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Pharmacology3
Endrocrine
Question | Answer |
---|---|
Octreotide/Lantreotide are what type of drugs? What kind of side effects can they have? | Somatostatin analogs Gallstones, GI disturbances, Abnormal cardiac conduction |
GH is suppressed and antagonized by what five things? | Somatostatin, Dopamine/Bromocriptine (only for GH tumors), Pegvisomant (GH-receptor antagonist), alpha blockers (Phentolamine), 5HT blockers (Cyproheptidine) |
Mecasermin (Mecasermin rinfabate) is an analog of? An adverse affect may be: | IGF-1. Hypoglycemia |
Somatostatin blocks what 4 things? | Insulin, Gucagon, GH, Gastrin (IG3) |
Potent D2 agonists used to treat prolactinomas (3) | Bromocriptine (also for acromegaly), Cabergoline, Pergolide |
GH release is stimulated by and inhibited by: | 5HT, Dopamine, B-blockers, Inhibited by alpha-blockers, somatostatin |
These hormones are used for diagnostic purposes only: | GHRH, CRH, ACTH, TRH, TSH |
The only anterior pituitary hormone that does not regulate the production of other hormones by peripheral tissues: | Prolactin |
These four hormones are subject to feedback inhibition by the hormones whose production they control | FSH LH ACTH TSH (FLAT) |
In children, Somatotropin is used to treat these 5 diseases (3 are genetic). Side effects of GH in children | GH deficiency (dwarfism), Chronic Renal Failure Genetic: Noonan's disease, Praeder Willi, Turner's Syndrome . Pseudotumor cerebri, slipped capital femorla epiphysis, scoliosis, edema, hyperglycemia, otitis media (in PW and T syndromes) |
In adults, Somatotropin/GH is used for (5): Side effects (4): | GH deficiency, AIDs-related wasting, post-GI resection malabsorption, anti-aging, boosting athletic performance. Myalgia, Arthralgia, Edema, INCREASED mortality |
Gonadotropins are: Their functions in men and women | LH and FSH. In males, FSH regulates spermatogenesis, LH stimulates androgen production in testes. In fmales, FSH stimulates follicle development, and FSH and LH regulate ovarian steroidogenesis. Used to treat infertiliy/anovulation |
Ovulation induction protocol: What are the three steps? | 1. Shut down endogenous gonadotropin production with GnRH agonist/antagonist 2. Daily injection of FSH for follicular development (menotropin/FSH derivative) 3. LH or hCG for final stage of oocyte maturation |
2 Serious complications of ovulation induction | 1. Multiple pregnancies 2. Ovarian hyperstimulation syndrome: large ovaries, ascites, hypovolemia, shock |
Menotropins are | Extracts of menopausal women's urine containing FSH and LH |
LH analogs include (2) | hCG and Lutropin alfa. The latter should only be used in combination with follitropin alfa for follicular develpment in infertile women with LH deficiency. NOT use to produce LH surge. |
FSH analogs include (3) | Urofollitropin (urine of postmenopausal women with LH activity removed by anti-hCG antibodies), Follitropin alfa/beta (synthetic rFSH) |
Long acting GnRH agonists (5): | Leuprolide, Goserelin, Histerelin, Nafarelin, Triptorelin |
Antagonistic activity of long-acting GnRH agonists are useful in the treatment of(5): Side effects may include: | Uterine fibroids, Endometriosis, Prostate cancer, Central Precocious Puberty, Early pubertal transgender adolescents . Side effects: Menopausal symptoms in females/males, bone loss, may initially exacerbate prostate cancer/central precocious puberty |
GnRH antagonists and advantages (2): | Ganirelix, cetorelix, (ovulation induction) degarelix (prostate cancer treatment). 1. No initial flare. 2. Less risk f ovarian hyperstimulation syndrome |
Hyperprolactinemia's 2 major adverse effects: How is this condition treated? What 3 drugs may increase PRL secretion | Infertility, Galactorrhea Bromocriptine (D2 agonist) Morphine, Endorphins, Anti-psychotics (D2 blockers - Clozapine/Haloperidol) |
Oxytocin, a nonapeptide synthesized in ____nuclei of the hypothalamus and released from the _____ pituitary plays a role in ________ (2). | Paraventricular. Posterior. Uterine contractions (inducing labor) and release of breastmilk |
