-Sulfonylurea dose should be adjusted when given with (MAO-I, Allopurinol, Cimetidine &
Chloramphenicol)
Because it Crosses placenta, stimulate fetal β-cells to release insulin → fetal hypoglycemia at
birth + it is TERATOGENIC. Also, it is excreted in milk. Because Sulfonylurea is metabolized by liver, (MAO-I, Allopurinol, Cimetidine &
Chloramphenicol) ------> INHIBIT HME -----> DECREASE Metabolism of Sulfonylureas. ----->
15-Sulfonylurea is contraindicated in sever Hepatic & Renal Disease HYPOGLYCEMIA.

Because it is METABOLIZED IN LIVER & EXCRETED IN URINE so if given in these conditions -----> 23-It is NOT preferred to give PROPRANOLOL with sulfonylurea
WILL NOT BE METABOLIZED OR EXCRETED -----> ACCUMULATION -----> HYPOGLYCEMIA.
Because Propranolol:
16-Sulfonylurea causes weight gain a- Augment their hypoglycemia & decrease compensatory hepatic glycogenolysis.
b- Mask sympathetic manifestation of hypoglycemia ------> Silent coma
Because it
-↑ Insulin release which ANABOLIC. 24-Sulfonylurea dose should be adjusted when given with (Thiazides, Corticosteroids &
-STIMULATEs APPETITE Contraceptives).
-Chlorpropamide----> Anti-Diuretic effect -----> Edema.
Because these drugs cause HYPERGLYCEMIA so they DECREASE action of sulfonylurea.
17-Chlorpropamide is not used nowadays.
25-Meglitinides are preferred over sulfonylurea in controlling post prandial hyperglycemia. /
Because of: Advantages of Meglitinides over sulfonylurea
-Bone marrow inhibition.
-Cholestatic jaundice. Because:
-Disulfiram-like action -----> Alcohol intolerance. -They have Rapid onset of action (Peak = t hour) & Short t1/2 = 2-3 hours.
-Edema due to its anti-diuretic effect. - Less liable to produce hypoglycemia & weight gain

18-Failure of sulfonylurea on long use 26-Metformin is Euglycemic./ used in Type 2 DM

Due to exhaustion of B-Cells 1- They do NOT stimulate the release of insulin → No hypoglycemia BUT euglycemia.
2- Decrease hepatic gluconeogenesis
19-Sulfonylurea dose should be adjusted when given with (Aspirin, Phenylbutazone & sulfa). 3-Increase anaerobic glycolysis in peripheral tissues →↑ Removal of glucose from the blood →
BUT↑ Lactic acid production.
Because Sulfonylurea is highly bound to plasma protein , so Aspirin, Phenylbutazone & sulfa 4-Increase sensitivity of tissues to insulin by ↑binding to its receptors.
------> Displace sulfonylureas ------> Hypoglycemia. 5- Decrease glucose absorption from the intestine.
6-. Increase glucose uptake by skeletal muscle
20-Oral Anti-coagulant dose should be adjusted when given with Sulfonylurea 7- Decrease release of Glucagon.

Because Sulfonylurea is highly bound to plasma protein, so Sulfonylureas -------> Displace Oral 27-Metformin is used in OBESE type 2 DM
anticoagulants -------> Bleeding.
Because
21-Sulfonylurea dose should be adjusted when given with (Phenobarbitone, Phenytoin & 1-It INHIBITS APPETITE & causes ANOREXIA.-----> weight loss
Rifampicin). 2-It Decrease glucose absorption from the intestine.

Because Sulfonylurea is metabolized by liver, Phenobarbitone, Phenytoin & Rifampicin ------>

