Pharmacology - Tot - NR 6classid S.F.A

M1439 Drug used in disorders of coagulation part 1 M1439
Pharmacology The 5th Exam Pharmacology The 5th Exam
Classifications : Anticoagulants
A. Direct mechanism of action

1. Drugs of Heparin
-standard heparin
-low-molecular-weight heparins: nandroparin , dalteprarin , daltegrin , enoxaparin
-Antagonists of Heparin - protamine sulfate
2. Heparinoids
-sulodexid
3 .Hirudin and its analogues
-hirudin
-hirugen
-lepirudin
-baviliridin
-desulfatohirudin
4.Drugs of AT III
-antithrombinIII
5.Ancrod (a defibrinogenating agent derived from the venom of the Malayan pit viper)
6.Remedies that fix Ca in blood
- sodium hydrocytrate
B. INdirect mechanism of action

1.Coumarin derivates
-warfarin
-acenocoumarol
-phepromaron
2.Indandionic derivates
-phenyndione
-diphenandione
3.Antagonists of anticoagulants with indirect action

- phytomenadione (vit. K)
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HEPARIN:
*HEPARIN: Mechanism of action
AT-III plays a crucial role in natural endogenous anticoagulant mechanisms by blocking the activity
of activated clotting factors, XI, X, IX and II.
Heparin accelerates AT-III activity 1000 folds especially against clotting factors IIa and Xa
low molecular weight heparins accelerate AT-III activity only against clotting factors Xa (thrombin
is not).
*HEPARIN: INDICATIONS
1) Prevention and treatment of deep vein thrombosis and pulmonary embolism,
2) myocardial infarction, unstable angina,
3) during cardiac bypass surgery and in placing artificial heart valves to prevent formation of any
thrombus/emboli;
4) to prevent clotting in extracorporeal circulation (e.g. during haemodialysis);
5) for anticoagulation during pregnancy
*HEPARIN : ADR
1) Heparin-induced thrombocytopenia,
2) osteoporosis,
3) spontaneous fractures on prolong use,
4) transient alopecia,
5) hypersensitivity;
6) GIT bleeding,
7) Haematuria
*HEPARIN: CONTRAINDICATION
- hypersensitivity, hemorrhage, gastric ulcer, hemophilia, hypertension, cerebral trauma, sever liver
and kidney diseases , TB , leucosis , aneurysms , diabetes
ANTITHROMBIN III
*Antithrombin III concentrate is primarily used for the prophylaxis and treatment of patients with
congenital antithrombin III deficiency and disseminative intravascular coagulopathy.
*Side effect: allergy, danger to contaminate with AIDS, viral hepatitis
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Indirect Oral Acting Anticoagulants

Coumarin derivates
Mechanism of action
- These drugs competitively inhibit vitamin-K epoxide leading to blocking of the
vitamin k dependent glutamate carboxylation of precursor clotting factors II, VII, IX, X
As result, will inhibit the synthesis of clotting factors II, VII, IX, X by the liver .
- The anticoagulant effect develops within 13 days.
Indications:
1) Prevention and treatment of deep vein thrombosis & vascular/pulmonary embolism
2) myocardial infarction
3) unstable angina
4) after placing artificial heart valves
5) persistent forms of atrial fibrillation
ADRs:
- transient alopecia, dermatitis, diarrhea, hemorrhages, hematuria, GIT bleeding
- necrosis of smooth muscles, dyspepsia, liver toxicity, leukopenia , nephrotixicity
- teratogenity (Coumarin derivatives cross the placenta and can lead to hemorrhagic disorders in
the foetus, foetal bone deformities)
contraindications: hemorrhagic syndrome, ulcer, hypertension, liver and kidney failure
osteoporosis, pregnancy
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Trombolytics (fibrinolitics)
1. with direct action
- fibrinolysin
2. with indirect action
- streptokinase
- anistreplase
- alteplase
- Urokinase
M.O.A: - Rapidly lyse thrombi by catalyzing plasmin protease from its precursor plasminogen.
- Fibrin degradation
* Administered by intravenous infusion
Indications: pulmonary emboli, DVT, thrombosis of peripheral vessels, M.I (in the first 5 days)
ADRs: Hemorrhages, increase of temperature, allergy, livertoxicity, hypotension, dyspepsia
Streptokinase is a protein synthetised by streptococci that combines with the

plasminogen. This complex catalyzes the conversion of inactive plasminogen to active
plasmin.
Urokinase is a human enzyme syntheized by the kidney that directly converts to
plasmin.
Antistreplase consists of a complex plasminogen and streptokinase that has been
acylated to protect.
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Antifibrinolytics
M.O.A: decrease the formation of plasmin, the major fibrinolytic enzyme from plasminogen,
that degradate fibrin into fragments.
Indications:
Hemorrhage, tachycardia, prevention of hemorrhage in surgical interventions , myopathy ,
In over dosage with fibrinolytic.
Side effects: allergy, dyspepsia, arrhythmias.
Antidotum: aprotinin , pamba (p-aminomethylbenzoic acid) , aminocapronic acid.
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CLASSIFICATIONS
I. Inhibitors of thromboxane activity drugs that decrease platelet aggregation (antiaggregant)
1) Inhibitors of tromboxane synthesis

a) Cyclooxygenase inhibitors
- acetylsalicylic acid (aspirin)
- nitroaspirin
- diclofenac
- indomethacin
b)Thromboxane synthetase inhibitors
- dazoxiben
2) TXA2-receptor antagonists
- daltroban
3) Drugs of mixed action (thromboxane synthase inhibitors + thromboxane

receptors blockers)
- ridogrel
II. Remedies that increase prostacyclin activity - stimulators of

prostacyclin receptors and activators of prostacyclin-synphesis
- epoprostenol
- carbacyclin
III. GLycoprotein IIb/IIIa receptor antagonists (GP IIb / IIIa)
a) Antagonists of glycoprotein-receptors
- Abciximab
- tirofiban
- Eptifibatide
- lamifiban
b) Inhibitors of ADP receptors

- ticlopidine
- clopidogrel
IV.Remedies with various antiaggregant action

- dipyridamole
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Nsaids / Acetylsalicylic acid:
*Mechanism of action
irreversibly inhibits the enzyme COX which involved in the synthesis of TXA2 (prostaglandins)
resulting in the inhibition of platelet aggregation.
* INDICATIONS
1.prevention of ischemic attack
2.prevention of myocardial infarction
3.reduce the risk of heart attack and reduce the incidence of first incidence
4.reduce the risk of Venous Thromboembolism (VTE) after orthopedic surgery
5.Treatment of acute coronary syndromes
* ADR
1) Tinnitus
2) dyspepsia
3) bleeding
4) prolonged
5) time
6) bleeding
7) rash
8) renal insufficiency
9) thrombocytopenia
10) hepatitis
11) angioedema
12) asthma
13) Reye's syndrome
* CONTRAINDICATION
1) People with kidney disease, hyperuricemia, or gout
2) glucose-6-phosphate dehydrogenase deficiency
3) asthma
4) peptic ulcers
5) gastritis
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ticlopidine
- M.O.A: reduce platelets aggregation by inhibiting ADP pathway of platelets

- INDICATIONS: used as alternative for patients intolerant to aspirin
- ADRs: nausea, dyspepsia, hemorrhage, leukopenia
- DOSSAGE: 250 mg/ twice day
Abciximab:
M.O.A: is antagonists of glycoprotein-receptors GPIIb/IIIa It inhibits combing to fibrinogen and

decreases aggregation
INDICATIONS: angina, M. I, surgery in the a. coronary, angioplasty, coronary artery syndrome
ADRs: allergy, hemorrhage, hypotension, bradycardia, dyspepsia, thrombocytopenia
dipyridamole:
M.O.A: inhibits adenosindesaminase and increases quantity of adenosine, that are an antagonist of
ADP_endogenous. Also, it inhibits phosphodiesterase that increase the quantity of fixed Ca.
ADRs: hypotension, crash syndrome, allergy, headache, bleeding
INDICATIONS: Prophylaxis against thromboembolic disorders, diagnosis of angina pectoris
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CLASSIFICATIONS
drugs that decrease platelet aggregation (antiaggregant)
1) With local action

a) coagulant factors and haemostatics:
- thromboplastin
- thrombin
- human fibrin
- gelatin
b) vasoconstrictors:
- epinephrine , norepinephrine , difetur , Izoturon
c) remedies from plants:
- folia Urticaria
- cortex Viburni
- herbae Milefolii
- flores Arnicae
- herbae Polygonii persicariae
2) With systemic action

a) Direct (coagulation factors)
- fibrinogen
- batroxobin
- fibracel
- blood clotting factors ( VIII, IX, XII)
b) Indirect (coagulation factors)
- phytomenadione (Vit. K)
- menadione (Vit. K3, vicasol)
a) with systemic action:

- aminocapronic acid
- tranexamic acid
b) animal origin
- aprotinin (contrical, trasilol)
a) platelet aggregants
- Calcium chlorite
- Calcium glyconate
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antihemorrhagics / haemostatics
With local drugs:
*thromboplastin:
- activates prothrombin and other factors of coagulation
*indication: to stop bleeding of hemorrhages especially in otorhinolaryngologic - " ORL ".
*fibrin, gelatin
- can be applicated locally and they produce local vasoconstriction
*indication: epistaxis, uterus hemorrhages, intestinal hemorrhages, rectal hemorrhages
*vasoconstriction drugs
- (Ex: epinephrine) to stop bleeding that lasts 0.5-2h.
-indication: used topically in bleeding from superficial capillaries and veins, epistaxis,
tooth extraction, wounds
*thrombin
-indication: parenchymal hemorrhages from superficial capillaries, epistaxis, Hematemesis,
tonsillectomy, Werlhof's disease, hemoptysis, hypoplastic and aplastic anemia, neurosurgery, after
tooth extraction thromboplastin activates prothrombin and other factors of coagulation
with systemic drugs:

