2011-2012 lecture 10 year 3 fin

Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. Lecture 10: Diuretics. Antidiuretics. Pharmacological
influence of blood disorders.
4. Drugs used in disorders of coagulation. 1. Diuretics

Diuretics are agents that increase diuresis (increase urine volume due to increase of the rate of
urine flow) and excretion of electrolytes and water.

Diuretics classification:
1. Thiazide diuretics (sulfonamide diuretics):
- benzothiazines (thyazides): Hydrochlorothiazide, Chlorothiazide, Methyclothiazide, Polythiazide, Hydroflumethiazide, Bendroflumethiazide, Cyclopenthiazide, Benzthiazide - thiazide-like diuretics (analogues of thyazides): Indapamide, Chlorthalidone, Quinethazone, Metolazone, Clopamide, Xipamide 2. Loop diuretics:
- Furosemide and its analogues (Bumetanide, Piretanide) - Ethacrynic acid and its analogues (Indacrinone, Ticrinafen) 3. K+ sparing diuretics:
- aldosterone antagonists (mineralocorticoid receptor antagonists): - nonselective: Spironolactone, Prorenone - physiologically antagonists (direct acting): Amiloride, Triamterene 4. Carbonic anhydrase inhibitors: Acetazolamide, Dorzolamide, Methazolamide, Brinzolamide,
5. Osmotic diuretics: Mannitol, Glycerin, isosorbide, urea
6. Other substances with low diuretic effect:
- antagonists of antidiuretic hormone: Lithium salts, Demeclocycline (tetracycline derivative) - methylxanthines: Theophylline, Caffeine - cardiac glycosides. Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. 1. THIAZIDE DIURETICS
Classification of thiazide diuretics
o Hydrochlorothiazide, o Others: Chlorothiazide, Methyclothiazide, Polythiazide, Hydroflumethiazide, Bendroflumethiazide, Cyclopenthiazide, Benzthiazide • thiazide-like diuretics (analogues of thyazides): o Indapamide, o Clopamide, o Chlorthalidone, Quinethazone, Metolazone, Xipamide Structure
All thiazides have an unsubstituted sulfonamide group:
• analogs and variants are derivatives that only unsubstituted sulfonamide group. Mechanism of action:
- inhibit the cotransporter Na+/Cl- from the proximal segment of the distal convoluted tubule
(probably also in the ascending limb of Henle and the last segment of the proximal tubule).
- Indapamide stimulate production of vasodilatory prostaglandins (PGE1, PGE2, PGI2)
the increas in renal blood flow causes a redistribution of blood flow within the renal cortex production of PGE1, PGE2 and PGI2 (vasodilator prostaglandins) chronic administration, stimulating the production of renin, then, the drug inhibits the cotransporter Na + / Cl-at the proximal segments of the distal convoluted tubule (probably also in the ascending limb of Henle and last segment of the proximal convoluted tubule). Pharmacodynamic effects of thiazide diuretics are of medium intensity:
- diuretic effect: increase the excretion of Na+, Cl-, K+ and water;
- retention of uric acid, Ca2 +;
- metabolic effects:
• hyperglycemia (reduce peripheral glucose utilization), • hyperlipidemia: increas total plasma cholesterol and LDL-cholesterol; - Indapamide has vasodilator effect (at doses lower than doses with diuretic effect). Duration of pharmacodynamic effects of thiazide diuretics: • medium: Hydrochlorothiazide,Chlorothiazide, Bendroflumethiazide,Hydroflumethiazide, Benzthiazide, Cyclothiazide, Cyclopenthiazide, Méthyclothiazide, Buthiazide; • long: Indapamide, Clopamide, Polythiazide, Chlortalidone. Pharmacokinetics
- absorption: for Hydrochlorothiazide
low fat solubility, the drug is administered only parenterally; - plasma protein binding: for Hydrochlorothiazide hepatic metabolism, and presents first pass effect; renal elimination, unmetabolized, by tubular secretion; Indications
- hypertension;
- chronic heart failure;
- renal failure (renal clearance > 30 ml / min);
- kidney stones due to idiopathic hypercalciuria;
Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. - nephrogenic diabetes insipidus induced by lithium (doses are adjusted, as thiazides decrease
lithium elimination).