INDUCE HME -----> INCREASE Metabolism of Sulfonylurea
28-Metformin is contraindicated in renal failure/ Hepatic failure / Hypoxic state (COPD, HF, 34-All patients receiving Glitazones should have liver functions "frequently" monitored
PULMONARY EDEMA & SHOCK).
Because of Hepatotoxicity
Due to:
- Fear of increasing risk of LACTIC ACIDOSIS, as metformin increase ANAEROBIC GLYCOLYSIS in 35-Pioglitazone is contraindicated in Class III/IV heart failure
peripheral tissues ------> LACTIC ACID FORMATION.
*In renal failure ------> Can't Excrete Lactic Acid. Because it may cause fluid retention
*In hepatic failure ------> Can't metabolize lactic acid.
*In Hypoxic State -----> More enhancement of ANAEROBIC METABOLISM -----> MORE lactic acid 36-The thiazolidinediones are useful in treating type II diabetes
formation.
*In Heart failure -----> LOW COP-----> Decrease Renal blood flow so can’t excrete lactic acid + Because The TZDs are insulin sensitizers. They bind to specific nuclear receptor (Peroxisome-
Decrease tissue oxygenation (hypoxia) so enhance anaerobic metabolism. Proliferator-Activator- Receptor-Gamma = PPAR-γ) -----> in insulin-sensitive tissues e.g. adipose,
sk.m. & liver -----> Gene expression ------> synthesis of cellular molecules important for insulin
29-Long use of metformin causes vit B12 deficiency signaling e.g. Lipoprotein lipase enzyme & Glut-4; they do not alter insulin secretion or
degradation but act to increase glucose uptake in adipose and muscle.
Because metformin DECREASE ABSORPTION OF VIT. B12.
37-Thiazolidinediones (glitazones) increase incidence of osteoporosis and fracture of long
30-Metformin is the first choice in treatment of type 2 DM bone

Because it has the following advantages: Because it decreases osteoblast formation.

-No risk of hypoglycemia
-No weight gain 38-Thiazolidinediones (glitazones) cause weight gain.
- has prominent lipid-lowering activity
-Inexpensive. Due to increased body fat and edema. BOTH are dose dependent, Adding sulfonylurea or insulin
increase both.
31-2nd generation sulfonylurea (Glipizide, Glyburide, Glimepiride) is preferred over 1st
generation 39-Acarbose & Miglitol are useful in type 2 DM.

Because it : Because they:

- Is More potent than first generation -Are Reversible inhibitors of intestinal α-glucosidases in intestinal brush border cells that are
-Have longer duration of action. responsible for carbohydrate digestion.
-Less frequency of administration -Decrease carbohydrate digestion and glucose absorption in small intestine (lower postprandial
-Have fewer adverse effects glucose level).
-Have fewer drug interactions
40-Concurrent use of Acarbose & Miglitol with metformin should be avoided.
32-Metformin should be taken with meals and should be started at a low dose then increase
gradually. Because they DECREASE ABSORPTION of metformin, DECREASE its bioavailability.

To avoid GIT side effects (Metallic taste in the mouth, nausea, vomiting, and diarrhea). 41-If a type 2 diabetic patient receives (Miglitol or Acarbose) & (Sulfonylurea) and
Hypoglycemia occur, it should be corrected with monosaccharide sugar "glucose tablet or gel"
33-The effect of Thiazolidinediones (glitazones) appear after 1-2 months NOT sucrose.

Because They bind to specific nuclear receptor (Peroxisome- Proliferator-Activator- Receptor- Because (Miglitol or Acarbose) Are Reversible inhibitors of intestinal α-glucosidases in intestinal
Gamma = PPAR-γ) -----> in insulin-sensitive tissues e.g. adipose, sk.m. & liver -----> Gene brush border cells that are responsible for carbohydrate digestion, so if u give a complex
expression ------> synthesis of cellular molecules important for insulin signaling e.g. carbohydrate, it won't be absorbed so hypoglycemia WILL NOT BE IMPROVED.
Lipoprotein lipase enzyme & Glut-4, so the onset is relatively slow.
42-Exenatide & Liraglutide are given S.C. NOT ORALLY 49-(Canagliflozin- Dapagliflozin- Empagliflozin) show increased incidence of genital infections
and urinary tract infections.
Because they are Synthetic analogs of Glucagon like Peptide-1 (GLP-1), an incretin released from
GIT after a meal -----> PROTEIN -----> if given orally --------> undergo DIGESTION. Because They inhibit SGLT-2 which is responsible for reabsorption of 90% of glucose ------>
glucose excretion of only 30 50% of the amount filtered causing GLUCOSURIA ------> Glucose is a
43-Exenatide & Liraglutide are used as an adjunctive therapy to control glycemia in patients good media for bacterial growth ---->increased incidence of infection.
with type 2 diabetes.
50-SGLT2 inhibitors may cause hypotension.
Because they are Synthetic analogs of Glucagon like Peptide- 1 (GLP-1), an incretin released from
GIT after a meal -----> Bind to GLP-1 receptors ------> delayed gastric emptying, INCREASE insulin Due to their osmotic diuretic effect.
release & DECREASE secretion of glucagon & suppresses appetite.
51-Glucagon is Useful SC & lM in treatment of Hypoglycemic coma when lV Glucose is not
44-Exenatide & Liraglutide may show some drug interactions available