*fibrinogen
- is a final factor of process of coagulation.
-indication: hypo & afibrinogenemia, post-operation hemorrhage, in oncology, in traumatology.
*fibracel
- interacts with V, x factors and calcium produces one complex that activates the transformation
into thrombin from prothrombin.
-indication: used to prevent of hemorrhage in surgical interventions, dyspepsia, myopathy,
arrhythmias
Antifibrinolytics:
*aminocapronic acid
- activates physiologic fibrinolytic system, decreasing the formation of plasmin, the major
fibrinolytic enzyme from plasminogen, that degradate fibrin into fragments.
- stimulates thrombocytopoiesis, increases the thrombocyte receptor sensibility at the aggregation.
- also, it has an antiviral action and stimulates the detoxicant function of the liver.
-indication: Hemorrhage, tachycardia, prevention of hemorrhage in surgical interventions,

myopaphy, In overdosage with fibrilolytics.
-side effects: allergy, dyspepsia, arrhythmias.
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CLASSIFICATIONS
I. Remedies that stimulate erythropoiesis
A. Remedies used in hypochromic anemia

1) Iron deficiency anemia

- Iron drugs
ferrous sulfate
ferrous lactate
fercoven
ferroplex
hemofer
fenules
dextriferron
ferumlec
- Cobalt drugs
coamid
cobolamid
2) Anemias after chronic diseases

epoietin and
B. Remedies used in hyperchromic anemia

cyanocobalamin
folic acid
cobamamide
oxicobolamine
II. Remedies that inhibit erythropoiesis

sodium phosphate with phosphor 32 market
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CLASSIFICATIONS
1) That stimulate leucopoiesis

sodium nucleinate
leucogen
methyluracil
pentoxyl
batilol
etaden
filgrastim
molgramostim
sargramostim
2) That inhibit leucopoiesis

novembichin
busulfan
mercaptopurine
dopan
thiotep
Sari faried alkrinawi

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CLASSIFICATIONS
1.Drugs that decrease the release of mediator's histamine, other

ABS) from mast cell. (Stabilization of mast cells)
- glucocorticoids
- sodium cromoglicate
2.Drugs that inhibit interaction between histamine & its receptors
*H1 Histaminoblockers: diphenhydramine, clemastine
3. Drugs that diminish the main allergic symptoms:

( hypotension, bronchospasm)
A. Adrenomimetics: epinephrine, norepinephrine

B. bronchodilators:
I. Musculotropic: aminophylline
II. Sympaphomimetics: salbutamol
III. M-cholinoblockers: ipratropium
IV. Drugs that decrease tissues affection:- NSAIDS
4. Drugs used in cell-mediated immune reactions:

1.Immunosuppressants:
*glucocorticoids
* 4-aminoquinoline derivatives: chloroquine, hydroxichloroquine
*cytostatics: methotrexate, azathioprine, cyclosporine, mercaptopurine
2.Drugs that diminish the cytotoxic reactions & tissues alteration:
*steroid anti-inflammatory drugs

*non-steroid anti- inflammatory drugs
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CLASSIFICATIONS
I. according to the chemical structure

1. Ethanolamines:
a. diphenhydramine
b. clemastine (tavegyl)
2. Ethylendamines:
a. chlorophiramine (suprastine)
3. Alkylamines:
a. chlorphenamine
4. Phenothiasines:
a. promethasine
5. Imidasols:
a. antasoline
6. Hynuclidines:
a.quiphenamide (phencarol)
7. Piperidines:
a. astemisole
b. loratadine
c. terfenadine
8. Piperazines:
a. Cetirizine
II. according to the generations
*I generations
- diphenhydramine
- clemastine (tavegil)
- chlorophiramine (suprastine)
- chlorphenamine
- promethazine
- antasoline
- quiphenamide
*II generation
- astemisole
- loratadine
- terfenadine
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- cetirizinedipyridamole
H1- antihistamines : Mechanism of action
Contain a groupe ethanolamino as histamine has
inhibit competitively H1 receptors and the corresponding effects i. e. vasodilation and capillary
permeability increase.
do not inhibit antigen/antibodies reactions, nor histamine release, they inhibit H1 effects.
First Generation (Classical) Antihistamines

compete against the receptors - natural substrate, histamine, in binding to the receptors
Effect duration differs but in medium is equal 4-8 hours.
Effects : first-generation
1) Antiallergic (used in allergic rhinitis, conjunctivitis, allergic dermatitis etc.)
2) Sedative (inhibition of H1, muscarinic, serotoninic receptors from CNS) (ADRs - fatigue, dizziness, sedation)
3) Antivomiting (inhibit H1 HR from CNS)- used in kinetoses
4) Anticholinergic (peripheral effects atropine like effects) used in premedication
5) Antiparchinsonic (inhibit M ChR from CNS)
6) Anti serotoninic (antimigraine effect)
7) Antitussive (inhibit tussive center)- Control coughs due to colds or allergy
8) alpha1 adrenolytic activity (vasodilating effect)
9) Local anesthetic activity : used in urticaria
10) Tolerance (no more than 2-3 weeks)
Indications: first-generation
1. Allergic reactions (light & moderate).
2. Atopic dermatitis.
3. Kinetosis - difenhydramine & prometazine.
4. Itching - due to local anesthetics effect.
5. Orexigenic effect cyproheptadine
Diphenhydramine:

Side Effects: fatigue, dizziness, sedation.
Due to: the peripheral anticholinergic effects & the interactions with a number of
neurotransmitter systems in the CNS
has the ability to penetrate the blood brain barrier due to their relative lipophilicity.
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Second-generation / H1-antihistamines

- Selective action on H1 histaminoreceptors, no muscarinic and serotoninic action
- without sedating effect (do not cross blood-brain and thus their effects remain peripheral)
- No tolerance
- Favorable pharmacokinetics effects: onset (30-60 minutes)
- long duration of action (24-48 h).
Side effects 2nd generations

- they could induce ventricular arrhrythmias, prolongation of QT interval which can lead to
torsades de pointes by inhibition of potassium channels .
- in case of overdose, loratadine can cause sedation and antimuscarinic effects
3rd generation

Desloratadine & Levocetirizine: Active metabolites of II Generation
Characteristics: No sedative effects, less affect K channels from the heart
3rd generation

*Sodium cromoglicate
*Nedocromil
*Ketotifen
used to prevent or treat the symptoms of seasonal allergic rhinitis such as itching, sneezing, and
runny or stuffy nose
works by preventing the release of natural chemicals from cells in the body (mast cells) involved
in an allergic reaction
This medication may take up to one week before you begin to notice symptom relief.
Ketotifen: the same mechanism of action plus also inhibition of H1histaminoreceptors.

Indications: prophylaxis of hay fever, allergic asthma, and food allergies.
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CLASSIFICATIONS
I. Endogenous origin:
1 .Immunoregulatory peptides
a) drugs from thymus:
-natural: T-activin, Timalin, Timoptin, Timactid
-semisynthetic: Timogen, Imunofan.
b) From bone marrow: mielopid
2 .Cytokines:
a) recombined interleukins: Roncoleukin, Betaleukin.
b) Interferons :
-natural: Interferon, Leukinferon, Locferon.
-recombined: Chipferon, Reaferon, Viferon, Roferon A, Intron A
c) interferons inductors :
-natural: Aloxin , Megosin, Ridostin.
-semisynthetic: Amixin, Arbidol, Cycloferon,
II. exogen origin

1. bacterial origin drugs:
- naturale: Pyrogenal, Prodighiozan, Bronho-Munal, Imudon, Ribomunil, Ruzam
- semisynthetics: Licopid
2. vegetal origin: echinacee, Imunal.
3. entomologic origin: Imupurin
III. synthetic origin:

1. low molecular weight: Levamizol, Galavit, Glutoxim, Alloferon, Imunomax.
2. high molecular weight: Polioxidonium.
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Immunomodulators
medicine, having immunotropic activity, which at therapeutic doses restore function
immune system (effective immune defense)
Immunosuppressant: these agents suppress the immune response and could be used for the
control of pathological immune response in autoimmune diseases, graft rejections etc
Immunostimulants: these agents are envisaged to enhance bodys resistance against

infections, they enhance the basal levels of immune response and in individuals with
impairment of immune response as immunotherapeutic agent
Interferons
- antiviral immunomodulatory activity
- bind to cell surface receptors initiate intracellular events
- enzyme induction
- inhibition of cell proliferation
- enhancement of immune activities
- increased phagocytosis
Immunosuppressant

A. Minor Immunosuppressants
4- aminoquininolinics derivates: cloroquine, hidroxicloroquine
B. Major Immunosuppressants:
1. Glucocorticoids
2. Cytostatics:
alchilants: cyclophosphamide, chlorambucil
Antimetabolites: mercaptopurine, azathioprine
Antibiotics: cyclosporine, tacrolimus, actinomycin
Antilymphocyte Serum
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Immunosuppressant

- work by suppressing the immune system and decreasing inflammation in the digestive tract in
people with inflammatory bowel disease, ulcerative colitis, and Crohn's disease.
- Tacrolimus can be used in Crohn's disease when corticosteroids prove ineffective.
- In children, immunomodulators are less likely to cause growth failure than corticosteroids.
- Topical immunomodulators such as tacrolimus and pimeocrolimus have been found to offer
benefits in patients with eczema, vitiligo and nickel allergy.
INDICATIONS:
- Organ transplantation
- Auto-immune diseases
- Life long use
- Infection
- Cancers
- Nephrotoxicity
- Diabetogenic problem
Side effects of prescription immunomodulator medications