Atosiban is: | Oxytocin-receptor antagonist. Acts as a tocolytic (prevents preterm labor). |
Vasopressin V2 receptor function (2) | 1. Insert water channels in apical membrane of collecting duct cell (reabsorb/antidiuresis) 2. Regulate release of coagulation factor VIII and Von Willebrand factor (binds to and prevents degradation of VIII) |
Name a V2 agonist. Used to treat what 3 diseases? | Desmopressin. Von Willebrand's disease, Hemophilia A, Pituitary Diabetes Insipidus |
V1 vasopressin receptor types and functions (2) | V1a: Vasoconstriction V1b: ACTH release |
Vasopressin receptor antagonists: | Conivaptan, Tolvaptan |
GH and prolactin act through what kind of receptors | JAK STAT |
TSH, FSH and LH are dimeric proteins that act through what kind of receptors. They have ___ and ___ chains | G-protein coupled |
Three things that inhibit TRH stimulation of TSH release and one thing that activates release: | Thyroid hormone, Glucocoritcoids, Somatostatin Estrogen |
Thyroid hormones (T3 and T4) inhibit the release of (2) | TSH and prolactin |
TRH can stimulate the release of GH in what 4 disease states? | Acromegaly, Depression, Anorexia, Uremia |
Agonistic effects of GnRH treatment (2) | Idiopathic hypogonadism, Hypothalamic amenorrhea |
CRH release is activated by (2): and inhibited by (3): | (2): 5HT and ACh (3): NE, melatonin, GABA |
In Early Follicular phase, does estrogen increase or decrease LH/FSH release by GnRH? | Decrease |
In Late Follicular phase, does estrogen increase or decrease LH/FSH release by GnRH? | Increase |
In Post-Menopausal women, does estrogen increase or decrease LH/FSH release by GnRH? | Decrease |
In males, does testosterone increase or decrease LH/FSH release by GnRH? | Decrease |
Finasteride does what? | Blocks 5a-reductatase, reducing synthesis of Dihydrotestosterone from Testosterone. This can reduce prostate hyperplasia and balding and treats hirsutism in women |
Flutamide/Nilutamid are: | Anti-androgens (blocks receptors). |
GH must either be derived from ______ or a synthetic analog may be used | humans |
How does IGF-1 differ from insulin? | Shows Non-Suppressible Insulin-like activity (not suppressed by antibodies against insulin) |
Compare and contrast GH and IGF1 in terms of protein synthesis, lipolysis, and blood sugar levels | GH: increases protein synthesis/muscle mass, lipolysis and causes hyperglycemia (Reduces insulin sensitivity and causes hyperinsulinemia) IGF1: increases protein synthesis, reduces lipolysis and causes hypoglycemia (insulin-like) |
In children/infants, lack of GH results in ________, where as lack of thyroid hormone results in ________. | Dwarfism. Cretinism. |
Excess of GH in children/adolescents leads to _______ and in adults leads to ________ | Gigantism, Acromegaly |
Pegvisomant is: (Bonus: How does it work?) | GH Receptor antagonist. It is a mutated version of GH that activates only one of the two receptors, which allows for receptor dimerization but does not cause the conformation changes needed for signaling |
Synthetic somatostatin analogs offer what advantages? | Compared to somatostatin, octreotide is only 2x as active in inhibiting insulin-like effects whereas 45x as active in blocking GH effects. It also has a 30x longer half life (90min compared to 3). |
Prenatal growth is ____ (GH/IGF-1) dependent and ____(GH/IGF-1) independent. Postnatal growth after 1 year of age is ___ dependent. | IGF-1, GH, GH |
3 Categories of Dwarfism include: How are they treated? | Laron's Disease (unable to synthesize IGF-1 even with GH administration), Praeder-Willi Syndrome, Turner Syndrome. Laron's is treated by Mecasermin (IGF-1 analog) and the latter two diseases are treated with GH analogs or GHRP(GH releasing peptide) |
3 GHRH derivatives: | Sermorelin, Hexarelin, GHRP2/6 |
Octreotide is: Side effects include: Before giving a long-acting form: | A somatostatin analog. GI events, (cramps/nausea/vomiting/flatuence/steaorrhea), gallstones, sinus bradycardia, pain at site of injection, Vitamin B12 deficiency with long term use Test with a short acting form to see if it's tolerated |