Because They cause DELAY IN GASTRIC EMTYING through BINDING TO GLP-1 RECEPTORS ------> Because it:
so DECREASE absorption of RAPIDLY disintegrated drugs (e.g. paracetamol) and INCREASE ++ Specific membrane receptors -----> ++ Adenylate cyclase --→ ++ cAMP:
absorption of SLOWELY disintegrated drugs (e.g. Digitalis). *++ Glycogenolysis & Gluconeogenesis (in liver Not skeletal muscle) ----> INCREASE Glucose.
* Anti-Insulin ------> Decrease Glucose uptake & utilization by peripheral tissues
45-DPP-4 inhibitors (Sitagliptin , Vildagliptin , Saxagliptin) are used in type 2 DM.
52-Glucagon can be used in Heart failure due to over dose B-blockers.
Because they Inhibit Di-Peptidyl Peptidase lV (DPP-IV) enzyme (DPP-4 is an enzyme that breaks
down incretin hormones) ------> accumulation of GLP-1 -------> Bind to GLP1 receptors ------> Because it:
delayed gastric emptying, INCREASE insulin release & DECREASE secretion of glucagon & ++ Specific membrane receptors -----> ++ Adenylate cyclase → ++ cAMP ------> ++ Heart ------>
suppresses appetite. +ve Inotropic & +ve Chronotropic effects.

46-Pramlintide is given by S.C. rout NOT ORALLY 53-Glucagon is Useful before radiological examination of bowel.

Because it is a synthetic amylin analog (Amylin is a pancreatic hormone secreted from B-lslet Because it:
cells) -----> PEPTIDE -----> if taken orally ------> undergo DIGESTION. ++ Specific membrane receptors -----> ++ Adenylate cyclase → ++ cAMP --------> Smooth muscle
relaxation.
47-Pramlintide is used as an adjunct to mealtime insulin therapy in patients with Tvpe 1 or
Type 2 diabetes 54-A 45-year-old female with past history of type II diabetes mellitus presents for routine
follow-up. Her fasting blood sugars are controlled in the 80–100 range. However, on lab report
Because it is a synthetic amylin analog (Amylin is a pancreatic hormone secreted from B-lslet the hemoglobin A1c is elevated at 8.5. The GP assumes that she needs better control of her
cells and through its circulation to the brain it reduces gastric emptying, inhibit glucagon release mealtime glucose. She is already taking oral biguanides and oral sulphonylureas.The specialist
and promotes satiety -----> decreased food intake). prescribed her insulin aspart.
Explain why insulin aspart is better than insulin detemir to control mealtime glucose?
48-(Canagliflozin- Dapagliflozin- Empagliflozin) are used as a third line therapy for diabetes
mellitus nowadays. Answer:
Insulin aspart is a rapid acting insulin ideal for mealtime glucose control
Because They inhibit SGLT-2 which is responsible for reabsorption of 90% of glucose ------> as its onset is 5–15 minutes and duration are on average 2–3 hours.
glucose excretion of only 30 50% of the amount filtered causing glycosuria and lowers glucose detemir insulin have longer durations of action and may combine with the oral sulfonylurea and
levels in patients with type 2 diabetes. insulin glargine to cause hypoglycemia later on.
55-Glucocorticoids cause hyperglycemia. / Contraindicated in Diabetic patients 63-Glucocorticoids are anti-inflammatory. / Used in treatment of inflammatory diseases
(Encephalitis, cerebral edema &++ Intra-cranial pressure, Rheumatic carditis, Chronic active
Because they: hepatitis, Nephritis & nephritic syndrome, Arthritis).
-Stimulate GLUCONEOGENESIS.
- Anti-insulin effect----->Decrease Glucose uptake & utilization by peripheral tissues. Because they:
-Synthesis of a Lipocortin-1 = Annexin-1------> INHIBIT Phospholipase A2 enzyme -----> DECREASE
56-Glucocorticoids cause Moon face & Buffalo hump appearance Arachidonic acid -------> DECREASE PGs, LTs & P.A.F.
-Repress genes of COX-Il, inducible NOS, adhesion molecules & complement components.
Because they Stimulate lipolysis ------> Lipemia ------> Redistribution of fat. - INHIBIT Formation of other inflammatory mediators & cytokines e.g. ILs, TNFα & CSF.
- SUPPRESS Migration of leukocytes to site of inflammation.
57-Glucocorticoids delay wound healing. - Stabilization of lysosomal membrane -----> INHIBIT Cell death.
- DECREASE Capillary permeability ------> DECREASE Inflammatory edema & joint effusion
Because they have CATABOLIC EFFECT on FIBROBLAST & CONNECTIVE TISSUES.
64-Addison's disease characterized by ANEMIA
58-Glucocorticoids should be stopped gradually not suddenly
Because in this condition, there is a low level of glucocorticoids (Hypocortisolemia) ----->
Because they INHIBIT PITUTARY ACTH so sudden withdrawal -----> ADDISONIAN CRISIS. decrease in ERYTHROPOIESIS & DECREASE RELEASE OF RBC'S FROM BONE MARROW.