- nausea, vomiting, diarrhea, stomach ulcers, rash, malaise, liver inflammation.
- natural immunomodulators are less potent than prescription immunomodulators and also less
likely to cause side effects.
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Azathioprine

- Purine antimetabolite
medication
- Incorporation
s of false nucleotide 6 Thio-IMP 6Thio-GMP 6Thio-GTP
-
Inhibition of cell proliferation
- Impairment of lymphocyte function
- Uses:
Prevention of organ transplant rejection, rheumatoid arthritis
- Toxicity:
Bone marrow suppression- leukopenia, thrombocytopenia, anemia
Increased susceptibility to infection, Hepatotoxicity, Alopecia, GI toxicity
Drug interaction: Allopurinol
Glucocorticoids
-
medications
-Induce redistribution of lymphocytes decrease in peripheral blood lymphocyte counts
- Intracellular receptors regulate gene transcription
- Down regulation of IL-1, IL-6
- Inhibition of T cell proliferation
- Neutrophils, Monocytes -display poor chemotaxis
- Broad anti-inflammatory effects on multiple components of cellular immunity
- Uses:
transplant rejection autoimmune diseases (RA, SLE), hematological conditions
psoriasis, inflammatory bowel disease, eye conditions
- Toxicity:
toxicity growth retardation, avascular necrosis of bone, risk of infection,
poor wound healing, cataract, hyperglycemia, hypertension
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Cyclosporine More effective against

medications
dependent immune mechanisms transplant rejection, autoimmunity
- T-cell
- IV, Oral
- Uses:
Skin Conditions- Atopic dermatitis, Alopecia Areata, Pemphigus vulgaris, Lichen planus,
Pyoderma gangrenosum
Organ transplantation: Kidney, Liver, Heart
rheumatoid arthritis, Psoriasis, aplastic anemia
- Toxicity:
renal dysfunction, tremor, hirsutism, hypertension, hyperlipidemia
gum hyperplasia, hyperuricemia - worsens gout
Tacrolimu
s
- Inhibits T-cell activation by inhibiting calcineurin

- Uses:
Prophylaxis of solid-organ allograft rejection
- Toxicity:
nephrotoxicity, neurotoxicity-tremor, headache, motor disturbances, seizures
GI complaints, hypertension, hyperglycemia, risk of tumors, infections
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CLASSIFICATIONS
I group: Nonsteroidal anti-inflammatory drugs

(Nonsteroidal anti-inflammatory) (NSAIDs)
A) non- selective NSAIDs

1) Salicylates: acetylsalicylic acid
2) Pirazolone and pirazolidine derivates: fenylbutazone
3) Indolacetic acids: indomethacin
4) Arhylacetic acids: diclofenac
5) Propionic acids: ibuprofen, naproxen
6) Fenamates: mefenamic acid, flufenamic acid
7) Oxicam derivatives: piroxicam, meloxicam, lornoxicam
8) Paraaminophenols derivates: paracetamol
B) selective NSAIDs
- nimesulid
- meloxicam
- celecoxib
II group: steroidal anti-inflammatory drugs

- Glucocorticoids: hydrocortisone, prednesolone, dexamethasone, prednisone
III group: Slow-acting , anti-inflammatory drugs:

a) 4-aminoquinoline derivatives: chloroquine , hydroxichloroquine
b) Gold-salts: auranofin, gold sodium thiomalate, aurothioprol.
c) D-Penicillamine
d) Sulfanilamide drugs: sulfasalazine
e) Cytostatics: methotrexate, azathioprine, cyclosporine, mercaptopurine
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Definition
Drugs that inhibit inflammation by preventing the synthesis of prostanoids.
-Prostanoid consisting of: the prostaglandins (mediators inflammatory and anaphylactic reactions)
-thromboxanes (mediators of vasoconstriction)
-prostacyclins (active in the resolution phase of inflammation).
Mechanism of Action of NSAID

Inhibit prostanoids synthesis by inhibiting cyclo-oxygenase (COX-1 & COX-2) enzymes
acetylsalicylic acid: - inhibits the enzyme irreversibly
- Induction of the generation of anti- inflammatory lipoxins
(aspirin-triggered lipoxins or ATLs)
pharmacological actions of Nsaids

of nsaids
- Analgesic
- Anti-inflammatory
- Antipyretic
- Anti-platelet
- Antidiarrheal effects
Mechanism of Action : non selective Nsaids

non- selective NSAIDs
Anti-inflammatory effect

Irreversible non-selective COX inhibitor
Inhibits platelet aggregation
Interferes with the mediators of the kallikrein system (bradykinins)
Inhibits chemotaxis of PMN leukocytes and macrophages
Analgesic effect: Probably inhibits pain stimuli at a subcortical site)
Antipyretic effect: COX inhibition in the CNS, inhibition of IL-1 (release in macrophages).
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Pharmacokinetics: non-selective Nsaids

- Weak organic acids

- Well absorbed
- Food doesnt change their bioavailability
- Metabolized in phase I and II
- Also in CYP3A, CYP2C (part CYP450)
- Renal, most important route of excretion. (biliary excretion and absorption)
- 98% Bound to Albumin
- Found synovial fluid after repeating doses
Clinical Uses : non-selective Nsaids

- As analgesic to mild to moderate pain.
-Combine with opioid analgesics for cancer pain.
- As anti-inflammatory in rheumatoid arthritis rheumatic, fever & inflammatory joints
- Antipyretic, when reducing the fever is desirable.
- Prophylaxis of ischemic heart disease, to reduce incidence of coronary artery disease
ADR's : non-selective Nsaids

- Gastrointestinal effects: GI upset, Peptic ulcers, upper gastrointestinal bleeding.

- Salicylism - Aspirin poisoning: Nausea, vomiting, tinnitus, decrease hearing, vertigo,
hyperthermia, hyperventilation.
- Hepatotoxicity, elevation of liver enzymes, hepatitis.
- Hypersensitivity (Asthma, Rashes)
- Renal toxicity (decrease function).
- Changes in uric acid levels (low doses high serum levels)
- Reyess-like syndrome (Hepatoencephalopathy) highly lethal.
- Avoid aspirin in children with influenza or chickenpox infections (give Tylenol).
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- Celecoxib, Etoricoxib, Rofecoxib, Valdecoxib, Meloxicam (preferential)

- inhibit prostacyclin (COX-2) in sites of inflammation
- do not block "housekeeping" effect of COX-1
- antipyretic, analgesic, anti-inflammatory effect
Indications
- Osteoarthritis, rheumatoid arthritis, dysmenorrhea, acute gouty attacks, musculoskeletal pain.
-
Rofecoxi
bs
- Higher
incidence of cardiovascular thrombotic events.
- Inhibits prostacyclin letting TXA2 act freely and promote platelet aggregation.
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- Synthetic or natural steroids

- Primary Use as anti-inflammatory & immunosuppressant
Actions: Anti-inflammatory

- decrease recruitment of monocyte/macrophage into affected area
- decrease elaboration of chemotactic substances
- increase Lipocortin
- decrease TNF from phagocytic cells
- decrease IL1 from monocyte-macrophage
- decrease Formation of Plasminogen Activator
- decrease Action of MIF & fibroblastic activity
- decrease Expression of cyclooxygenase II
ADR's
1) Metabolic toxicity:
- Iatrogenic Cushings syndrome
- Hyperglycemia, glycosuria, diabetes
- Myopathy (negative nitrogen balance)
- Osteoporosis (vertebral compression fracture)
- Retardation of growth (children)
- Hypertension, edema, CCF
- Avascular necrosis of femur
2) Behavioral toxicity:
euphoria, psychomotor reactions, suicidal tendency
3) Ocular toxicity: steroid induced glaucoma, posterior subcapsular cataract
4) Others: Superinfections, delayed wound healing, Steroid arthropathy Peptic ulcer

, live vaccines are dangerous
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Contraindications

- Infections
- Hypertension with CCF
- Psychosis
- Peptic ulcer
- Diabetes mellitus
- Osteoporosis
- Glaucoma
- Pregnancy: prednisolone preferred
therapeutical use

1. Arthritis
first choice
- Not the drug of
- Prednisolone5 or 7.5 mg
- Intra-articular injection
2. Rheumatic carditis
- Not responding to salicylates
- Severely ill pts.
- Prednisolone 40mg in divided doses
- Salicylates given concurrently to prevent reactivation
3. Collagen diseases
- pemphigus vulgaris, polyarteritis nodosa
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Slow-acting, anti-inflammatory drugs

- they can't repair existing damage, they can only prevent further injure.
- It is believed that gold salts are taken up by macrophages and suppress phagocytosis and
lysosomal enzyme activity.
- this mechanism retards the progression of bone and articular destruction. also they inhibit
antibody production by B- lymphocytes.
4-aminoquinoline derivatives

1. they stabilize lysosomal membranes and trap free radicals
2. they inhibit blastransformation of T lymphocytes.
3. inhibit collagen synthesis
D - penicillamide:
*Mechanism of action: it interacts with rheumatoid factor and inhibits its synthesis
- it inhibits collagen maturation
- cytostatic action (it binds with bivalent metals: Cu, Zn, Mg, I and inhibits protein synthesis)
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Hormones: biologically active substances, produced by the endocrine glands & special cell groups.
Hormones drugs:
- Natural (human, animal)
- Synthetic
Hormones antagonists: drugs that block the appropriate receptors or inhibit hormones synthesis
and and are used for the treatment of endocrine gland hyperfunctions
CLASSIFICATIONS
I. AGENTS OF PROTEIN OR PEPTIDE ORIGIN drugs that decrease platelet aggregation (antiaggregant)
- Hormonal preparations of the hypothalamus

