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HORMONAL DRUGS

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Title: HORMONAL DRUGS


1
HORMONAL DRUGS
Lector prof. Posokhova K.A.
2
Hormones
  • I Protein-peptide
  • 1. Hypothalamus
  • 2. Pituitary gland
  • 3. Parathyroid glands
  • 4. Pancreas
  • 5. Intestinal
  • II Derivatives of amine acids
  • 1. Thyroid gland derivatives of
    thyronin
  • 2. Medulla of adrenal glands
    catecholamines
  • III Steroid
  • 1. Adrenal cortex
  • 2. Sex glands

3
Hormones and hormonal drugs of protein and
polypeptide structure
4
Influence of insulin on metabolism
Type of metabolism Stimulation Depression
Carbohydrate Synthesis of glycogen (in liver and muscles) Transport of glucose into a cell Glycolysis Phosphorilation of glucose Glycogenolysis Gluconeogenesis Glycosylying of proteins
Fat Synthesis of triglycerides Synthesis of fatty acids Income of glucose in adipocytes Activity of lipoprotein lipase Lipolysis Production of keton bodies
Protein Synthesis of proteins Absorption of amine acids Disintegration of protein
Nucleonic acids Synthesis of cyclic nucleotides (c-AMP and c-GMP) Absorption of nucleonic acids Synthesis of RNA and DNA Biosynthesis of ribonucleotides
5
Metabolic Changes Occurring When Insufficient
Insulin is Released
  • Hyperglycemia Increased blood sugar
  • Glycosuria Sugar is spilled into the urine
  • Polyphagia Increased hunger
  • Polydipsia Increased thirst
  • Lipolysis Fat breakdown
  • Ketosis Ketones cannot be removed effectively
  • Acidosis Liver cannot remove all of the waste
    products

6
Disorders Associated With Diabetes
  • Atherosclerosis Heart attacks and strokes
    related to the development of atherosclerotic
    plaques in the vessel lining
  • Retinopathy With resultant loss of vision as
    tiny vessels in the eye are narrowed and closed
  • Neuropathies With motor and sensory changes in
    the feet and legs and progressive changes in
    other nerves as the oxygen is cut off
  • Nephropathy With renal dysfunction related to
    changes in the basement membrane of the
    glomerulus

7
Classifications of Diabetes Mellitus
  • Type 1, insulin-dependent diabetes mellitus
    (IDDM)
  • Usually a rapid onset seen in younger people
  • Connected in many cases to viral destruction of
    the beta cells of the pancreas
  • Type 2, noninsulin-dependent diabetes mellitus
    (NIDDM)
  • Usually occurs in mature adults
  • Has a slow and progressive onset

8
Insulin drugs
Group Onset Duration of action Trade names Routs of introduction
1. Simple (short duration of action) 20-40 min 4-6-8 hours Iletin, Insul-rapid, Humalog, Humalin R, Actrapid S.c., i.m., i.v.
2. Medium (moderate) acting (on neutral protamine of Hagedorne - NPH 1-1,5 hour 12-14 hours Insuman, Humulin N S.c., i.m.
3. Long acting (contain Zinc) 6-8 hours 24 hours (till 36 hours) Insulin-Zn-suspension, Ultratard n-m S.c., i.m.
4. Standard mixtures of drugs of 1st group with NPH-insulins 20-60 min Till 18 hours Insuman Comb 30 / 70, 25 / 75, 20 / 80, 10 / 90 S.c., i.m.
9
Types of Insulin Delivery
  • Past
  • Subcutaneous injection
  • Present
  • Subcutaneous injection, insulin jet injector,
    insulin pen, extended insulin pump, long-acting
    insulin
  • Future
  • Implantable insulin pump, insulin patch, inhaled
    insulin

10
Rules of mixing drugs of insulin
  • 1. Never mix crystal zinc-insulins of the 3d
    group (ultralente) with simple insulin because
    the Zn2 partially transforms simple insulin to
    prolonged form. Therefore its absorption
    decreases and onset becomes longer. Insulins of
    these groups should be introduced separately,
    using different places for injection.
  • 2. Insulin-zinc-suspensions should no be mixed
    with drugs that contain phosphates because due to
    this zinc phosphate is produced that leads to
    decreasing of duration action of zinc-insulins.
  • 3. Never mix insulins with different pH level in
    one syringe. For example, acid insulins of short
    action arent combinable with NPH-insulins, and
    surphen insulins should not be combined with
    neutral drugs with short action.