59-Glucocorticoids worsen peptic ulcer. / Contraindicated in patients with peptic ulcer. 65-Glucocorticoids have an anti-shock & anti-stress function

Because they INCREASE GASTRIC HCL SECRETION & DECREASE MUCIN SECRETION. Because they cause:
-Hypernatremia------>Hypervolemia ------> INCREASE (C.O.P & BL.PR.)
60-Glucocorticoids cause OSTEOPOROSIS -Hyperglycemia & INCREASE Glycogen content in liver.
-INCREASE Sympatho-adrenal discharge.
Because they have CATABOLIC EFFECT ON BONE & ANTI-VIT D EFFECT -------> DECREASE Ca -C.N.S. stimulation ------> Sense of wellbeing & adaptive effect to stress.
absorption from GIT ------> (HYPOCALCEMIA).
66-Glucocorticoids may lead to thrombo-embolic disorders
61-CUSHING'S disease characterized by polycythemia
Because they INCREASE PLATLETS & COAGUALBILTY OF BLOOD & POLYCYTHEMIA DUE TO ++ OF
Because in this condition, there is excess glucocorticoids (Hypercortisolemia) ------> ++ ERYTHROPOIESIS AND ++ RELEASE OF RBC'S FROM BONE MARROW -----> INCREASE BLOOD
ERYTHROPOIESIS & ++ RELEASE OF RBC'S FROM BONE MARROW. VISCOSITY.

62-Glucocorticoids are anti-allergic (used in bronchial asthma) & immune-suppressant (used in 67-Glucocorticoids worsen DIGITALIS TOXICITY.
Auto-immune disease & organ transplantation). Because they have mineralocorticoid effect ------> salt and water retention with K depletion---->
HYPOKALEMIA that worsen digitalis toxicity.
Because they:
- INHIBIT Antibody formation. 68-Glucocorticoids are used in GOUTY ARTHRITIS
- INHIBIT Antigen / Antibody reaction.
- Stabilization of mast cell ------>INHIBIT Degranulation - -----> INHIBIT Release of allergic Because they are:
mediators. 1- Anti- INFLAMMATORY:
- DECREASE Tissue response to allergic mediators. -Synthesis of a Lipocortin-1 = Annexin-1------> INHIBIT Phospholipase A2 enzyme -----> DECREASE
- DECREASE Lymphocytes ------> Lymphopenia (Catabolic effect on lymphoid tissues). Arachidonic acid -------> DECREASE PGs, LTs & P.A.F.
-Repress genes of COX-Il, inducible NOS, adhesion molecules & complement components.
- INHIBIT Formation of other inflammatory mediators & cytokines e.g. ILs, TNFα & CSF.
- SUPPRESS Migration of leukocytes to site of inflammation.
- Stabilization of lysosomal membrane -----> INHIBIT Cell death.
- DECREASE Capillary permeability ------> DECREASE Inflammatory edema & joint effusion.
2-Have a URICOSURIC EFFECT------> INCREASE URIC ACID EXCRETION.
69-Glucocorticoids cause weight gain. 75-Glucocorticoids are contraindicated in pregnancy

Because: Because:
-They have mineralocorticoid effect ------> salt and water retention-----> EDEMA. 1-TERATOGENIC
- They Stimulate lipolysis ------> Lipemia ------>Redistribution of fat -----> MOON FACE & BUFFALO 2-They RETARD FETAL DEVELOPMENT as:
HUMP APPEARANCE. *They have CATABOLIC EFFECT on FIBROBLAST & CONNECTIVE TISSUES.
-Increase Appetite *They have CATABOLIC EFFEC ON BONE
*They have CATABOLIC EFFECT on muscle proteins ----> WASTING & MYOPATHY.
70-Repeated intra-articular injection of Glucocorticoids is contraindicated. 3-Predispose pregnant woman to OSTEOPOROSIS as they have ANTI-VIT D EFFECT ---->DECREASE
Ca absorption from GIT (HYPOCALCEMIA).
Because they cause SUB-LAXATION OF JOINTS DUE TO ITS CATABOLIC EFFECT ON CONNECTIVE 4-Further inhibition of pregnant immunity -----> liable for infection.
TISSUES AND BONE. 5-Increase risk of Diabetes (pregnancy = Stress, hyperglycemia).
6-Increase Risk of HTN & aggravate the already present edema in pregnant woman.
71-Glucocorticoids are contraindicated in INFECTIONS 7-Increase Risk of Thrombo-embolic disorder due to hypercoagulable state.