- pituitary
- Parathyroid gland
- Pancreas
- calcitonin
II. AMINOACID DERIVATIVES

- Hormonal preparations of the thyroid glands
- Epiphysis
III. STEROID COMPOUNDS

- Hormonal preparations of the adrenal cortex
- Sex glands
CLASSIFICATIONS
I. Steroids and thyroid hormones: drugs that decrease platelet aggregation (antiaggregant)
- enter the cell and bind to cytosolic receptors that transport the steroid into the nucleus.
- the steroid-receptor complex alters gene expression.
II. Polypeptides and catecholamines
- interact with the receptors on the cell surface, and activate various enzymes that
contribute to the formation of o lot of secondary mediators (cAMP, cGMP),
and increase the membranes permeability for Ca +2, and other metabolites.
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hypothalamic factor/hormones drugs analogues of hypothalamus

factor/hormones and substances acting on
hormone synthesis and release
Corticotropin-releasing hormone (CRF) Corticoliberine
Thyrotropin-releasing hormone (TRH) Prothyreline (rifathyroin)
Gonadotropin-releasing hormone (GNRH) Gonadorelin hydrochloride , histrelin , goserelin
, nafarelin , danazol , leuprolide
Growth Hormone-releasing factor Sermoreline

(GHRF, somatoreline)
Growth Hormone-inhibiting factor Octreotide, lanreotide
(somatostatin) Bromocriptine
Prolactin release inhibiting hormone lisuride

(probably dopamine)
Prolactin releasing factor (PRF)
Melanocyte -stimulating hormone

(MSH) releasing factor
MSH release - inhibiting factor
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sermorelin

*M.O.A
- stimulates release of GH
*indication :
- diagnostic evaluation of decreased plasma GH.
- GH deficiency
- GH therapy in children with tertiary (hypothalamic deficient)
*side effect:
- transient flushing, injection site reactions, chest tightness, antibody development
*contraindications:
- not to use with other drugs which affect pituitary gland
*caution in children whose GH deficiency results from an intracranial lesion.
protirelin (TRH )
*M.O.A
- stimulates TSH release from pituitary gland.
*indication :
- diagnosis of thyroid function
*side effect:
- seizure , amaurosis fugax in patient with pituitary tumor
- anxiety, hyper and hypotension.
* transient change in blood pressure can occur immediately following administration

* cyproheptadine and thioridazine decrease protirelin-mediated TSH response
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somatostatin
*M.O.A
-inhibits GH release
*indication :
- VIPomas
- carcinoid tumors
- enterocutaneous and pancreatic fistula
- short bowel syndrome
*side effect:
- arrhythmias, erythroderma, life threatening water retention,
- glucose intolerance, rebound hormonal hypersecretion (seldom).
*contraindications:
- hypersensitivity to somatostatin
* reduces analgesic effects of morphine
octreotide
*M.O.A
-inhibits GH release
*indication :
- acromegaly
- flushing and diarrhea from carcinoid tumors
- carcinoid crisis
- diarrhea from vasoactive intestinal peptide secreting tumors
- to control GI bleeding and to reduce secretory diarrhea.
*side effect:
- arrhythmias, bradycardia, hypoglycemia, gallstones formation
- abdominal pain, constipation, diarrhea, nausea and vomiting.
*contraindications:
- hypersensitivity to octreotide
* octreotide also available in depot formulation
* decrease cyclosporine levels
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*M.O.A
- D2 receptor agonist inhibits spontaneous and TRH induce release of prolactin
- D1 receptor agonist (to a lesser extent)
*indication :
- amenorrhea and galactorrhea from hyperprolactenemia
- acromegaly
- Parkinson disease
- premenstrual syndrome
- cushing syndrome
- hepatic enhephalopathy
- neuroleptic malignant syndrome releated to neuroleptic drug therapy.
*side effect:
- Cerebrovascular accident (CVA), seizure, acute MI
- CNS effects such as psychosis, hallucination, insomnia, nightmares
- dizziness, hypotension, abdominal cramps, nausea and vomiting, headache
- nasal congestion, digital vasospasm
*contraindications:
- hypersensitivity to ergot derivates
- uncontrolled hypotension
- toxemia of pregnancy
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hypothalamic factor/hormones drugs analogues of pituitary hormones

and substances acting on hormone
synthesis and release
Adenocorticotropin hormone Corticotropin
(ACTH, coticotropin)
Cosyntropin
Anterior Tetracosactide
Thyroid-stimulating hormone Thyrotropin
(TSH , thyrotropin)
Luteinizing Hormone (LH) Chorion gonadotropin
or interstitial cell- stimulating
pituitary hormones
Growth Hormone Somatotropin
(GH, somatotrophin) somatrem
Prolactin Lactin
Intermediate Alpha, beta and delta MSH Intermedin

lobe melaxen
Oxytocin Oxytocin
demoxytocin pituitrinum
posterior
Vasopressin Vasopressin antiurecrinum
pituitary Desmopressin
Lypressin
desmopressin
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octreotide
*M.O. A
*Exert their effects through G-protein coupled receptors
In women:
FSH direct ovarian follicle development
FSH and LH ovarian steroidogeneses
-Follicular stage:
LH androgen production
FSH- conversion of androgen to estrogen
- Luteal phase:
LH, estrogen and progesterone production
human chorionic gonadotropin (HCG) (if pregnancy) - estrogen and
progesterone production (nearly identical with LH) LH receptors)
In men:
FSH spermatogenesis, production of androgen binding protein and
conversion of testosterone to estrogen ( by sertoil cells )
LH production of testosterone by leyding cells.
*indication:
Diagnosis uses of gonadotropins
- pregnancy testing (urine HCG)
- ectopic pregnancy, hydatidiform mole, choriocarcinoma, malignancies (germ cells tumors)
(plasma hCG)
- localization if ovulation (urine LH levels)
-localization of endocrine diseases
Therapeutic uses of gonadotropins:
-male infertility -hypogonadotropic hypogonadism (hCG , menotropins
(FSH+LH) or recombinant FSH
- cryptorchidism(hCG)
- fertility induction in women
*side effect:
- Ovarian hyperstimulation syndrome (ovarian enlargement, ascites, hydrothorax,
and hypovolemia, sometimes shock)
- multiple pregnancies (15-20%)
- ovarian enlargement , hemoperitonium , fever
- arterial thromboembolism
- headache, depression, edema, precocious puberty, production of antibodies to hCG (rarely)
- ovarian cancer
- gynecomastia "in men "
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*M.O.A
- Its act via a specific GPCR (OXT) closely related to the v1a and v2 vasopressin receptors, in the
human myometrium, OXT couples to Gq-G11 activating the PLC IP3 calcium pathway and
enhancing activation of voltage sensitive calcium channels.
- Oxytocin also increase local prostaglandins production, which further stimulates uterine
contraction.
*Therapeutic use:
- Contraction of the uterus
- contracts the myoepithelial cells in the mammary glands "milk let-down"
- vasodilator action
- weak antidiuretic action
*indications:
- Induction of labor at term
- facilitation of threatened abortion
- postpartum control of bleeding after expuision of the placenta
*M.O.A
- Is an analogous of naturally vasopressin (ADH), primary action is enhanced reabsorption of
water in the kidneys.
*Therapeutic use:
- Prevention of nocturnal enuresis
- maintenance of appropriate body water content in in diabetes insipidus
- to control bleeding in certain types of hemophilia or von willebrand disease.
*indication:
- central Diabetes insipidus (caused by ADH deficiency) .
- to control bleeding in certain types of hemophilia and von willebrands"s disease.
- primary nocturnal enuresis.
*side effect:
- Seizures, drowsiness, headache, listlessness
- dyspnea, rhinitis, nasal congestion, flushing,
- hypertension, hypotension, tachycardia, mild abdominal cramps,
- nausea, vulval pain, water intoxication / hyponatremia, phlebitis at IV site,
*contraindications:
- hypersensitivity, hypersensitivity to chlorobutanol
- patient with type IIB or platelet type (pseudo) von willebrands disease
- hyponatremia
- use cautiously in: angina, hypertension, patients at risk of hyponatremia
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Thyroid hormones
1. monocomponent drugs
- Levothyroxine (T4, thyroxin, eutyrox, T4, etc)
- Liothyronine (T3 , triiodthyronin)
2. Combined drugs
- Thyreodin, thyireotom , (T3 + T4 = 1 : 4)
- Thyreotom forte , thyreocomb , (T3 + T4 +k1 = 1 : 7 : 15)
- Novothyral (T3 + T4 = 1 : 5 )
- Iodthyrox (T4 + KI)
*M.O. A
free hormones enter the cell by both passive diffusion and active transport and bind to
thyroid hormone receptors (TRs)
- nucleus and cytoplasm:
activation of gene transcription of down regulation gene expression
affect (increase) mitochondrial metabolism
- plasma membrane receptors:
stimulates intracellular signal transduction (Ex: increase cAMP)
*indications:
thyroid hormone replacement therapy (thyroid supplementation)
- hypothyroidism
- subclinical hypothyroidism
- myxedema coma (IV)
- thyroidectomy
Treatment or suppression of euthyroid goiters and thyroid cancer and suppression therapy of
thyroid cancer.
*ADRs:
usually seen when excessive doses cause iatrogenic hyperthyrodism :
CNS : nervousness , headache , insomnia , irritability
CVS : angina , arrythmias , hypotension , tachycardia
GIT : cramps , diarrhea , vomiting , choking , gagging , dysphagia
Derm : hair loss ( in children ) , sweating
Endo : hyperthyroidism , menstrual irregularities
Metabolism: heat intolerance, weight loss, accelerated bone maturation in children's
*contraindication:
- hyperthyroidism, recent MI, hypersensitivity
use cautiously in:

- cardiovascular diseases (initiate therapy with lower doses)
- serve renal insufficiency
- Uncorrected adrenocortical disorders
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Anti thyroid drugs

1) drugs which decrease release of TSH:
- diiodtyrosine
- iodine
2) anti-thyroid drugs, which interfere with the synthesis of thyroid hormones (thioamines)
- carbimazole
- methimazole
- thiamazole
- propylthiouracil
- methylthiouracil
3) ionic inhibitors, which block the iodine transport mechanisms
- potassium perchlorate
- pertechnetate
- fluoborate
- thiocyanate
4) anti-thyroid drugs, which decrease release of thyroid hormones from the gland
(also may decrease hormone synthesis)
- potassium iodine
- sodium iodine
- lugol sol.
5) anti-thyroid drugs, which damages the thyroid gland with ionizing radiation
- radioiodine
6) inhibitors of peripheral thyroid hormones metabolism
- adrenoblckers
- ipodate
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*M.O. A/ thioamines
- thioamines compete with thyroglobulin for oxidized iodide in a process that is catalyzed by the
enzyme thyroid peroxidase.
- Propylthiouracil inhibits thyroid peroxidase as well as peripheral T4 and T3 conversion.
- iodinated thioamines may also be able to bind to thyroglobulin, further antagonizing any
coupling reactions.
*indications/thioamines
- palliative treatment of hyperthyroidism
- control hyperthyroidism in preparation for thyroidectomy or radioactive iodine therapy
- as definitive treatment, to control the disorders in anticipation of a spontaneous remission in
gravis disease
- in conjunction with radioactive iodine, to hasten recovery while awaiting the effects of radiation
*ADRs / thioamines
- goiter formation (goitrogens)
- pruritic rash
- arthralgia
- hypoprothrombinemia increase bleeding tendency
*contraindication / thioamines
- hypersensitivity
- lactation
* use cautiously in:

- patients with bone marrow reserve
- patients > 40 years old ( risk of agranulocytosis)
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*ionic inhibitors, which block the iodide transport mechanism*

*M.O. A
-high levels of iodide inhibit thyroid hormone synthesis and release (wolff- chaikoff effect )
-reduce the size and vascularity of the thyroid gland.
-inhibition of the release of thyroid hormone.
*Indications
-preparation for of thyroid gland surgery.
-as a prevention measure to avoid uptake of radioactive iodide.
-thyrotoxic crisis (thyroid storm)
-in conjunction with anti thyroid drugs and propranolol
-severe thyrotoxicosis.
*ADRs
-angioedema
-multiple cutaneous hemorrhages
-serum-sickness type of hypersensitivity fever arthralgia, lymph node enlargement, eosinophilia
-thrombotic thrombocytopenic purpura
-fatal periarteritis nodosa.
Symptoms are dose related.

*unpleasant brassy taste and burning in the mouth and throat, soreness of the teeth and gums,
increased salivation.
*coryza, sneezing, and irritation of the eyes with swelling of the eyelids
*mild iodism simulates a head cold
-severe headache that originates in the frontal sinuses
-irritation of the mucous glands of the respiratory tract causes a productive cough.
*excess transudation into the bronchial tree may lead to pulmonary edema,
*parotid and submaxillary glands may become enlarged and tender.
*inflammation of the pharynx, larynx, and tonsils.
*skin lesions usually are mildly acneform and distributed in the seborrheic areas. rarely severe
and sometimes fatal eruptions (iodemna)
*symtptoms of gastric irritation are common ,and diarrhea (sometimes bloody )

-fever, anorexia, depression.
treatment: osmatic dieresis, chloruretic diuretics, and salt loading.

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*Diabetes mellitus
-Affects approx. 5-8%
-Mostly asymptomatic
-Tendency increase with obesity
-One of the leading cause of death by disease
-One of the leading cause of blindness
-One of the leading cause of renal failure
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CLASSIFICATIONS
I. Drugs for replacement drugs that decrease platelet aggregation (antiaggregant)
-insulin
II. Oral antidiabetic drugs
1.drugs that stimulate endogenous insulin release

- sulfonylurea derivatives
A. according to generation
a) I.generation
- tolbutamine
- chlorpopamide
- tolazamide
- carbutamide
b) II.generation
- glibenclamide (maninil)
- glipizide
- glyburide
- gliclazid
B. according to duration of action

a) Medium duration (8-24 hours)
- tolbutamine
- glibenclamide
- glipizide
b) Long duration (24-36 hours)
- chlopropamide
Meglitidine derivatives:
- Nateglind
- repaglind
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2.drugs that inhibits gluconeogenesis and promote glucose uptake in the tissues
Biguanides
a) short action (4-6 hours)
- metformin
- euformin
b) long duration (14-16 hours)
- buformin
- diformin
3. drugs that increase tissue sensibility to insulin
thiazolidinediones
- rosiglitazone
- pioglitazon
4. drugs that inhibits glucose absorption in the small intestine
(inhibitors of a- glucosidase)
-acarbose
5. inhibitors of aldoreductase
-tolrestat
Human insulin Animal insulin

Short duration (4-8 hours) and maximum action at (1-4 hours)
Actrapid HM Actrapid MS
Rapid insulin regularIletin II
Inutral HM Betasint neutral insulin E-40S
Homopap 40 Maxirapid insulin VO-S
Regular humulin Insulin S
Insulin GPP
Medium duration (18-24 hours) and maximum action at (6-12 hours)
Izophane Insulin HM (isophane insulin Iletin IIL
suspension ) Iletin II NPH
Basal Insulin Betasint lente insulin E 40S
Monotard HM Betasint lente insulin NPH E 40S
Protiphan HM Lente insulin GPP
Homolong 40 Insulin GPP
Humulin L Basal insulin
Humulin H Monotard MS
Protaphane MS
Humulin NPH
Long duration of action (24-40 h.) and maximum action at (12-18 hours)
Ultratard HM (isulin zinc suspension
extended USP)
Humulin UL
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1. Severe Hypoglycemia (< 50 mg/dl) Life threatening

-Overdose of insulin
-Excessive (unusual) physical exercise
-A meal is missed
2. Weight gain
3. Local or systemic allergic reactions (rare)
4. Lipodystrophy at injection sites
5. Insulin resistance
6. Hypokalemia
Oral Hypoglycemics
all taken orally in the form of tablets.

Pts with type11 diabetes have two physiological defects:
1. Abnormal insulin secretion
2. Resistance to insulin action in target tissues associated with decreased number of insulin
receptors
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insulin
*M.O. A
-it binds to a specific receptor on the surface of cells that contains two alpha and beta subunits ,
the alpha subunit are entirely extracellular and binds with insulin , after it activates b subunits that
activates tyrosine kinase , tyrosine kinase is activator of a cascade of kinase and phosphates
*indication
-type I DM, retinopathy, uncontrolled type II DM, diabetic after pancreotomia, precoma and
coma, nephropathy , diabetic coma
*contraindication:
-allergy, hypoglycemia
*side effect:
-pain in the injected region, hypoglycemia, allergy, lipodystrophy, hypoglycemic coma
carbohydrate
- glucose uptake
- glycogen synthesis ( storage)
- gluconeogenesis(liver)
- glycolysis(muscle)
- conversion of carbohydrates to fat (lipogenesis)
FATS
- lipolysis
- lipogeneses
PROTENIS
- amino acid uptake (protein synthesis)
POTTASIUM
- potassium uptake into cells
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*M.O. A
- release of insulin from beta -cells
- reduction of serum glucagon concentration
- potentiation of insulin secretion action of target tissues
*ADRs
- nausea and vomiting, diarrhea, abdominal pain
- hypoglycemia, weight gain
- blood dyscrasias (agranulocytosis, pancytopenia, thrombocytopenia)
- hyponatremia and water intoxication
- Cholestatic obstructive jaundice (uncommon)
- dermatitis (mild)
- muscle weakness, headache, vertigo (no common)
- increased cardio-vascular mortality with long-term use
*contraindication
- type I DM (insulin dependent)
- parenchymal disease of the liver / kidneys
- pregnancy, lactation
- major stress
E.x "repaglinide, nateglinide"

*pharmacokinetics
-taken orally
-rapidly absorbed (peak approx.1 hr)
-metabolized by liver
-t1/2= 1hr
-duration of action 4-5 hr
*M.O. A
- Bind to same k-ATP channel as do sulfonylureas, to cause insulin release from B-cells
*clinical use
- Approved as monotherapy and in combination with metformin in type 2 diabetes
Taken before each meal, 3 time /day
- Does not offer any advantage over sulfonylureas:
- Advantage pts. allergic to sulfer or sulfonylurea
*clinical use
- hypoglycemia, Wt gain (less than SUs), Caution in pts with renal & hepatic impairment.
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E.x "metformin "
*pharmacokinetics
-given orally
-not bind to plasma proteins
-not metabolized
-excreted unchanged in urine
-t 2 hr
*M.O. A
1.increase peripheral glucose utilization
2.inhibits gluconeogenesis
3. impaired absorption of glucose from the gut.
*side effects
1. Metabolic taste in the mouth
2. Gastrointestinal (anorexia , nausea , vomiting , diarrhea , abdominal discomfort )
3. Vit B12 deficiency (prolonged use)
4. Lactic acidosis ( rare 01/30,000-exclusive in renal & hepatic failure)
*Contraindications
1.heaptic impairment
2.renal impairment
3.alcholism
4.herat failure
*indications
1.obese patients with type 11 diabetes
2.alone or in combination with sulfonylureas
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E.x "acarbose "