Adverse effects
- hypokalemic metabolic alkalosis;
- due to ions excretion:
• blood: hyponatremia, hypokalemia, hypercalcemia • urine: hyperphosphaturia; - hyperuricemia; - uric lithiasis; - hyperglycemia, glycosuria (in patients with diabetes mellitus); - the increase in insulin resistance; - hyperlipidemia (increased total plasma cholesterol and LDL - cholesterol plasma); o mental fatigue, physical fatigue, paresthesias; - sexual impotence; - Type I immunological reactions (rash, pruritus), type II (hemolytic anemia, thrombocytopenia) and type III (Stevens-Johnson syndrome) cross-reactivity to other sulfonamides; - other adverse effects (rare): acute pancreatitis, cholestatic jaundice, acute pulmonary edema.
Contraindications
- diabetes mellitus;
- dyslipidemia;
- liver cirrhosis, heart failure associated with renal failure (except, indapamide), heart failure
associated with liver cirrhosis;
- gout;
- sarcoidosis.
2. LOOP DIURETICS (or High-Ceiling Diuretics)
Classification of loop diuretics
o Furosemide and its analogues (Bumetanide, Piretanide) o Torsemide (= Torasemide) (sulfonylurea derivative) o Ethacrynic acid and its analogues (Indacrinone, Ticrinafen) Mechanism of action:
- inhibition of the cotransporter Na+/K+/2Cl- in the ascending limb of Henle;
- increase the production of vasodilatory prostaglandins (PGE1, PGE2, PGI2).
Pharmacodynamic effects of loop diuretics are fast, very intense and short-term (after iv
administration):
- vasodilator effect appears before the diuretic effect;
Furosemide acutely increase systemic venous capacitance and thereby decrease left ventricular filling pressure the increase in renal blood flow cause a redistribution of blood flow within the renal cortex renal blood flow stimulate cyclooxygenase increase production of vasodilatory prostaglandins if volume deppletion occurs it is stimuled the production of renin. - increase in glomerular filtration rate; - diuretic effect: increase the excretion of Na+, K+, Ca2 +, Mg2 +, Cl-, water and phosphates. Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. Pharmacokinetics
- absorption is rapid (after oral administration);
- protein binding: for Furosemide
- metabolism: liver;
- rapid renal elimination by tubular secretion (in the proximal convoluted tubule) and glomerular
filtration.
Indications
- Furosemide
• hypertensive crisis; • edema of various etiologies: o acute heart failure (acute pulmonary edema, cardiac asthma); o chronic heart failure (edema refractory to diuretic therapy with other groups and o liver cirrhosis (complicated with ascites); o nephrotic syndrome, acute or chronic renal failure (but are contraindicated in patients with renal failure associated with cirrhosis); • hypercalcemia (these drugs are contraindicated in massive dehydration or in lung cancer). • fluid and electrolyte disturbances (such as hyperkalaemia) due to poisonings with bromides, fluorides and iodides (not indicated in lithium intoxication). Adverse effects
- hypokalemic metabolic alkalosis;
- due to ions excretion:
• blood: hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia o hypomagnesemia induced by Furosemide increase the ototoxic effects of • urine: hypercalciuria, moderate hypophosphaturia; - hyperglycemia - hyperuricemia (with the exception of Indacrinone and Ticrynafen, which are uricosuric drugs) • hyperglycemia and hyperuricemia are weaker than those caused by thiazide diuretics; • hypotension; • extracellular dehydration, • functional renal failure - nausea, vomiting; - Type I immunological reactions (rashes), type II (thrombocytopenic purpura) and type III (acute interstitial nephropathy) cross-reactivity to other sulfonamides; - increase in plasma renin.
Contraindications
- hypersensitivity to sulfonamides;
- massive dehydration;
- lung neoplasms.