Because: 76-Mitotane is used in Cushing's disease & Inoperable adrenocortical carcinoma

-They are IMMUNO-SUPPRESSIVE (discuss mechanisms) --------> FLARE UP OF INFECTIONS.
- Mask manifestations of bacterial & viral infections. Because it causes Destruction of adrenocortical cells.

72-Glucocorticoids cause Retardation of growth in children 77-Aminoglutethimide & Ketoconazole are useful in Cushing's syndrome.

Because: Because they Decrease Conversion of Cholesterol ----> Pregnenolone (First step in
- They have CATABOLIC EFFECT on FIBROBLAST & CONNECTIVE TISSUES. steroidogenesis).
- They have CATABOLIC EFFECT ON BONE & ANTI-VIT D EFFECT -------> DECREASE Ca absorption
from GIT ------> (HYPOCALCEMIA). 78-Metyrapone (Mitopirone) is used in Cushing's disease / Test the function of anterior
- They have CATABOLIC EFFECT on muscle proteins -----> WASTING & MYOPATHY. pituitary

73-ONLY Prednisone is safe in pregnancy Because it INHIBIT 11-B-Hydroxylase enzyme ----> INHIBIT Synthesis of BOTH Aldosterone &
Cortisol -----> INCREASE ACTH.
Because it is a prodrug that is not converted to the active compound, prednisolone, in
the fetal liver. 79-Des-Oxy-Corticosterone (D.O.C.) NOT effective ORALLY

74-Prednisone & Dexamethasone can be given SAFELY in patients with HTN. / don't show Due to extensive hepatic 1st pass effect.
Edema
80-Glucocorticoids are contraindicated in patients with HTN & HF.
Because Mineralocorticoid activity is less with Prednisone (prodrug) and absent with
dexamethasone. Because they have mineralocorticoid effect ------> salt and water retention with K depletion
------> Hypervolemia -----> volume overload and HTN.

81-During long term glucocorticoid therapy, patients are advised, diet should be rich in
Proteins, K+& Ca2+ & low in NaCl.

Because Glucocorticoids have :

-Catabolic effects on proteins→ myopathy
-Anti – Vitamin D →Decreases Ca2+ absorption from G.I.T →Hypocalcemia
-Mineralocorticoid effect → Na, water retention &↑K excretion
82-Glucocorticoids are not used in a patient with T.B. 90-Clinical response to thioamides takes a long time to appear.

Because Glucocorticoids are immunosuppressant →↑ Susceptibility to infection, flare up Due to:

present infection & reactivation of latent T.B. lesion. - Long t1/2 of thyroxine
-Large store of hormones in the gland.
83-Glucocorticoids are contraindicated in Glaucoma.
91-Methimazole preferred over Propylthiouracil (PTU) in the treatment of hyperthyroidism
Because they increase intra-ocular pressure
As Methimazole is more potent & effective it has a longer half-life, allowing for once- daily
84-In primary Addison BOTH Gluco- & Mineralo-corticoid activities are replaced while in dosing, Methimazole has fewer side effects compared to PTU, particularly liver toxicity, which is
secondary Addison ONLY Glucocorticoid activity is replaced. a significant risk with PTU

Because in primary Addison, the adrenal gland itself is not functioning so both gluco & mineralo 92-Propylthiouracil is used in thyroid storm
corticoids are affected, while in 2ry Addison the pituitary doesn’t release ACTH which control
only glucocorticoids→↓glucocorticoids only as mineralocorticoid is under the control of renin- Because it inhibits thyroid hormone synthesis and inhibits conversion of T4 to the more active
angiotensin system and K level so it is not affected. T3

85-A 45-year-old patient has been on high doses of glucocorticoids for 6 months. What is the 93-Methimazole is used for the 2nd and 3rd trimesters of pregnancy while propylthiouracil is
appropriate protocol for withdrawing glucocorticoids? Give the reason. preferred during the 1st trimesters.

Slow reduction of the glucocorticoid dose over 1–2 weeks. Long-term use of glucocorticoids As methimazole-associated with embryopathy, is not given in 1st trimester and propylthiouracil
results in adrenal suppression and atrophy (crisis). A slow “weaning” from the drug is necessary is preferred. But propylthiouracil is associated with liver failure in pregnancy so not used for the
so that the adrenals can recover. remainder of the pregnancy.