11
Indication for usage of insulin drugs
  • Patients with diabetes
    mellitus
  • Absolutely indicated in case of diabetic coma
    and precoma.
  • Diabetes mellitus of I type if diet therapy and
    other sugar decreasing means arent enough
    effective.
  • 3. Diabetes of any type if it is accompanied
    by complications (ketoacidosis, infection,
    gangrene etc.)
  • 4. Surgeries, pregnancy.
  • Other cases
  • In case of long-lasting exhausting illnesses.
  • In case of heart, liver, kidney diseases the
    drugs are administered with glucose or as a
    component of polarizing mixture.
  • 7. Shock therapy of schizophrenia.

12
Variants of insulin therapy 1. traditional
2. intensive
13
Traditional insulin therapy
  • adjusting of lifestyle and nutrition of patient
    at strictly established dose of insulin.
  • The simplest variant is administration of
    standard mixtures of short and NPH-insulin in two
    injections 2/3 of dose before breakfast, 1/3
    before dinner.
  • Advantages simplicity of performing, glycemia
    needs not to be controlled often, control is
    possible according to level of glucosuria
  • Disadvantages hyperinsulinemia, which demands
    additional meals, larger risk of hypoglycemia,
    increased frequency of late complications of
    diabetes mellitus, bad compensation of sugar
    level

14
Intensive (basis-bolus) insulin therapy
  • the patient himself makes daily a selection of
    insulin dose based on measuring of glycemia level
    with glucometr. Insulin of medium durability is
    used twice a day (to create a basal level of
    hormone) and before the breakfast, lunch and
    dinner additionally insulin of short action
    duration is introduced (imitation of bolus
    physiological secretion of insulin as a respond
    to food consumption).
  • Advantages effective compensation of
    glycemia, more liberal diet (only easy
    assimilable carbohydrates and alcohol are
    prohibited), flexible day schedule, decreasing
    risk of development of late complications
  • Disadvantages it is necessary to constantly
    control glycemia, teaching the patient
    (additional expenses), often light hypoglycemia

15
TREATMENT OF HYPERGLYCEMIC KETOACIDIC COMA
  • Introduction of insulin (only insulin of short
    action is used)
  • intravenously dropply counting 0,1 ?D/kg of body
    weight per hour. First two hours with the speed
    of 8 ?D/hour. If the initial glycemia is higher
    than 33,3 mmol/l? insulin dose in first hour is
    increased till 16 OD. In case of decreasing of
    sugar level on 25-50 from the initial level the
    speed of introduction of insulin is
    correspondingly decreased on 25-50 . If glycemia
    is lower than 16,6 mmol/l insulin should be
    introduced with the speed of 4 OD/hour. In case
    of decreasing of sugar level lower than 11
    mmol/l, it is recommended to transfer to
    subcutaneous introduction of the drug every 6-8
    hours.
  • Glycemia should not be decreased faster than 5
    mmol/l/hour, otherwise it is possible to promote
    brain edema. The level of glycemia should be
    examined every 30-60 minutes.
  • 2. Elimination of dehydration and hypovolemia
    intravenous dropping introduction of liquids
    during 1st hour 1 l of 0,9 NaCl (better
    Ringers solution) is introduced, during the next
    2 hours 500 ml of 0,9 NaCl each hour, and
    after not more than 300ml/hour. In case of
    decreasing of glycemia level lower than 14
    mmol/l, 0,9 NaCl should be substituted by 5-10
    glucose solution
  • 3. Acidosis correction solution of sodium
    hydrocarbonate (if pH lower than 7,1)
  • 4. Correction of electrolyte disorders after 2
    hours from beginning of treatment intravenous
    dropping introduction of ??? dosed 2 g/hour
    should be started under the constant control of
    potassiumemia.
  • 5. Symptomatic treatment of correction of blood
    pressure only introduction of mesatone is
    possible, since other adrenomimetics stimulate
    glycogenolysis and increase sugar level in blood.