In female follicular stage, ___ in the theca cells produces _____, and _____ in granulosa cells converts it to ______. In the luteal stage, ____ is responsible for production of ____ and ______ | LH, Testosterone, FSH, Estrogen LH, estrogen progesterone |
hCG is most similar to ____ and works through the same receptors. | LH |
In males, ____ assists in spermatogenesis in ______ cells, and ______ produces androgens in ______ cells. ____ also converts androgens to estrogens in ______ cells. | FSH, Sertoli, LH, Leydig FSH Sertoli |
L-Dopa is commonly used to treat ________ disease (CNS). A side effect may be that it lowers ___ levels in the blood. | Parkinson's. Prolactin |
Infertility in men is treated with: Spermatogenesis occurs in ____ months What is ICSI | hCG, then hMG 4-6 months Intracytoplasmic Sperm Injection: more efficient |
What class of testosterone is Testosterone Cypionate How is this class of drugs administered and what is it used for? Aromatizable or no? Crosses BBB? | Class 1 IV or transdermal patch. To treat hypogonadism. Aromatizable. Yes |
What class of testosterone is Nandrolone Decanoate How is this class of drugs administered and what is it used for? Aromatizable or no? Crosses BBB? | Class 2 IM (Long acting). Out of clinic Aromatizable. Yes |
What class of testosterone is 17a-methyltestosterone/ stanozolol/ oxyandrolone? How is this class of drugs administered and what is it used for? Aromatizable or no? Crosses BBB? | Class 3 Oral administration, many uses Non-aromatizable. Acts mostly on periphery |
AAS can be used to treat (9): "muscle growth provides happiness to most boys of all ages" | 1. Malnutrition 2. hypoGonadal men 3. delayed male Puberty 4. HIV patients to gain muscle mass 5. female to Male Transgenders 6. Mood disorders 7. Breast engorgement 8. Anemia 9. Aging |
Describe regimen to treat hypopituitarism in puberty/adulthood: Long/Short acting agents, How is it administered, | Use long acting agents: Tes. Enanthate/Cypionate via IM injections (50mg) and decrease interval time and increase dose to mimic what happens in puberty. In adults, use 200mg at 2 wk intervals |
Adverse effects of AAS in women and men | acne, deep voice, enlarged clitoris, risk for atherosclerosis, altered serum lipids, progestational activity (endometrial bleeding), affects fetus in pregnancy, liver/kidney damage, jaundice (raised bilirubin), prostate hyperplasia in men |
How does Ketoconazole (anti-fungal) impact the Estrogen/Testosterone ratio? Adverse effects? | Steroid synthesis inhibitor. Synthesis of testosterone is lowered, but conversion rate to estrogen using aromatase in not inhibited, raising the Estrogen to Testosterone ratio. Toxic to women, gynecomastia in men |
Cyproterone is: | an anti-androgen (androgen receptor blocker), It suppressed LH and FSH feedback. Used to treat excess libido in men and hirsutism in women. |
Bicalutamide is used for: Nilutamide is used for: | Reducing prostate tumor flares in addition to GnRH analog Surgical castration |
Spironolactore, an aldosterone antagonist, can also compete for ____ receptors and lowers serum Testosterone levels by reducing the enzyme _______. It is used to treat __________ in women. | androgen (competes with DHT) 17a-hydroxylase hirsutism |
Two methods of chemical contraception in males: | 1) Testosterone enanthate with progestins to reduce adverse effects of testosterone aromatization to estrogen 2) Testosterone with GnRH antagonists |
Exogenous testosterone has ________ effects, but shuts down the ___________ | Peripheral, HPG |
3 patterns of AAS abuse | Shotgunning, Cycling, Pyramiding |
AAS abuse is usually combined with ____, ____ or _____. | Antiestrogens, Competitive aromatase inhibitor, hCG/LH (to maintain endogenous testosterone production/testes size) |
Aminogluthethemide and Anastrozole are examples of | competitive aromatase inhibitors |