86-A 32-year-old woman is prescribed a pill for excessive hair on her face and arms. She notes 94-Iodide is not suitable for prolonged TTT of hyperthyroidism & only used for short term
that she has been going to the bathroom at night more often. What is the most likely therapy (2-3 weeks)?
explanation for the nocturia?
Due to Iodine escape; Hyperthyroidism reappear again after 3-4 weeks of TTT as the gland
Answer: The medication is probably spironolactone, which is a competitive inhibitor of escape from iodide block
androgens at the receptor level, and also an anti-mineralocorticoid effect at the distal tubule,
inhibiting free water resorption. As such, it is a potassium sparing diuretic agent. 95-It is mandatory to perform CBC and liver function tests during the use of antithyroid drugs

87-A higher dose of L-T4 often is required in hypothyroid pregnant woman. Antithyroid drugs PTU carry risks of serious side effects, as agranulocytosis and hepatotoxicity
Regular CBC tests help monitor for signs of agranulocytosis, while liver function tests are
As early development of the fetal brain depends on maternal thyroxine necessary to detect early signs of liver damage.

88-Levothyroxine (T4) is preferred than Liothyronine (T3) as replacement therapy in 96-Beta blockers (Propranolol) should be used as adjuvant therapy in patients of
hypothyroidism. hyperthyroidism.

Because T4 has Less risk of cardiotoxicity, in addition it has low cost, long t 1/2 , and is given Propranolol used to:
once daily -To control peripheral manifestations of hyperactivity of the sympathetic nervous system
(tachycardia, tremors and nervousness) occurring secondary to hyperthyroidism.
89-Intravenous therapy (T4 or T3) is mandatory in patients with myxedema. -To prevents peripheral conversion of T4 into the more active T3

Because patients with myxedema coma absorb drugs poorly from other routes. 97-Iodide is used during preparation for thyroidectomy
Because:
-it reduces the size and vascularity of the thyroid gland, making it easier and safer to remove.
-It Inhibits hormone release →↓Thyroid crisis (storm).
98-Hydrocortisone may be needed in myxedema coma. 106-Vit.D regulate bone resorption and bone formation depending on the level of Ca in the
blood.
If the patient has associated adrenal or pituitary insufficiency.
-If calcium level is normal → it acts on osteoblasts (bone hardening).
99-The chief toxic effect of Radioactive iodine (I131) is hypothyroidism. -If calcium level is low → it acts on osteoclasts → increases bone resorption → increases Ca++
level in blood
Because it emits Beta rays (cytotoxic) which destroy the gland tissue.
107-PTH increases Ca level in blood but decreases phosphate level while Vit.D increase both
100-Thioamides is used as an adjuvant to I131 in hyperthyroidism. Ca and phosphate blood levels and Calcitonin decrease both Ca and phosphate blood levels.

To control the disease while waiting its effect PTH:

1- G.I.T: increases absorption of Ca & phosphate
101-Bisphosphonates effective in treating osteoporosis 2- Bone: stimulates the resorption of Ca from bone to increase its level in blood.
3-Kidney: increases renal tubular reabsorption of Ca & Mg but increases excretion of phosphate
Because Bisphosphonates decrease osteoclastic bone resorption via: resulting in increased Ca & decreased phosphate in blood
-Decrease in osteoclastic formation/activation.
-Increase in osteoclastic apoptosis (programmed cell death) Vit.D:
-Inhibition of the cholesterol biosynthetic pathway important for osteoclast function 1-G.I.T: Increases calcium & phosphate absorption (the main site of action).
2- At the Bone: Regulate bone resorption and bone formation depending on the level of calcium
102-Patients should remain in an upright position at least 30 minutes after taking an oral in Blood:
bisphosphonate. •If calcium level is normal → it acts on osteoblasts (bone hardening).
•If calcium level is low → it acts on osteoclasts → increases bone resorption → increases Ca++
To minimize the risk of esophageal irritation. level in blood
3-Kidney: It ↑↑calcium & phosphate reabsorption from kidney (weak effect).
103-Calcitonin beneficial for patients who have recently suffered a vertebral fracture / Paget
disease Calcitonin:
1-Bone: inhibits osteoclastic activity so, it decreases bone resorption.
Because Calcitonin inhibits osteoclastic activity so, it decreases bone resorption. It also has an 2- Kidney: inhibits calcium and phosphate reabsorption by the kidney tubules.
analgesic effect that helps relieve pain associated with fractures, making it especially beneficial
for patients with recent vertebral fractures. 108-Vit.D is used in Hypocalcemia (vit D deficiency- Rickets - Osteomalacia- in renal disease)