16
COMLICATIONS OF INSULIN THERAPY OF DIABETES
  • Hypoglycemic coma
  • allergy
  • lipodystrophy
  • resistance to the drug (daily dose of insulin
    grows to 200 U and more)
  • it is caused
  • ?) production of antibodies towards insulin,
  • b) increasing of binding with plasma proteins,
  • c) decreasing of receptors sensitivity to
    insulin,
  • d) obesity,
  • e) increasing of contrainsular hormones level,
  • f) pseudoresistance injecting the drug into
    places of lipodystrophy (considerable worsening
    of drug absorption).

17
TREATMENT OF HYPOGLYCEMIC COMA
  • Intravenous bolus introduction of 20-50 ml of 40
    glucose (dextrose) solution.
  • If the condition doesnt improve, after 10-20
    minutes the injection should be repeated.
  • In case of absence of effect intravenous dropping
    infusion of 5 glucose solution should be
    started.
  • Correction of blood pressure and stimulation of
    glycogenolysis adrenalin hydrochloride.
  • Prophylaxis and treatment of brain edema
    mannit, glucocorticosteroids.

18
  • SYNTHETIC ANTIDIABETIC PREPARATIONS
  • (taken orally)

19
Derivatives of sulfonilurea 4 generations
  • ? (appeared in the 50-s) chlorpropamid,
    butamid, bucarban
  • ?? (introduced after 1967) glybenclamid
    (maninil)
  • ??? glymeperid (amaryl)
  • ?? repaglynid.

20
Possible mechanism of hypoglycemic action of
derivatives of sulfonilurea
butamid, chlorpropamid
Block of ATP-dependent ? -canals of ?-cells
Depolarization of membranes of ?-cells
Opening of potential-depending ?? 2 -canals of
?-cells
Entering of ?? 2 into ?-cells
Secretion of insulin
21
Mechanism of action of sulfonilurea derivaties
  • Blockade of ATP-depended ? - canals of ?-cells
    of Langergans isles depolarization of ?-cells
    membranes opening of potential-depending
    ??2-canals increasing of ??2 income into
    ?-cells activation of insulin excretion.
  • Similar mechanism if responsible for secretion of
    insulin under the influence of glucose. But in
    this case the signal for closing of of ? -canals
    is increasing of correlation ATP/ADP, which is
    caused by intracellular metabolism of glucose.
    Therefore derivatives of sulfonilurea imitate
    signal of increased concentration of sugar in
    blood.

22
Indications for administration of drugs
derivatives of sulfonilurea
  • diabetes mellitus of ?? type, if
  • ?) all the possibilities of diet therapy are used
    up
  • b) diabetes is diagnosed after the age of 40
  • c) patient suffers from diabetes no more than 10
    years
  • d) there are no complications and pregnancy.

23
Classification of biguanids
  • Phenilethylbiguanids (phenphormin)
  • Buthylethylbiguanids (buphormin-glibutid)
  • Dimethylbiguanids (methphormin glucophage).

24
Mechanism of action of biguanids
  • Mechanism of sugar-decreasing action of biguanids
    influence of peripheral tissues
  • 1. increasing of action of endogen insulin due to
    increasing of quantity and sensitivity of insulin
    receptors
  • 2. decreasing of absorption of glucose in
    intestines, blockade of gluconeogenesis
  • 3. increasing of synthesis of glycogen in liver
  • 4. increasing of glucose metabolism till stage of
    lactate in muscles.
  • Biguanids depress lipogenesis and stimulate
    lipolysis, which leads to body weight loss in
    obese patients

25
Inhaled Insulin Sanofi-Aventis-Pfizer
  • powder
  • before every meal, small onset
  • for diabetes type 2, which is not controlled by
    peroral hypoglycemic drugs
  • as additional therapy for type 1 diabetes
    treatment

26
Sites of Action of Drugs Used to Treat Diabetes
27
Types of Glucose-Elevating Agents
  • Diazoxide (Proglycem)
  • Can be taken orally
  • Glucagon (GlucaGen)
  • The hormone produced by the alpha cells of the
    pancreas to elevate glucose levels
  • Can be given only parenterally preferred for
    emergency situations

28
Hormonal preparations of thyroid gland
29
Actions of the Thyroid Gland
  • Produces two thyroid hormones using iodine found
    in the diet
  • Tetraiodothyronine or levothyroxine (T4)
  • Triiodothyronine or liothyronine (T3)
  • Removes iodine from the blood, concentrates it,
    and prepares it for attachment to tyrosine, an
    amino acid