*pharmacokinetics
-given orally
-not absorbed from intestine except small amount t1/2 3-7hr
-excreted with stool.
*M.O. A
-inhibits intestinal alpha glucosidases and delays carbohydrate absorption , reducing
postprandial increase in blood glucose
*side effects
-flatulence
-loose stool or diarrhea
-abdominal pain
-alone does not cause hypoglycemia
*indications
-Patients with type11 inadequately controlled by died with or without other agents (SU, metformin)
-Can be combined with insulin
-May be helpful in obese type 11 patients (similar to formation)
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New class of oral antidiabetics
E.x " rosiglitazone, pioglitazone "

*pharmacokinetics
-99% absorbed
-metabolized by liver
-99% of drug binds to plasma proteins
-half life 3-4h
-eliminated via the urine 64% and feces 23%
*M.O. A
-Increase target tissue sensitivity to insulin by:

Reducing hepatic glucose output &increase glucose uptake and oxidation in muscles
And adipose tissue.
-They do not cause hypoglycemia
*side effects
-mild to moderate edema
-wt gain
-headache
-myalgia
-hepatoxicity
*indications
-Type 2 diabetes alone or in combination with metformin or sulfonylurea or insulin in patients

resistant to insulin treatment.
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CLASSIFICATIONS
A. ACCORDING TO THE WAY OF ADMINISTRATION

I. For enteral administration
-Cortisone acetate
-Hydrocortisone acetate
-Prednisone
-Prednisolone
-Methylprednisolone
-Triamcinolone
-Dexamethasone
-Betamethasone
II. For parenteral administration
A. Intravenous B. Intramuscular
-Hydrocortisone hemisuccinat -Hydrocortisone acetate
-Prednisolone hemisuccinat -Prednisolone acetate
-Methylprednisolone hydrochloridone -methyl prednisolone acetate
-Dexamethason sodium phosphate -triamcenelone acetonide
-Betamethason sodium phosphate -plus, those for IV administration
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III. For topical administration

-Hydrocortisone
-Prednisolone
-Flumetasone
-Flucortolone
-Acetonide
-Mometasone
-Budesunide
-Beclomethasone
-Fluticasone
-Clobetasol
IV. For inhalation administration

-Beclomethasone
-Flunisolide
-Budesonide
-Fluticasone
B. ACCORDING TO THE DURATION OF ACTION
I. Short action: half-life 8-12 h

-Cortisone
-Hydrocortisone
II.Medium action: half-life 12-36 h

-Prednisolone
-Prednisone
-methyl prednisolone
-triamcenelone
III. long action: half-life 36-54 h

-betamethasone
-dexamethasone
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C. ACCORDING TO THE DURATION OF ACTION

I. low potency (20-25mg)
-Cortisone
-Hydrocortisone
II. intermediate potency (4-5mg)
-prednisolone
-prednisone
-methyl prednisolone
-triamcenelone
-flucortolon
III. potent (0.5-0.75mg)
-betamethasone
-dexamethasone
D. ACCORDING TO THE MAIN EFFECTS
)anti-inflammatory mineralocorticoid)
Moderate anti-inflammatory and mineralocorticoid
-Cortisone
-Hydrocortisone
Marked anti-inflammatory effect and water saline retention
-Prednisone
-prednisolone
-Methylprednisolone
Marked anti-inflammatory, practically free from effects of salt and water retention
-Betamethasone
-Dexamethasone
-Triamcinolone
-Fluprednisolon
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1) carbohydrate
2) protein
3) lipid
4) CND
5) blood
6) immunosuppressant
7) growth and cell division
8) electrolyte and H2O
9) CVS
10) skeletal muscle
11) stomach
12) anti-inflammatory
13) respiratory system
14) calcium metabolism
*Metabolic actions*
carbohydrate:
-decreased uptake and utilization of glucose accompanied by increased gluconeogenesis
-this causes a tendency to hyperglycemia
proteins:
Increased catabolism, reduced anabolism
lipids:
-a permissive effect on lipolytic hormones and a redistribution of fat, as observed in Cushing's
syndrome
*Actions: carbohydrate and protein metabolism*

Negative nitrogen balance and hyperglycemia
increase gluconeogenesis
-peripheral actions (mobilize AAs, glucose and glycogen)
-hepatic action
decrease peripheral utilization of glucose
increase glycogen deposition in live

- (activation of hepatic glycogen synthase)
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*Action: lipid metabolism*

redistribution of fat
-buffalo hump
-moon face
Promote adipokinetic agent's activity

(glucagon, growth hormone, adrenaline, thyroxine)
*Action: electrolyte and water balance*

aldosterone is more important
act on DT and CD of kidney
-increase Na+ reabsorption
-increase urinary excretion of k+ and H+
Addison's disease??
- Na+ loss
- shrinkage of ECF
- cellular hydration
- hypodynamic state of CVS
- circulatory collapse, renal failure death
*Regulatory actions*
hypothalamus and anterior pituitary gland: a negative feedback action resulting
in reduced release of endogenous glucocorticoids
cardiovascular system: reduced vasodilation decreased fluid exudation
musculoskeletal: decreasing osteoblast and increasing osteoclast activity
Inflammation and immunity:

- acute inflammation: decreased influx and activity of leukocytes.
-chronic inflammation: decreased activity of mononuclear cells, decreased angiogenesis
, less fibrosis
-lymphoid tissue: decreased clonal expansion of T and B cells, and decreased action of
cytokine secreting T cells. switch from TH1 to TH2 response.
mediators:
- decreased production and action of cytokines, including interleukins, tumor necrosis
factor a and granulocyte macrophage colony stimulating factor
-reduced generation of ecicosanoids
-decreased generation of IgG
-decreased in complement in the blood
-increased release of anti inflammatory factor such as interleukin -10and annexin 1.
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* Actions: cardiovascular system *

- restrict capillary permeability
- maintain tone of arterioles
- myocardial contractility
-Mineralocorticoid induced hypertension??
Na+ sensitize blood vessels to the action of catecholamines & angiotensin.
* Actions: skeletal muscle*

-Needed for maintaining the normal function of skeletal muscle.
-Addison's disease: weakness and fatigue is due to inadequacy circulatory system
-Prolonged use: steroid myopathy
* Actions: CNS*
direct:
-mood
-behavior
-brain excitability
indirect:
- maintain glucose, circulation and electrolyte balance
Increase icp (pseudo tumor cerebral)-rare
* Actions: Stomach*
-Aggravate peptic ulcer. may be due to;

-Increase acid and pepsin secretion.
-Decrease immune response to H. pylori.
* Actions: Blood*
RBC:
-Increase HB and decrease content (erythrophagocytosis)
WBC:
-Decrease lymphocytes, eosinophils, monocytes, basophils
-Increase polymorphonucleocytes
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* Actions: anti - inflammatory *

-decrease recruitment of WBC and monocyte into affected area &elaboration of
-chemotactic substances
-increase lipocortin.
-decrease Elam1 and ICAM_1 in endothelial cells.
-decrease TNF from phagocytic cells.
-decrease IL 1 from monocyte -macrophage.
-decrease formation of plasminogen activator.
- action of MIf and decrease fibroblastic activity.
-decrease expression of CoX 2
* Actions: immunosuppressive and anti-allergic *

-suppress all types of hypersensitivity and allergic phenomenon.
interfere with all steps of immunological response.
causes greater suppression of cell-mediated immunity (graft rejection and delayed
hypersensitivity).
decrease antigen expression from grafted tissue, delay revascularizations, decrease
sensitization of T lymphocytes etc.
* Actions: growth and cell division *

inhibit cell division or synthesis of DNA.
delay the process of healing.
retard the growth of children.
* Actions: calcium metabolism *

decrease intestinal absorption
increase renal excretion
excessive loss of calcium from spongy bones (E.x, vertebrae, ribs, etc.)
* Actions: respiratory system *
not bronchodilators
most potent and most effective anti -inflammatory .
effects not seen immediately (delay 6 or more Hrs.)
inhaled corticosteroids are used for long term control
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1.subestitution purposes :
-acute adrenocortical insufficiency (primary and /or secondary).
-chronic adrenocortical insufficiency ;
2.suppression purposes :
-congenital dysfunction (hyperplasia) of adrenal cortex.
3.diagnostic purposes :
-diagnosis and differental diagnosis of Cushing's syndrome .
4.with pharmacodynamic (palliative) purposes:
A. rheumatic diseases
1.systemic disease of conjunctive tissue (collagenosis):
-disseminated lupus erythematosus -polyarthritis nodosa
-lupus nephritis -polymyositis and so on ;
2.joint diseases
-rheumatoid arthritis -rheumatic fever;
-acute gouty arthritis -deformingosteoarthrosis;
-tendinitis -bursitis .
B. kidney disease
-glomerulonephritis (rapidly progressive , mezangiocapillary );
-nephrotic syndrome;
-focal glomerulosclerosis
C.liver and digestive diseases
-chronic active hepatitis , subacute hepatic necrosis;
-alcoholic hepatitis (severe form);
-nonspecific ulcerative colitis - crhon's diseases (ileitis);
D. ophthalmic diseases
-iridocyclitis
-oculomotor nerve neuritis;
-iritis,
- conjunctivitis;
8
M1439 M1439
E. allergic diseases
-anaphylactic shock;
-status asthmaticus and severe forms of asthma;
-quincke edema -allergic reaction to drugs;
*dermatitis and allergic dermatitis (severe forms) ;
*allergic rhinitis (severe forms)
F. tumors
*acute lymphoblastic leucosis (acute leukemia in children)
*malignant lymphomas.
G. other conditions
-dermatitis of different origin cerebral edema , shock - collapsed state,
-thrombocytopenia (idiopathic thrombocytopenic purpura);
-immune hemolytic anemia spinal cord trauma;
- sarcoidosis, premature birth, organ transplant.
moon face , buffalo hump, trunk (love handles ), acne , hirsutism , wight gain.
impaired healing or brusing.
cns : neverousness , insomnia , depression , aggravation of pre_existing mental disorder
musculoskeletal: long term use can cause osteoporosis, muscle weakness and atrophy.
Git: peptic ulcer , increased appetite.
cardiovascular :fluid retention
ocular : increased intraocular pressure , glaumcoma , cataracts .
-fungal infection -thrush -vaginal yeast infections .