Precautions: administration of Furosemide, Bumetanide and Torsemide in patients with liver
cirrhosis associated with kidney failure or heart failure
Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. 3. K+ SPARING DIURETICS
Classification of K+ sparing diuretics
• aldosterone antagonists (mineralocorticoid receptor antagonists): o nonselective (act on both aldosterone and steroidal hormone receptors): o selective (act only on aldosterone receptors): Eplerenone • physiologically antagonists (direct acting): Mechanisms of Action
- competitive antagonists of aldosterone receptors from the distal convoluted tubule
Na+/K+ -ATPase in the membrane of target cells block Na+ reabsorption and the secretion of K+ and H+, - physiological antagonists of aldosterone block Na+ channels in collecting duct of the block Na+ /K+ exchange (not dependent of the presence of aldosterone). Pharmacodynamic effects
- stimulate the reabsorption of H + and K +; - increase elimination of Na+, Cl-, bicarbonates and water; - block myocardial remodeling (anti-fibrosis effect); - antiandrogenic effects (only for non-selective competitive antagonists). Duration of pharmacodynamic effects of potassium-sparing: • medium: Amiloride, Triamterene; • long: Spironolactone, Prorenone, Eplerenone. Pharmacokinetics
- absorption: for Spironolactone and Triamterene
absorption; - metabolism: hepatic (Spironolactone is biotransformed in active metabolites); Spironolactone and Triamterene - elimination: renal.
Indications
- as diuretic in combination with a thiazide or loop diuretic (to prevent the K+ excretion induced
by these drugs);
- in hypokalemia during the treatment of refractory oedema from hepatic cirrhosis, heart failure
or nephrotic syndrome (conserve potassium);
- Spironolactone: congestive heart failure;
- Spironolactone: primary and secondary hyperaldosteronism.
Adverse effects
- hyperkalemia, hyponatremia;
- hyperkalemic metabolic acidosis, especially in cases of renal failure which is a cons-indication
for their use;
- Spironolactone determines endocrine adverse effects (because has an antiandrogenic effect):
gynecomastia, menstrual disorders, impotence, and benign prostatic hyperplasia;
- Triamterene: megaloblastic anemia in patients with liver cirrhosis, renal failure when it is
associated with indomethacin, kidney stones;
- Amiloride: hyperammonemia, impaired glucose tolerance.
Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. Contraindications
- hyperkalemia with or without clinical symptoms (disorders of atrioventricular conduction);
- acidosis of various etiologies;
- severe chronic renal failure;
- hepatorenal syndrome;
- breastfeeding.
4. CARBONIC ANHYDRASE INHIBITORS
Classification of carbonic anhydrase inhibitors diuretics
• Acetazolamide, • Dorzolamide, • Methazolamide, • Brinzolamide Mechanism of action
- inhibition of carbonic anhydrase → block the formation of bicarbonates and H + ions
There is carbonic anhydrase in the eye, kidneys (predominantly in the proximal convoluted tubule), CNS, gastric mucosa, pancreas, erythrocytes. Pharmacodynamic effects
are of low intensity and short duration - renal: inhibition of carbonic anhydrase activity depresses bicarbonate reabsorption in the proximal tubule and inhibit the exchange of H + ions with Na+ ions: • in urine are eliminated: Na+, K+, bicarbonate, phosphate, water (increase diuresis); • in blood increase H+ and Cl- - eye: reduce intraocular pressure in glaucoma (because decreases the rate of formation of aqueous humor); - CNS: local acidosis induced by inhibitors of carbonic anhydrase determine • anticonvulsant effects, reduce cerebral edema and regulate nerve impulses in the cortical - gastric mucosa: reduce gastric acidity;
Pharmacokinetics
- absorption: good for Acetazolamide, slow for Metazolamide;
- plasma protein binding: 90%;
- renal elimination as unchanged drugs.
Indications
- glaucoma
• Acetazolamide is used by mouth for open angle and for closed angle glaucoma; • Dorzolamide is drug of choice – used as 2% topical drops; • for urinary alkalinization (to increase renal excretion of weak acids); • increase urinary phosphate excretion during severe hyperphosphatemia; - acute mountain sickness (= high-altitude disorders) • Symptoms: weakness, dizziness, insomnia, headache and nausea may occur in mountain travelers who ascend rapidly to above 3000 m → pulmonary or cerebral edema; • prophylaxis can be obtained after oral administration, starting 24 hours before the ascent; as an alternative or adjunct to first-line drugs; Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. - peptic disease;
- to correct metabolic alkalosis.