30
Thyroid Control of Hormone Levels
31
Regulation of thyroid hormones synthesis
32
Functions of Thyroid Hormones
  • Regulate the rate of metabolism
  • Affect heat production and body temperature
  • Affect oxygen consumption, cardiac output, and
    blood volume
  • Affect enzyme system activity
  • Affect metabolism of carbohydrates, fats, and
    proteins
  • Regulate growth and development

33
Types of Thyroid Dysfunction
  • Hypothyroidism
  • Underactivity
  • Hyperthyroidism
  • Overactivity

34
Causes of Hypothyroidism
  • Absence of the thyroid gland
  • Lack of sufficient iodine in the diet to produce
    the needed level of thyroid hormone
  • Lack of sufficient functioning thyroid tissue due
    to tumor or autoimmune disorders
  • Lack of TRH related to a tumor or disorder of the
    hypothalamus

35
Replacement Hormone Products for Treating
Hypothyroidism
  • Levothyroxine (Synthroid, Levoxyl, Levo-T,
    Levothroid) Synthetic salt of T4
  • Thyroid desiccated (Armour Thyroid and others)
    Prepared from dried animal thyroid glands and
    contains both T3 and T4
  • Liothyronine (Cytomel) Synthetic salt of T3
  • Liotrix (Thyrolar) Synthetic preparation of T4
    and T3 in a standard 41 ratio

36
Drugs of thyroid hormones
Name Contents, origin Onset Duration of action Way of introduc-tion
Thyreoidine (Thyroxin threeiodthyronin) extract from thyroid gland 2-3 days 3-4 weeks Orally
Threeiodthyronin (liothyronin) Synthetic 4-8 hours 8-10 days Orally
Levothyroxin-sodium (L-thyroxin-sodium) Synthetic 3-4 days (max. 8-10 days) 2-4 weeks Orally
37
Focus on the Replacement Hormone Prototype
Levothyroxine
  • Indications Replacement therapy in
    hypothyroidism pituitary TSH suppression in the
    treatment of euthyroid goiters, management of
    thyroid cancer thyrotoxicosis in conjunction
    with other therapy myxedema coma
  • Actions Increases the metabolic rate of body
    tissues, increasing oxygen consumption,
    respiration, and heart rate the rate of fat,
    protein, and carbohydrate metabolism and growth
    and maturation
  • PO route Onset slow peak 13 weeks
  • IV route Onset 68 h peak 2448 h
  • T½ 67 days metabolized in the liver and
    excreted in the bile

38
L - thyroxin
39
Thyreocomb (thyroxin threeiodthyronin)
40
Thyreotom (thyroxin threeiodthyronin)
41
Hyperthyroidism
  • Definition
  • Excessive amounts of thyroid hormones are
    produced and released into the circulation
  • Cause
  • Graves disease
  • Signs and symptoms
  • Increased body temperature, tachycardia, thin
    skin, palpitations, hypertension, flushing,
    intolerance to heat, amenorrhea, weight loss, and
    goiter

42
Antithyroid Agents
  • Thioamides
  • Propylthiouracil (PTU)
  • Methimazole (Tapazole)
  • Iodine solutions

43
Adverse Effects of Iodine Solutions
  • Hypothyroidism
  • Iodism (metallic taste and burning in the mouth,
    sore teeth and gums, diarrhea, cold symptoms, and
    stomach upset)
  • Staining of teeth
  • Skin rash
  • Development of goiter

44
Antithyroid drugs
  • Depression of production of TTH
  • - iodine
  • - diiodithyrosine (dithyrine)
  • Depression of synthesis of hormones in thyroid
    gland
  • - mercasolil
  • - propilthiouracyl
  • Disturbance of absorption of ?2 by thyroid gland
    - potassium perchlorate
  • Destroying cells of thyroid gland follicles
  • - radioactive iodine (?131)

45
Calcium Control in the Body
46
Actions of Parathormone (PTH)
  • Stimulation of osteoclasts or bone cells to
    release calcium from the bone
  • Increased intestinal absorption of calcium
  • Increased calcium resorption from the kidneys
  • Stimulation of cells in the kidney to produce
    calcitriol