-patients who are high risk for infection
-diabetes
-peptic ulcer
-hypertension
-CHF
-Renal failure
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M1439 M1439
groups estrogens progestins androgens
Hormonal 1) natural steroids 1) natural 1) natural:

- estradiol dipopionate - progesterone - testosterone
- estrone - etisteron(pregnine) - dehydrotestosterone
preparations - estriol
2) semisynthetic steroids 2) semi-synthetics: 2) semisynthetics:

- ethinylestradiol a) progestins analogs - testosterone propionate
- mestranol - hydroxyprogesterone - testosterone enantate
- medroxyprogesterone - methyltestosterone
3) synthetic non-steroids - megesteron - testenal
- diethylstilbestrol
- hexestrol(sinestrol) a) testosterone analogs
- benzestrol - levonorgestrel
- megestrol - norethisterone
- etisteron
4) conjugated estrogens
- premarin
- presomen
- tamoxifen citrate - flutamide

Hormonal - mifepristone
- toremifene - finasteride
antagonists - onapristone
- clomiphene citrate - cyproterone acetate
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M1439 M1439
*Sex organs:
-Vagina uterus and fallopian tubes
-Vaginal cornification
-Endometrium: proliferative and secretary phase menstruation
-Cervical secretion watery
*Secondary sexual characteristic

-Growth of breast
-Facial pubic and axillary hair
*Metabolic effect
-Anabolic effect weak
-Fusion of epiphysis
-Salt and water retention
-Increase b.p
-Impaired glucose tolerance
-Increase coagulability
-Increase HDL and decrease LDL
-Increase cholesterol content of bile
-Increase thyroxine and cortisol binding globulins
-carcinogenic action
Use of estrogen
1. contraception
2. dysmenorrhea
3. hypogonadism
4. menopause hot flushes muscle cramp anexity over breathing
5. osteoporosis increase ca deposition in bone
6. prostatic cancer anti androgenic effect
*Adverse effect
1. nausea and breast tenderness
2. headache
3. increase skin pigmentation
4. impair glucose tolerance
5. increase incidence of breast vaginal and cervical cancer??
6. cardiovascular most concern:
A. thromboembolism
B. hypertension
7 increase frequency of gall bladder disease
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*Uterus:
Secretary change (with oestrogen)
If ovum is fertilized
Prepare endometrium : Decrease oxytocin and ergonovine actions
: Decrease FSH and LH ovulation decreased
Cervical secretion thick and viscid
*Vagina: wbc infiltration and cornified epithelium
*Breast: halts mitotic activity and stabilizes mammary cells; prepares breast for lactation
*Body temperature: Slight rise in body temperature
*Respiration: Stimulates respiration at higher doses
*Pituitary
* Clinical uses of progesterones *

-as OCs
-DUB
-HRT
-dysmenorrhea
-premenstrual syndrome
-endometriosis
-decrease threatened abortion
-post-partum lactation
-endometrial cancer
-hypoventilation
* Adverse effects of progesterone *

-breast engorgement, headache, rise in body temperature, edema, acne and swings.
masculinization of external genital in the fetus
-increased incidences of congenital abnormalities
-irregular bleeding or amenorrhea
-lower HDL (19-nortestosteron derivatives)
-hyperglycemia
-fatigue, depression of mood
-weight gain
-Hirsutism
-Ectopic pregnancy
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Mifepristone
-19 nor steroid derivative
*M.O. A
- Blocks progesterone and glucocorticoid receptors
- During luteal phase: decrease pregest. ->PGs-> menstrual bleeding
- sensitize myocardium to PGs.
- HCG production falls
*ADME
- F:25%, CYP3A4 metabolism t1/2: 20h
*uses
- Termination of early pregnancy- along with prostaglandin.
- as a cervical ripening agent
- post coital contraceptive
- progesterone sensitive tumors
- Cushing's syndrome
*side effects
- vomiting, diarrhea, pelvic pain or abdominal pain ,
about 5% have severe vaginal bleeding
precaution: not to be given to a woman with suspected ectopic pregnancy, hematological

disorders, receiving oral anticoagulants
13
M1439 M1439
CLASSIFICATIONS
1. female contraception
- containing estrogen and progestogen (combined)
monophasic:
-minulen, femulen, microginon, rigevidon, minisiston, nonovion, lo-femenal
biphasic:
- anteovin , neo-eunormin
triphasic:
-trivilar, triregol, triziston, trinovum
- containing estrogen
ethinylestradiol, dirthylstilbestrol, conjugated estrogens.
containing progestogens
-peroral
linestrenol
norgestrel
-contraceptive Depo
medroxyprogesterone
-postcoital (used in the first 24h)

levonorgestrel
-subcutaneous implants
levonorgestrel
norgestrel pointers
-intrauterine
levonorgestrel
Gine T 380S
Vaginal
-Nonoxynol
-benzalkonium chloride(farmatex)
2. male contraceptive:
-gossypol
-inhibin
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M1439 M1439
-Combination of estrogen and progestin are the most common (100% effective)
-The concentration of estrogen is very low to minimize its side effect.
-Contraceptive pills are taken for 21 days starting on 5 days of cycle.
-The tablets should be taken at approx. the same time each day.
-Phase formulation is more closely mimic normal endogenous hormonal activity
*M.O. A
Estrogen inhibits secretion of FSH via negative feedback on the anterior pituitary, and thus
suppresses development of the ovarian follicle.
Progestron inhibits secretion of LH and thus prevent ovulation, its makes the cervical mucus
less suitable for passage of sperm.
Estrogen and progesterone act in concert to alter the endometrium in such a way as to
discourage implantation.
Abnormal transport time through fallopian tube.
Abnormal contraction of fallopian tubes and uterine musculature.
*Indication for contraceptives containing only a progestin(minipill)

When it is desirable to eliminate estrogen;
1.during breast feeding (estrogen postpartum lactation).
2.contraindication to estrogen (E.x. Hypertension or breast cancer).
3.smoker more than 35-year-old.
Disadvantages
1.slightly higher failure rate (efficacy 97%)
2.irregular bleeding.
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M1439 M1439
*Side effects
Wight gain, owing to fluid retention or an anabolic effect, or both.
Mild nausea, flushing, dizziness, depression or imitability.
Skin changes (E.x acne and /or an increase in pigmentation).
Amenorrhea of variable duration on cessation of taking the pill.
*contraindications
thromboembolic disorders.
markedly impaired hepatic function.
suspected carcinoma of the breast.
Undiagnosed genital bleeding.
16
M1439 M1439
androgens and the hormonal control of the male reproductive system

gonadotropin-releasing hormone from the hypothalamus acts on the anterior pituitary to release
both follicle -stimulating hormone, which stimulates gametogenesis, and luteinsing hormone
(also called interstitial cell -stimulating hormone), which stimulates androgen secretion.
the androgenous hormone is testosterone; intramuscular depot injections of testosterone esters
are used for replacement therapy.
mechanism of action is via intracellular receptors.
effects depend on age /sex, and include development of male secondary sexual characteristics in
prepubertal boys and masculinization in women.
*clinical uses: androgens and antiandrogens*

androgens (testosterone preparations) as hormone replacement:
- male hypogonadism due to pituitary or testicular disease (e.g.2.5 mg/day patches)
- female hyposexuality following ovariectomy (e.g.300ug/day patches).
antiandrogens (e.g. flutamide , cyproterone ).
are used as part of the treatment of prostatic cancer.
5a-reductase inhibitors (E.x finasteride) are used in benign prostatic hypertrophy.
*side effects: androgens and antiandrogens*

-eventual decrease of gonadotrophin release, with resultant infertility,
-salt and water retention leading to oedema .
-adenocarcinoma of the liver
-impair growth in children (via premature fusion of epiphyses)
-acne
-masculinization in girls
*anabolic preparations*
1.steroidal
-nandronlone phenylpropionate (fenoboline )
-nandronlone decanoate (retabolil )
-methandienone (nerobol )
-oxandrolone
2.nonsteroidal
-potassium orotic
- inosine
17
M1439 M1439
- these drugs may increase or decrease contractile activity and / or tone of myometrium & cervix
I. With predominant influence on the contractile activity of myometrium
A. Ocitocic drugs increase contractile activity of the myometrium.

Hormones and hormonal drugs of neurohypophysis.
- Oxytocin
- Pituitrinum
- Desamino-oxytocin
Prostaglandins
- Dinoprostone ( PG E2 )
- Dinoprost ( PG F2a )
B. Tocolytic drugs reduce contractile activity of the myometrium.

Beta 2 Adrenomimetics:
- Fenoterol
- salbutamol
General anesthetics :
- Oxibutirat sodium
Miscellaneous :
- magnesium sulphate
II. With predominant action on the tone of myometrium.

From plants sources (ergot alkaloids)
- Ergometrine maleate
- methylergometrine
- Ergotamine hidrotartrat
- Ergotal
synthetic derivatives
- Cotarnine chloride
III. Remedies that reduce cervical tone

- Atropine sulphate
- Dinoprost
- Dinoprostone
18
1) Rheumatic polyarthritis
-phenylbutazone , dexamethasone , indomethacine
2) spondyloarthritis anchilozis
3) acute ischio-lumbar gout

4) degenerative lesions of joints

5) myositis
6) pollinosis
-sodium cromoglycate , ketotifen , dexamethasone
7) urticaria (welts on skin triggered by reaction to food,medications.)