Dietary Supplements that are used as ergoenic agents incliude: | hGH (may cause acromegaly), Androstenedione, Creatine (pure protein) |
AAS Drug Test Techniques (2): | EMIT (enzyme immunoasay) and GC/MS (gas chromatography/massspec) |
Time for detection of 1) oral AAS 2) Injected AAS | 1) 3-6 weeks 2) 6-8 months |
AAS effects on 1. 5HT 2. Dopamine 3. Glutamate 4. Vasopressin | 1. Lowers 5HT (depression) 2. Increases Dopamine (reward) 3. Increases Glutamate (aggressive/anxious) 4. Increases vasopressin (memory) |
Estrogen-like compounds in our daily lives include | soybean, BPA, PCBs |
Estrogen can (increase/decrease) clotting factors, (increase/decrease) plasma renin substrate, (increase/decrease) bone resorption, (increase/decrease) endometrial proliferation. | increase, increase, decrease (oppose PTH), increase |
Estrogen (does/does not) pass through breast milk. Progesterone (does/does not). | does does not. |
Hormone Replacement Therapy reduces risk of __________ but raises risk of ____ and ______, the latter of which may be avoided if HRT is used in combination with _________. | osteoporosis, breast cancer, endometrial cancer, progestins |
If HRT does not work, a different therapy involves the use of ______ | Clonidine |
After 4 months of continuous use, HRT be cause _____ | amenorrhea |
Diethylstilbestrol (DES), a synthetic estrogen used to maintain pregnancy, may cause _______________. Now it is only used to _______ and as __________l. | Vaginal adenocarcinoma in offspring Treat cancer, morning after pill |
Metabolic effects of progesterone (on fat/glycogen) include (3): | Fat deposition by lipoprotein lipase, glycogen storage by facilitating effects of insulin (may lead to diabetes type 2), Ketogenesis |
Progesterone's effects on 1) body temperature 2) Na retention 3) bodily changes 4) urinary nitrogen excretion 5) blood pressure 6) HDL | 1) increases body temp 2) decreases Na retention (competes with aldosterone) 3) alveolobular/secretory breast development 4) increases nitrogen excretion 5) increases BP 6) reduces HDL |
Describe types of contraception: | Oral: monophasic (constant dose), biphasic, triphasic (dose of one or both changed through cycle), progestin only (minipill) Implantable: etonogestrel Vaginal rings or IUDs |
For breastfeeding mothers, what kind of oral contraceptives are allowed to be used? | Progestin-only (minipill) - does not go into breastmilk like estrogen |
On CNS, Estrogen ____ excitability and Progesterone _____ it. | Increases, Decreases |
Estrogen ____ TG, HDL, and cholesterol and Progesterone _____. | Increases, decreases |
L-Norgestrel is commonly used as | The morning after pill ("Plan B") |
Mifepristone (RU486) is an antagonist or what receptor(s)? What is it used for? | Progesterone and Glucocorticoid Terminating pregnancy (before 7 weeks gestation), Cushing's diseases |
Danazol is an ______ derivative with weak ___, ___, and ____ activities. It prevents midcycle ________, and is used to treat ____ (4) | Eristerone (synthetic steroid) Weak P, androgenic, GC activities Prevents LH/FSH surges Treats endometriosis, hemophilia, fibrocytic breast disease, angioedema, |
Describe and state the uses for: 1. Anatrozole/Letrozole 2. Exemestane 3. Fadrozole | All aromatase inhibitors. 1. Anastrozole: Non-steroidal. Used when tamoxifen is ineffective 2. Exemestane: Steroidal, irreversible. Used for advanced breastcancer 3. Fadrozole: Non-steroidal. Used to treat precocious puberty/excessive aromatase syndrome |
Fulvesant is: | a pure estrogen receptor antagonist; inhibits ER complex from binding DNA - used when pt is resistant to tamoxifen |
Desribe 3 SERMs. | Tamoxifen (breast cancer) Raloxifen (long acting >24 hrs, prophylactic use for breast cancer/osteoporosis), Clomiphene (ER partial agonist,inhibits negative feedback, increases gonadotropins, used in ovulation induction) |
In Sertoli cells, activin and inhibin respectively increase and decrease _____ Sertoli cells also convert ____ to ______ | FSH Testosterone to estradiol |