47
Parathyroid Dysfunction
  • Hypoparathyroidism
  • The absence of parathormone
  • Most likely to occur with the accidental removal
    of the parathyroid glands during thyroid surgery
  • Hyperparathyroidism
  • The excessive production of parathormone
  • Can occur as a result of parathyroid tumor or
    certain genetic disorders

48
Hormonal preparations of steroid structure
49
Natural hormones of adrenal cortex
Mineral corticosteroids aldosterone desoxycortico
sterone 11-desoxy-17-oxy- corticosterone
Glucocorticosteroids hydrocortisone
(cortisole) corticosterone cortisone 11-dehydrocor
ticosterone
Hormones with sexual activity androsterone andro
stendione estrone progesterone
50
Hypothalamus-adrenal axis Hypothalamus-hypophys
is-epinephral system
  • Hypothalamus
  • CRH Somatostatin GRH TRH PRH PIH GnRH
  • Anterior pituitary
  • Growth hormone ACTH TSH FSH
  • LH (male) LH (female) Prolactin
  • Peripheral endocrine glands
  • Adrenal cortex Thyroid Gonads Liver
  • Feed-back mechanism

51
Properties of glucocorticosteroides used in
clinics
  • Anti-inflammatory
  • Immune-suppressive
  • Anti-allergic
  • Anti-shock
  • Anti-toxic

52
Anti-inflammatory action of GCS
  • Nonspecific inflammation
  • Auto-immune component
  • Hyperergic character
  • Therapy of despair

53
Mechanism of anti-inflammatory action of GCS
GCS
activation of lipomoduline
decreasing of activity of phospholipase ?2
slowing down of arachidonic acid metabolites
production (prostaglandins, leucotriens,
thromboxan ?2)
stabilization of cellular and lyzosomal membranes
decreasing of capillaries wall permeability
decreasing of leucocytes migration processes,
depression of phagocytes activity
depression of histamine, serotonin,
bradykinine releasing
54
Administration of GCS
  • Insufficiency of adrenal cortex
  • Rheumatoid illnesses (rheumatoid arthritis,
    rheumatism, system red lupus etc.)
  • Chronic active hepatitis
  • Bronchial asthma
  • Ulcerative colitis
  • Nephritic syndrome
  • Auto-immune hemolytic anemia
  • Shock and collapse of any etiology
  • Brain, lungs, larynx edema
  • Acute allergic reactions
  • Transfusion reactions
  • Heavy infections (hiding behind the etiotropic
    drugs!)
  • Liver diseases

55
Doses and terms of GCS therapy
Situation Daily dose Terms of treatment
Acute cases (shock, collapse, brain, lungs edema, septic shock, asthmatic condition etc.) 200-500- 800-1000 mg i.v. 1-3 days
Subacute and acute attacks of chronic processes (rheumatoid diseases, ulcerative colitis, bronchial asthma etc.) 20-50 mg (rarely till 200 mg) 4-6 weeks- several months
Primary and secondary insufficiency of adrenal cortex 2,5-10 mg life-long
56
Hydrocortisone acetate
57
Prednisolone
58
Prednisolone
59
Prednisolone
60
Becotide Beclometh (beclomethasone dipropionate)
61
Kenalog (triamcinolone acetonide)
62
Kenalog (triamcinolone acetonide)
63
Fluocinar Sinaflan Sinalar (Fluocinole
acetonide)
64
Dexamethasone
65
Dexamethasone
66
Dexamethasone
67
Lorinden A flumethasone pivalate (locacorten)
neomycin
68
Complications of GCS-therapy
Steroid diabetes immune-suppression depression of
resistance towards any infections atrophy of
muscles hypopotassiumemia peptic
ulcers disturbance of regeneration osteoporosis,
delay of growth matronism (buffalo hump,
moonlike face etc.) retention of Na , H2o
edema hypertension hypercoagulation of
blood changes of psychical conditions
disturbance of menstrual cycle hypothalamus-pitui
tary-epinephral insuffciency
Izenko-Cushings syndrome
69
Controls and Actions of the Adrenal Glands
70
MINERALOCORTICOIDS Desoxycorticosterone acetate -
DOXA
  • Mode of action
  • Acts on kidney tubules causes the
    reabsorption of sodium and water, decreases the
    reabsorption of potassium,
  • regulates fluid-electrolyte metabolism,
    increases AP, enhances muscle work
  • Administration
  • For chronic adrenal insufficiency (Addisons
    disease), myasthenia, adynamia
  • Side effects
  • edema, AP increasing, pulmonary edema,
    cardiac insufficiency