Adverse effects:
- rapid development of tolerance;
- hyperchloremic metabolic acidosis;
- kidney stones;
- renal elimination of potassium;
- dizziness, fatigue, drowsiness, CNS depression and paraesthesia at high doses;
- bone marrow depression (rare);
- hypersensitivity reactions (fever, pruritus, interstitial nephritis).
Contraindications:
- liver cirrhosis.
5. OSMOTIC DIURETICS
Classification of osmotic diuretics
• Mannitol, • Others: Glycerin, isosorbide, urea Mechanisms of action
- increase the osmotic pressure (physical action) in the lumen of vessels and of nephrons;
• act in the nephron segments highly permeable to water: the proximal convoluted tubule, the collecting tubule, the descending limb of Henle. Pharmacodynamic effects
are of moderate intensity and short duration - increase the glomerular filtration rate;
- diuretic effect: increase the elimination of water, K +, bicarbonates, phosphate, Ca2 +, Mg2 +.
Pharmacokinetics
- administration: only iv;
- distribution: in extracellular fluid;
- metabolism: hepatic (Mannitol is metabolised 10%);
- elimination: glomerular filtration.
Indications
- intracranial hypertension: to reduce intracranial pressure;
- before ophthalmic surgery: to reduce intraocular pressure;
- to increase in urine volume, when renal hemodynamics is compromised (eg, renal failure);
- syndromes with hypersecretion of antidiuretic hormone.
Adverse effects
- transient increase in extracellular volume;
- transient severe hypernatremia;
- cellular dehydration.
6. OTHER SUBSTANCES WITH LOW DIURETIC EFFECT
- antagonists of antidiuretic hormone: Lithium salts, Demeclocycline (tetracycline derivative) - methylxanthines: Theophylline, Caffeine - cardiac glycosides. Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. 2. Antidiuretics

Antidiuretics are agents that reduce urine volume, particularly in diabetes insipidus. They have
also other effects.
Classification
1. Antidiuretic hormone (peptides):
- natural: Vasopressin (ADH) - synthetic: Desmopressin, Terlipressin 2. Drugs that potentiate the antidiuretic effects of antidiuretic hormone:
- Chlorpropamide, - Carbamazepine, - Clofibrate
VASOPRESSIN (ANTIDIURETIC HORMONE), TERLIPRESSIN, DESMOPRESSIN
• Vasopressin (antidiuretic hormone) is a polypeptide hormone secreted by the neurons of the supraoptic and paraventricular nuclei of the hypothalamus and stored in the posterior pituitary gland. • Terlipressin is a synthetic vasopressin analog with similar efficacy to vasopressin, but • Desmopressin is a synthetic polypeptide structurally related to vasopressin. • V1 (mediate vasoconstriction), • V2 (mediate antidiuretic effect) • V2-like (=V3, stimulate release of coagulation factor VIII and von Willebrand factor) Mechanism of action
- Vasopressin and Terlipressin: agonist of vasopresin receptors V1, V2 and V2-like.
- Desmopressin: agonist of vasopresin receptors V2 and V2-like.
Pharmacodynamic effects
- Vasopressin and Terlipressin
- intense vasoconstriction (particularly of capillaries and of small arterioles, mediated by V1 receptors); Terlipressin has preferential splanchnic vasoconstrictor; the vasopressor effects are less pronounced than those of vasopressin. - antidiuretic effect (maintain serum osmolality within a normal range, mediated by V2 - potent antidiuretic effect; - stimulation of release of coagulation factor VIII (antihemophilic factor) and von Willebrand factor (mediated by V2-like receptors). Pharmacokinetics
- Absorption:
- Vasopressin is administered intranasal (very good absorption) or parenteral. - Desmopressin (used as acetate salt) is administered intranasally, orally, by subcutaneous injection, direct IV injection, or slow IV infusion. - Distribution: in extracellular fluid, but no plasma protein binding. Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. - Metabolism: rapidly destroyed in the liver and kidneys. - Elimination: small quantity - T1/2 = Vasopressin: 10-20 minutes, Desmopressin: 8 - 24 hours.