104-Denosumab should be reserved for women intolerant of or unresponsive to other Because it increases both Ca and phosphate blood levels by:
osteoporosis therapies. 1-G.I.T: Increases calcium & phosphate absorption (the main site of action).
2- At the Bone: Regulate bone resorption and bone formation depending on the level of calcium
Because it increases the risk of infections, secondary malignancies, hypocalcemia, and in Blood:
dermatological reactions. It is a monoclonal antibody that targets RANKL and block osteoclast •Calcium level is low → it acts on osteoclasts → increases bone resorption → increases Ca++
activation. level in blood
3-Kidney: It ↑↑calcium & phosphate reabsorption from kidney (weak effect).
105-Continuous administration of PTH produces an effect that differ from intermittent
administration. 109-Vit.D is used topically in psoriasis.

Chronic elevation of its level will deplete bone stores of Ca, However, intermittent exposure to it To decrease cellular proliferation.
will activate osteoblasts more than osteoclasts
110-Alfacalcidol (One-alpha =1α-hydroxycholecalcifrol) is not effective in patient with liver
failure.

Because it requires hepatic activation to produce calcitriol as the active metabolite.

111-Alfacalcidol (One-alpha =1α-hydroxycholecalcifrol) is used for secondary 118-Oxytocin is used in impaired milk ejection.
hyperparathyroidism due to renal failure.
Because it stimulates the contraction of pregnant uterus and is reflexly released from pituitary
Because it is activated by liver to produce calcitriol as the active metabolite, elevating blood following suckling to contract myo-epithelium of breast, Syntocinon is a synthetic derivative.
calcium by the followings leading to decrease in PTH release by negative feedback:
1-G.I.T: Increases calcium & phosphate absorption (the main site of action). 119-Desmopressin is preferred to vasopressin in the treatment of diabetes insipidus.
2- At the Bone: Regulate bone resorption and bone formation depending on the level of calcium
in Blood: Desmopressin has minimal activity at V1 receptor→ largely free of vasopressor effects +
•Calcium level is low → it acts on osteoclasts → increases bone resorption → increases Ca++ Desmopressin is longer acting than vasopressin.
level in blood
3-Kidney: It ↑↑calcium & phosphate reabsorption from kidney (weak effect). 120-Octreotide is administered once every 4 weeks

112-Calcitonin is taken by SC injection and nasal spray NOT ORAL. Because Its half-life is longer than that of the natural compound, and depot formulations are
available, allowing for administration once every 4 weeks.
Because it is a Polypeptide hormone, if taken orally it will be digested. It is a synthetic analog of somatostatin.

113-Thiazide causes hypercalcemia. 121-Ischemic heart disease is less common in women than men.

Because it ↓renal Ca excretion Because of Estrogen that causes estrogen-mediated dilation of coronary arteries occurs by the
increased formation and release of nitric oxide and prostacyclin in endothelial cells.
114-Selective Estrogen Receptor Modulators (SERMs) are preferred over Estrogen as a
hormonal replacement therapy in post- menopausal women with osteoporosis. 122-Estrogen is contraindicated in thrombo-embolic diseases/ Increases risk of thrombo-
embolism.
Because Estrogen may enhance breast and endometrial cancer while SERMs have no
carcinogenic effects. Because Estrogens enhance the coagulability of blood by increasing levels of factors II, VII, IX and
X resulting in high incidence of thromboembolic disease.
115-Teriparatide is used in post-menopausal osteoporosis and steroid induced osteoporosis.
123-Estrogen cause weight gain and hypertension.
Because it is a recombinant segment of human parathyroid hormone, it:
-Stimulates osteoblast function Because it causes Salt & water retention leading to edema & hypertension.
-Increase Ca absorption
-Increase renal tubular reabsorption of Ca 124-Raloxifene is preferred over tamoxifen in prevention & treatment of osteoporosis/ Reduce
These effects increase bone mass and strength risk of breast cancer

116-Abaloparatide reduces the risk of vertebral and non-vertebral fractures in post- Because tamoxifen may enhance risk of endometrial cancer while raloxifene has NO EFFECT on
menopausal women. endometrium.