71
Drugs of female sex hormones
Estrogens estron (oil solution of
folliculin) estradiol ethynilestradiol (microfolli
n) synestrol
Gestagens progesterone oxyprogesterone
caproate alilestrenol (turinal)
72
Estrogens
  • Uses
  • Hormone replacement therapy (HRT)
  • Palliative and preventive therapy during
    menopause
  • Actions
  • Protecting the heart from atherosclerosis
  • Retaining calcium in the bones
  • Maintaining the secondary female sex
    characteristics

73
Sites of Action of the Estrogens
74
Administration of drugs of female sex
hormones estrogens 1) Genital hypoplasia,
primary and secondary amenorrhea 2) Sexual
underdevelopment of women 3) After
ovary-ectomia 4) Climacteric disorders 5)
Lactation depression 6) Weak labor
activity (estrogen background) 7) Prostate cancer
of men, breast cancer of women after the age of
60 8) A part of contraceptive agents
75
Effects of Progesterone on the Body
  • Decreased uterine motility
  • Development of secretory endometrium
  • Thickened cervical mucus
  • Breast growth
  • Increased body temperature
  • Increased appetite
  • Depressed T-cell function
  • Anti-insulin effect

76
Administration of gestagens 1) miscarriage,
habitual abortion 2) dysfunctional uterus
bleedings, algomenorrhea 3) as component of
contraceptives 4) Climacteric disorders 5) As
part of fertility programs 6) Treat specific
cancers with specific receptor site sensitivity
77
Hormonal contraceptives 1) combined
estrogen-gestagen a) monophased (bisecurin,
non-ovlon, rigevidon, marvelon, demulen) b)
double-phased (anteovin, neo-eunomin) c)
triple-phased (tri-regol, trisiston) 2)
monohormonal gestagen (mini-pilli) exluton,
ovret, continuin 3) postcoital hestagen
(postinor) 4) depot-contraceptives - of
prolonged action norplant (levonorgestrel)
depot-provera (medroxyprogesterone acetate)
78
Complications in case of administration
of hormonal contraceptives
hypertension hypercoagulation dyspeptic
disorders (nausea, vomiting) migraine
depression obesity cholestatic jaundice breast
cancer, cancer of uterus cervix ischemic heart
disease myocardium infarction stroke embryotoxic
and teratogenic action
thrombo-embolia
79
Focus on the Fertility Drug Prototype Clomiphene
  • Indications Treat ovarian failure in patients
    with normal liver function and normal endogenous
    estrogens unlabeled use treat male sterility
  • Actions Binds to estrogen receptors, decreasing
    the number of available estrogen receptors, which
    gives the hypothalamus the false signal to
    increase FSH and LH secretion, leading to ovarian
    stimulation
  • PO route Onset 58 days duration 6 weeks
  • T½ 5 days, with hepatic metabolism and excretion
    in the feces

80
Abortifacients
  • Use
  • Evacuate the uterus by stimulating intense
    uterine contractions
  • Types
  • Carboprost (Hemabate)
  • Dinoprostone (Cervidil, Prepidil Gel, Prostin E2)
  • Mifepristone (RU-486, Mifeprex)

81
Androgens and Their Indications
  • Testosterone (Duratest, Testoderm, others)
  • Hypogonadism breast cancer
  • Danazol (Danocrine)
  • Block the release of FSH and LH in women
  • Fluoxymesterone (Halotestin)
  • Hypogonadism breast cancer
  • Testolactone (Teslac)
  • Breast cancers

82
ANABOLIC STEROIDS Phenobolinum, Retabolil,
Methandrostenolonum
  • PHARMACOLOGICAL EFFECTS
  • Stimulation of protein synthesis
  • Depression of phosphor and Ca excretion
  • Increase of bones, muscles and parenchymatous
    organs mass
  • Stimulation of regeneration
  • ADMINISTRATION
  • Aplastic anemia (bone marrow suppression)
  • Osteoporosis, bone fractures
  • Exhausted diseases
  • Prolonged treatment with GCS
  • COMPLICATIONS
  • Hepatitis, sexual disorders (impotence),
    edemas, masculinization, nausea, vomiting
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