Indications
- Vasopressin and Terlipressin
- diabetes insipidus (it is drug of choice) caused by a deficiency of endogenous posterior pituitary antidiuretic hormone; - gastro-intestinal hemorrhage: esophageal variceal hemorrhage, colonic diverticulosis - cardiac arrest (may replace the first or second dose of epinephrine in the treatment of ventricular fibrillation arrest, pulseless ventricular tachycardia, asystole, or pulseless electrical activity in advanced cardiovascular life support); - diabetes insipidus caused by a deficiency of endogenous posterior pituitary - primary nocturnal enurezis; - to evaluate the ability of the kidneys to concentrate urine; - hemophilia A and von Willebrand disease. Adverse effects
- Vasopressin and Terlipressin
- skin pallor; - increased blood pressure (can lead to hypertension, myocardial ischemia or infarction, mesenteric infarction), bradycardia, minor arrhythmias; - nausea, vomiting, abdominal cramps; - severe hyponatremia (“water intoxication” = overhydration children): headache, confusion, anuria, and weight gain; - type I alergic reactions (urticaria, angioedema, bronchoconstriction, fever, rash, wheezing, dyspnea, circulatory collapse, cardiac arrest, and anaphylaxis). - severe hyponatremia; - unlike vasopressin, usual doses of Desmopressin do not cause skin pallor, Contraindications
- Vasopressin and Terlipressin
Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. 3. Agents Used in Anemias; Hematopoietic Growth Factors

AGENTS USED IN ANEMIAS
Classification of agents used for the treatment of anemia due to deficiency of iron, vitamin
B12, or folic acid:
1. Iron salts:
sodium ferric gluconate complex in sucrose 2. Vitamin B12: Cyanocobalamin, Hydroxocobalamin
3. Folic acid


Iron salts
These compounds contain divalent or trivalent iron. The necessary daily intake of iron is 50mg.
Pharmacokinetics
- administration: p.o. or parenteral (i.m. or i.v.).
- absorbtion: the compounds containing divalent iron are better absorbed in the duodenal mucosa
and they are less irritating than the digestive compounds containing trivalent iron. Organic iron
compounds present are better digestive tolerance.
Indications
- treatment of iron deficiency anemia;
- prophylaxis of iron deficiency anemia (the necessary daily intake of iron is 30 mg): during
pregnancy, lactation, blood donors, infants, young children, puberty, elderly, vegetarians.
- parenteral administration is indicated if:
• oral intake is inadequate or the oral route can not be used; • gastrointestinal bleeding (is continuous or intermittent and rainfall associated with lower • after gastrectomy; • anterior resection of the small intestine; • inflammatory bowel disease involving the proximal small intestine; • malabsorption syndromes. • gastrointestinal bleeding. Adverse effects
- when administered po: nausea, vomiting, gastrointestinal irritation, abdominal cramps,
constipation / diarrhea, dark stool.
- when parenteral administration:
• headache, flushing, intense sweating, fever, arthralgia; • pigmentation at the injection site; • hemochromatosis (high dose). Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. Contraindications
- hemochromatosis;
- haemosiderosis;
- hemolytic anemia;
- thalassemia;
- peptic ulcer;
- colitis.
Specific treatment in poisoning with iron: deferoxamine, EDTA.
Drug interactions
- drugs which decrease iron absorption: antacids; cimetidine; caffeine; cholestyramine; dairy
products; citric acid;
- drugs which increase iron absorption: ascorbic acid, fructose, cysteine, alcohol.
Vitamin B12
The necessary daily intake of vitamin B12
Pharmacodynamic effects
- Vitamin B12 is essential for the activity of two enzymes:
• deoxy-adenosyl-cobalamin enzyme which determine the conversion of the enzyme • 5-methyltetrahydrofolate-homocysteine-methyltransferase enzyme which determine: o conversion of the inactive form of tetrahydrofolate (the methyltetrahydrofolate) to o conversion of homocysteine to methionine. Pharmacokinetics:
- administration: only parenteral route (im or sc);
- absorption: in the stomach, vitamin B12 binds to a glycoprotein (Castle intrinsic factor)
forming a a complex that is absorbed in the ileum;
- transport in the blood: it is linked to transcobalamin;
- it has enterohepatic circuit;
- there are storage reserves in the liver;
- elimination: renal and biliary.