SHBG is increased by ____ and ______ SHBG is reduced by _____, _____ and ______ | Estrogen and thyroid hormone Androgens, Insulin, Growth Hormone |
Testosterone can _____ HDL, _____ renal erythropoietin, ______ clotting actors, ______ the action of hepatic TG lipase | lower, increase, increase, increase |
Describe ovarian hyperstimulation syndrome | Ovarian enlargement, hydrothorax, hemoperitoneum, arterial thromboembolism, shock |
In male or female infertility, what GnRH analog is first administered and how? | Gonadorelin - delivered by pump every 90 minutes (pulsatile) |
Delayed onset of puberty may be caused by (2): | 1. Constitutional delay (impending puberty) 2. Hypogonadism (LH levels <15.6mIU/mL after GnRH administration) |
Why is a GnRH analog used in controlled ovarian hyperstimulation? | To prevent endogenous LH surges that may prematurely trigger ovulation |
What is endometriosis and what are 3 treatment methods? | Estrogen sensitive endometrium-like tissue that grows outside the uterus. 1. Contraceptives 2. GnRH analogs (may cause bone loss over time) 3. Danazol (not first choice - has many side effects, DO NOT TAKE when pregnant) |
What are uterine fibroids and how are they treated? | Estrogen-sensitive fibrous growths in uterus that may cause menorrhagia and anemia, treated with GnRH analogs for 3-6 months (often supplemented with iron to reduce anemia) |
Prostate cancer is treated with what regimen? | Continuous GnRH with flutamide (Androgen Deprivation Therapy) or surgical castration |
Central Precocious Puberty is treated with? | GnRH analogs |
Cetorelix and Ganirelix are used in _____ Degrelix is used in _____ Collectively these drugs are known as: | Controlled ovarian hyperstimulation Prostate cancer GnRH antagonists (inhibits FSH/LH secretion) |
Prolactin is secreted from the ______ and its levels rise at the end of pregnancy when the levels of progesterone ______. Hyperprolactinemia may cause _________, and is treated with ______ | Anterior pituitary, Decrease Galactorrhea and amenorrhea in women, erectile dysfunction in men. Treat with Dop-agonists (Bromocriptine) |
Bromocriptine and Quinagolide _______ levels of GH in patients with acromegaly. | Decrease |
Dopamine agonists can cause _________ in early weeks of pregnancy and ________ in post partum women | sponataneous abortions stroke/coronary thrombosis |
Oxytocin's functions (4) | 1. Mammary gland contraction (milk release) 2. Uterine contractions (induce labor/terminate pregnancy) 3. Control post-partum bleeding 4. Weak anti-diuretic by activating ADH receptors |
Atosiban is: | Oxytocin antagonist used to prevent pre-term labor |
Diabetes may cause 4 conditions: | 1. Retinopathy, 2. Kidney Damage 3. Vascular Damage 4. Neuronal damage |
Fasting glucose should be less than ____ mg/dL HbA1C measure blood glucose levels over _____ period and normal should be lower than ___%. | 100 3 month 6% |
Glucose metabolism is mediated by the GI enzymes ___ and ___. | GIP and CCK |
Insulin levels are increased by ___ and ___ receptors and decreased by ____ receptors. | B-adreneric & Muscarinic increase alpha-adrenergic decrease |
Stimulation of ventro_____ hypothalamus (parasympathetic) increases insulin whereas ventro______ hypothalamus (sympathetic) decreases it. | lateral = increase medial = decrease |
Insulin is a peptide, and therefore must be administered ____ | IV |
What are the two major types of Primary Diabetes | 1. Insulin-dependent 2. Insulin-independent (insulin insensitivity) |
Oral hypoglycemic agents are only used to treat Type ___ diabetes | 2 |
Ketoacidosis is always found with Type ___ diabetics | 1 |
High plasma glucagon is suppressible or non-suppressible in Type 2 diabetics? | Non-suppressible |
Type 2 diabetics have 3 classifications - what are they? | 1. Non-obese 2. Obese 3. MODY (maturity onset diabetes of the young) |
Secondary causes of Diabetes Mellitus (5) | 1. Chronic Pancreatitis (alcoholism) 2. Hormonal (Pheochromo, Cushing's, Acromegaly - all cause hyperglycemia) 3. Drug-induced: Streptozotocin kills beta cells 4. Insulin receptor abnormalities 5. Myotonic Dystrophy - impairs beta-cell activity |