Because it is a synthetic peptide analog of human parathyroid hormone -related protein. It: 125-Letrezole can be used in treatment of breast cancer & induction of ovulation.
-Stimulates osteoblast function
-Increase Ca absorption Because it is a non-steroidal aromatase inhibitor which bind reversibly to aromatase → Decrease
-Increase renal tubular reabsorption of Ca the production of estrogen→ increases GnRH release → increases FSH release → induction of
These effects increase bone mass and strength ovulation, it is devoid from androgenic side effects.

117-Romsozumab is used in treatment of osteoporosis in post-menopausal women at high risk

of fracture.

Because it is monoclonal antibody (IgG2) that binds sclerostin (regulatory factor in bone
metabolism) and inhibits it →Increase bone formation and decrease bone resorption.
126-Mifepristone and Misoprostol are proved very effective in terminating early pregnancy / 133-Leuprolide and Nafarelin are given continuously in treatment of Cancer prostate, Uterine
postcoital contraceptive e.g. in rape fibroids, Endometriosis and Precocious puberty.

Mifepristone: Given continuously to inhibit gonadotropins release →reduced production of androgens and
-Inhibits the activity of progesterone. It binds to progesterone receptors with no progesterone estrogens.
activity (progesterone antagonist).
134-Octreotide is used in treatment of acromegaly.
Misoprostol: is a prostaglandin analog administered orally or intravaginally to induce uterine
contractions. Because it is synthetic analog of somatostatin, binds to receptors in the pituitary that suppress
GH release.
127-Danazol is used in treatment of endometriosis & fibrocystic disease of breast.
135-Somatotropin is used to promotes growth in Pituitary dwarfism (GH deficiency), as
Because it: replacement therapy prior to epiphyseal closure.
-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 Because it is a recombinant human growth hormone.It increases growth via stimulating the
changes in the endometrium. production of somatomedins and stimulates protein synthesis & lipolysis.

128-Clomiphene citrate is used in treatment of infertility due to ovulatory failure / may cause 136-Human menopausal gonadotropin (hMG) and Human chorionic gonadotropin (hCG) are
Ovarian enlargement Multiple Ovulation & multiple pregnancies. used in the treatment of infertility.

Because it: - Human menopausal gonadotropin (hMG): has FSH & LH activity.
-Blocks ER in hypothalamus preventing the usual negative feedback effect of estrogen on GnRH - Human chorionic gonadotropin (hCG): has LH activity.
leading to increased FSH→ marked stimulation and enlargement of ovaries & increase estrogen - They are given by injection (IM or SC).
secretion & induction of ovulation. - HMG injection over a period of 5 to 12 days causes ovarian follicular growth and maturation,
and with subsequent injection of HCG, ovulation occurs.
129-Metformin is used in Polycystic ovary syndrome.
137-Metoclopramide & antipsychotics such as risperidone are associated with galactorrhea
Because it: and hypogonadism (amenorrhea-galactorrhea syndrome).
- lowers insulin, androgen and cholesterol levels
- is useful in restoring regular menstrual cycle and starting ovulation in about 50% of women Because they are dopamine antagonists that block D2 receptor → Hyperprolactinemia
with polycystic ovary syndrome
138-Reserpine and α-methyl dopa are associated with galactorrhea and hypogonadism
130-Finasteride is used to reduce benign prostatic hyperplasia (BPH) / Hirsutism (amenorrhea-galactorrhea syndrome).

Because it Inhibits conversion of testosterone into di-hydro-testosterone by inhibiting 5α- Because they inhibit dopamine release → Hyperprolactinemia
reductase, so it blocks action of androgen on tissues requiring dihydrotestosterone (prostate and
hair follicles). 139-Cabergoline and Bromocriptine are used in treatment of hyperprolactinemia.

131-Flutamide, Cyproterone are used in hypersexuality in males and in hirsutism, and in Because they are D2 receptor agonists→↓ Prolactin
cancer prostate. 140-Syntocinon has different uses with different routes of administration.

Because they compete with testosterone for receptors, decreasing its action. It is used in:

132-Spironolactone is used in treatment of hirsutism in women. 1. Induction of labor in uterine inertia (I.V)

2. Control of postpartum hemorrhage (I.M)

Because it is a competitive inhibitor of aldosterone, also competes with di-hydro-testosterone
for the androgen receptors in target tissues. It also reduces 17α-hydroxylase activity, lowering 3. Impaired milk ejection (nasal spray)
plasma levels of testosterone and androstenedione.
141-Syntocinon is used in Induction of labor in uterine inertia, Control of postpartum
hemorrhage, Impaired milk ejection.

Because it is a synthetic derivative of oxytocin which Stimulates the contraction of pregnant

uterus and contraction of the myo-epithelium of the breast.