Indications: treatment of megaloblastic anemia.
Adverse effects: allergy (rare).
Contraindications: malignant tumors; polycythemia.
Folic acid
The necessary daily intake of folic acid
100 mg / day (food sources far exceed this amount). Pharmacodynamic effects
- cofactor in the synthesis of purines and pyrimidines
- involved in cell maturation.
Indications
- treatment of megaloblastic anemia;
- prophylaxis in pregnancy (to prevent neural tube defects).
Contraindications
Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. - malignant tumors.
- association with drugs that inhibit folic acid synthesis (Sulfonamides, Trimethoprim,
Methotrexate, Phenytoin, Isoniazid, oral contraceptives).
HEMATOPOIETIC GROWTH FACTORS
Classification of hematopoietic growth factors used to treat anemia, thrombocytopenia, and
neutropenia, and to support stem cell transplantation.
1. erythropoietin:
2. myeloid growth factors:
- granulocyte colony-stimulating factor (G-CSF) - granulocyte-macrophage colony-stimulating factor (GM-CSF) 3. thrombopoetic growth factors (Megakaryocyte Growth Factors):


Erythropoietin
Administration: parenteral route (iv).
Mechanism of action: bind on erythropoietin receptors from erythroblasts (red cell progenitors)
in bone marrow
Pharmacodynamic effects
- stimulates erythroid proliferation and differentiation
- induces release of reticulocytes from the bone marrow.
Indications
- anemia in patients with chronic renal failure, chronic inflammatory diseases, myelodysplasia,
myelofibrosis, multiple myeloma, phlebotomy;
- anemia induced by zidovudine therapy.
Available preparations
- epoetin alfa and epoetin beta (recombinant human erythropoietin),
- Darbepoetin alfa (glycosylated form of erythropoietin).
Adverse effects
- hypertension;
- headache, vomiting, visual disturbances, convulsions;
- thrombosis;
- immunological reactions: skin rash, chills, flu-like symptoms.
Contraindications
- hypertension,
- treatment with iron.
Myeloid growth factors G-CSF, GM-CSF
Indications
- neutropenia
Lecturer Cristina GHICIUC, MD, PhD Lecture 10: Diuretics. Antidiuretics. Pharmacological influence of blood disorders. • neutropenia after chemotherapy, • neutropenia after bone marrow transplantation; • congenital neutropenia; • neutropenia induced by treatment with zidovudine; • neutropenia more aplastic anemia; - myelodysplasia;
- pancytopenia (in combination with other growth factors, because G-CSF, GM-CSF does not
determine the stimulation of the formation of erythrocytes and platelets).
Available preparations
- granulocyte colony-stimulating factor (G-CSF)
• filgrastim, • pegilated compound: pegfilgrastim, • lenograstim - granulocyte-macrophage colony-stimulating factor (GM-CSF) Adverse effects: fever; arthralgia; syndrome of capillary infiltration.
Interleukin-3 (IL-3)
Pharmacodynamic effects: stimulates production of platelets and erythrocytes.
Indications: bone marrow failure.
The toxicity is high.
Interleukin-11 (IL-11)
Indications: thrombocytopenia (as secondary prophylaxis after chemotherapy in non-myeloid
cancers).
Adverse effects
- fatigue, headache, dizziness;
- anemia (due to hemodilution);
- dyspnea;
- supraventricular arrhythmias (transient);
- hypokalemia (rarely).
Thrombopoietin
Administration: parenteral route (iv).
Mechanism of action: bind on thrombopoietin receptors
Pharmacodynamic effects
- stimulate the growth of lymphoid and myeloid cells
increases the number of peripheral platelets and neutrophils. Indications: thrombocytopenia after chemotherapy or after bone marrow transplant (it is also
given to donors).
Available preparations
- recombinant human thrombopoietin.
Lecturer Cristina GHICIUC, MD, PhD

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