Does insulin stimulate or inhibit: 1. Glycogen synthase 2. Glucokinase 3. Glycolysis 4. Glyceraldehyde Phosphate Dehydrogenase 5. Phosphorylase A 6. Gluconeogenesis 7. PEPCK 8. Pyruvate Carboxylase 9. 1,6 Fructose Bisphosphatase | Stimulates 1-4. Inhibits 5-9 |
Oral hypoglycemic agents include: (7) | 1. Sulfonylureas 2. Biguanides 3. Thiozoinediones (Rosiglitazone) 4. Glucosidase inhibitors (Acarbose/Miglitol) 5. DPP-blockers (Gliptins) 6. Pramintide (Amylin analog) 7. Exenatide (GLP1 analog) |
How does Sitagliptin work? | Decreases DPP (dipeptidyl dipeptidase) which normally breaks down GLP-1. |
GLP-1 effects include (4) | 1. Central anorexia 2. Slow gastric emptying 3. Insulin release 4. Glucagon suppression |
Biguandies have an adverse side effect of: | Lactic acidosis |
How do sulfonylureas work First generation sulfonylureas include: Second generation: Adverse effects: | Inhibit ATP-sensitive K+ channels, depolarize cell, allow calcium inflow,/ stimulate insulin secretion 1: Chlorpropamide, Tolbutamide, Tolazamide, Acetohexamide 2: Glyburide, Glipizide Adverse effects: Hypoglycemia, CV events |
Thiozolidinediones (glitazones) work through: Adverse effects are: | nuclear PPARy receptors that increase insulin sensitivity. Adverse effects: water retention, weight gain |
Biguanides include: | Metformin, Buformin |
Acarbose and Miglitol are: | Glucosidase Inhibitors: block the degradation of complex carbohydrates in the gut. They have no effect on absorption of simple sugars |
List the 4 types of Insulin preparations: | Rapid acting (Lispro, Aspart, Glulisine) Short acting (Novolin, Humulin) Intermediate acting (Neutral Protamine Hagedorn) Long acting (Detemir (myristic acid added), Glargine) |
Thiocyanate and Perchlorate inhibit what function | Uptake of Iodide into thyroid gland |
PTU and Methimazole inhibit what function: | Iodination of tyrosine and coupling of Di-iodotyrosin and Mono-iodotyrosine to form thyroid hormones PTU also inhibits T4 to T3 conversion |
Iodides inhibit what function: | Colloidal reabsorption and proteolysis |
Dinitrotyrosine does what? | Inhibits de-iodination |
The 3 main agents for hyperthyroidism are: | PTU, Methimazole, Iodides |
T4 binding to TBG is ______ by estrogen and _______ by androgens and glucocorticoids | increased, decreased (facilitates excretion) |
Thryoid hormone can be displaced from TBG by (2) | Salicylate and Furosemide |
TRH secretion is inhibited by ___ and ____ and its action on receptors on the pituitary is inhibited by _____ | Somatostatin, Dopamine Glucocorticoids |
Lithium inhibits what process in T4 production | Colloidal resorption |
Drugs that induce HYPOthyroidism (2) | Lithium, Phenylbutazone (NSAID) |
What happens in thyroiditis? Differentiate between acute and chronic: | Inability to store T3/T4 Acute: Excessive free thyroid hormone (hyperthyroidism) Chronic: Hypothyroidism |
Hashimoto's Disease occurs due to: | Autoimmune destruction of enzymes needed for tyrosine iodination (peroxidase) |
Grave's disease occurs due to: | Thyroid stimulating immunoglobulin binding and resulting production of excessive thyroid hormone |
In hyperthyroidism, cardiovascular issues may occur due to upregulation of __ receptors, which may be prevented by using _____ and _____ | Beta Adrenergic B-Blockers, Ca-Channel Blockers |
ADH release is stimulated by | Beta and Muscarinic receptors |
Glucocorticoid effect on ADH stimulation (2) | 1. raises threshold of osmo-sensitivity 2. less renal tubules less permeable to water (diuresis) |
ADH stimulatory drugs include (9) | CNS: Nicotine, Barbiturates, Morphine Anti-Cancer: Vinblastine Vincristine Cyclophosphamide Etc: Clofibrate, Chlorpropamide (diabetes), TCA |
ADH inhibitory drugs include: | Anti-narcotics, Ethanol, Chlorpromazine |
Desmopressin, compared to aqueous vasopressin has what sort of activity profile | 3000:1 ratio of ADH:vasocontrictive activity, longer half life |
Leukopenia is an adverse side effect of which antithyroid drugs: | PTU and Methimazole. |