-tacrolimus , dexamethasone , diphenhydramine
8) post-operatory vomiting
-diphenhydramine , clemastine , loratidine
9) kinetosis ( motion sickness )

-diphynhydramine , clematine , astemesol , scopolamine
10) pre anesthesia

-diphynhydramine , clematine , astemesol
11) parkinson syndrome

-bromocriptine , amantadine , levodopa , tolcapone , seligiline
12) rheumatoid arthritis

1
13) bronchial ashtma
-salbutamol , ipratropium , theophyline , O2 , dexamethasone
14) anaphylactic shock

-dexamethasone , salbutamol , epinephrine , hydrocortisone
15) contact dermatitis

-dexamethasone , hydrocortisone , prednisolone
16) asthmatic bronchitis

-diphenhydramine , salbutamol , aminophylline , ipratropium , cholropiramine
17) chronic infections

-cyclosporine , hydroxychloroquine , azathioprine
18) AIDS
-imupurin , timalin , timogen , molgramostim
19) tissue and organ transpaltation

-tacrolimus , cyclosporine , mercaptopurine
20) cancer
-interferon , imupurin , timogen , leukenferon
21) diabetes melletus

-clorpopamide , insulin , tolbutamine
22) type I diabetes melletus

-insulin , seroinsulin , insulin B
23) type II diabetes melletus

-metformin , glyclazide , glybenclamide
24) non-sugar diebetes ( diabetes insipidus )

-vasopressin , desmopressin , lypressin , pituitirin
2
25) diabetic coma(hyperglycemia)
-human insulin , clorpopamide , carbutamine , tolbutamine
26) mixedema
-thiamasol , carbimazol , cibaclacin
27) hyperthyreosis
-propylthyouracil , thiamasol , carbimazole
28) hypoglycemic coma

-glucose , glucagon , epinephrine
29) labor stimulation

-oxytocin , misoprostol , pituitrinum , desamino-oxytocin
30) metorrhagies
-ergotamine , oxytocin , metoxyprogesteron
31) uterine cervix relaxation

-atropine sulphate , dinoprost , dinoprostone
32) abortion stimulation

-oxytocin , ergotal , dinoprost , demoxytocin
33) untreated postnatal (postpartrum )hemorrhage

-ergotamine , ergotal , methylergometrine
34) alcoholism
-disulfiram , apomorphine , teturam ,
35) neuritis
-phenylbutazone , indomethacine , thiamine , pirodoxine
36) keratitis
-riboflavin , diphenhydramine , phenylbutazone , dexamethasone
3
37) pellagra
-nicotinic acid , nicotamide ,
38) leucopenia
-leucogen , batilol , inosine , ethaden
39) iron deicnecy anemia

-ferrus sulphate , ferrus chloride , ferbitol , dextrafer
40) megaloblastic anemia ( B12 difecincy)

-cyanocobolamine , hydrocobolamine , cobamamide , fercoven
41) anemia of chronic disease

-erythropoieten alpha , erythropoiten beta , darbopoiten alpha
42) hemolytic anemia

-dexamethasone , retinol , prednisolone
43) aplastic anemia

-matandienone , metandriol , stanazol , vitB12
44) hemophilia
-tranexamin acid , desmopressin , concentration of factor VIII , IX , XII
45) skin and mucos membrane lesions

-ascorbic acid ,
46) hemorhages diathesis

-vitamin k , menadione , phyeomenadione
47) inflammatory disease and infection of upper respiratory tract

-echinacea , bronhomuna, ruzam
48) Rachitis
-ergocalciferol , colecalciferol , calcidiol , calciterol
4
49) sterility
-neogest , regulon , ovulen , femulen , testosterone , androsterone
50) ovary hypotension

-chorionic gonadotropin , gonadorelin , progesterone , menopausal gonadotropine
51) prostate cancer

-finasteride , cyproterone acetate , testosterone , estrone
52) threatened abortion prophylaxis

-indomethacine ,
53) undesirable pregnancy prevention

-salbutamol , progestan , fenoterol
54) male genitals hypoplasia

-testosterone , androsterone , methyltestosterone
55) myocardial infarction

-potassium urotate , inozine , nandrolone
56) alimentary infection dystrophy

-nandrolone phenylpropiate , nandrolone decanoate , inosine , potassium orotic
57) addison disease

-cortisone , hydrocortisone , testosterone , DOKSA
58) rheumatism
-dexamethasone , phenylbutazone , diclofenac
59) exema
-dexamethasone , diphenhydramine , pridnesolone
5
60) stimulation uterine contarcion
-oxytocin , ergotal , pituitrinum
61) labor stimulation

--oxytocin , ergotal , pituitrinum
62) uterine atony in postnatal period

-oxytocin , ergotal , methylergotamine
63) acute pancreatitis

-aprotinine , atropine , baralgine , regesan
64) bronchoectase
-bronhomunal , pyrogenal , ruzam
65) pulmonary emboli

-heparin , warfarin , streptokinase , fibrinolysin
66) bleeding because of hyperfibrinolysis

-aprotinine tranexamic acid , aminocaproic acid , aminomethylbenzoic acid
67) gastric achilia

-cyanocobolamine , folic acid , natural gastric juice , pepsin , pancreatin , HCL
68) phosphororganic substances intoxication

-atropine , scopolamine , thiopental , platyphylline ,
69) epilepsy
-phenobarbital , clonazepam , diazepam , sutiam , valporic acid
70) dysethalipoproteinemia
-nicotinic acid , clofibrat , bezafibrat , ciprofibrat
71) hypertrigliceridemia
-cholysteramine , bizafibrate , nicotinic acid , lovastatin
6
72) hypercholestrolemia
-cholysteramine , bizafibrate , nicotinic acid , lovastatin
73) diminish of pruritus in mechanic icterus

-diphenhydamine , clemastine , loratadine
74) drug intoxication

-apomorphine , ascorbic acid ,
75) pollinosis ( hay fever caused by an allergic reaction to pollen )

-sodium cromoglycate , ketotifen , dexamethasone
76) premidication
-diphenhydramine , clemastine , chlorprophenamine ,
77) overdose with indirect anticoagulants

-franexamic acid , aprotinine , aminocaproic acid
78) overdose with direct anticoagulants

-franexamic acid , aprotinine , aminocaproic acid , protamine sulphate
79) stopping of parenchymal and capillary hemorrahges

-fibrin , thrombin , venoum viber , thromboplastin
80) intravascular coagulopathy

-heparin , warfarin , phepromaron
81) Eczema
-hydrocortisone , prednisolone , corticotropine
82) nocturnal enuresis

-hydrocortisone , indapamide , cyclothiazide
Indications by : Abu Dabas Karam - M1353

7

Pharmacology - Tot - NR 6classid S.F.A

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Pharmacology - Tot - NR 6classid S.F.A

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M1439 Drug used in disorders of coagulation part 1 M1439

Pharmacology The 5th Exam Pharmacology The 5th Exam

A. Direct mechanism of action

B. INdirect mechanism of action

3.Antagonists of anticoagulants with indirect action

*Side effect: allergy, danger to contaminate with AIDS, viral hepatitis

Indirect Oral Acting Anticoagulants

Streptokinase is a protein synthetised by streptococci that combines with the

Side effects: allergy, dyspepsia, arrhythmias.

Antidotum: aprotinin , pamba (p-aminomethylbenzoic acid) , aminocapronic acid.

I. Inhibitors of thromboxane activity drugs that decrease platelet aggregation (antiaggregant)

1) Inhibitors of tromboxane synthesis

3) Drugs of mixed action (thromboxane synthase inhibitors + thromboxane

II. Remedies that increase prostacyclin activity - stimulators of

b) Inhibitors of ADP receptors

IV.Remedies with various antiaggregant action

Nsaids / Acetylsalicylic acid:

- M.O.A: reduce platelets aggregation by inhibiting ADP pathway of platelets

M.O.A: is antagonists of glycoprotein-receptors GPIIb/IIIa It inhibits combing to fibrinogen and

INDICATIONS: angina, M. I, surgery in the a. coronary, angioplasty, coronary artery syndrome

ADRs: allergy, hemorrhage, hypotension, bradycardia, dyspepsia, thrombocytopenia

ADRs: hypotension, crash syndrome, allergy, headache, bleeding

INDICATIONS: Prophylaxis against thromboembolic disorders, diagnosis of angina pectoris

drugs that decrease platelet aggregation (antiaggregant)

1) With local action

2) With systemic action

a) with systemic action:

with systemic drugs:

-indication: Hemorrhage, tachycardia, prevention of hemorrhage in surgical interventions,

-side effects: allergy, dyspepsia, arrhythmias.

I. Remedies that stimulate erythropoiesis

A. Remedies used in hypochromic anemia

1) Iron deficiency anemia

2) Anemias after chronic diseases

B. Remedies used in hyperchromic anemia

II. Remedies that inhibit erythropoiesis

1) That stimulate leucopoiesis

2) That inhibit leucopoiesis

Sari faried alkrinawi

1.Drugs that decrease the release of mediator's histamine, other

*H1 Histaminoblockers: diphenhydramine, clemastine

3. Drugs that diminish the main allergic symptoms:

A. Adrenomimetics: epinephrine, norepinephrine

4. Drugs used in cell-mediated immune reactions:

2.Drugs that diminish the cytotoxic reactions & tissues alteration:

*steroid anti-inflammatory drugs

I. according to the chemical structure

First Generation (Classical) Antihistamines

Side effects 2nd generations

Ketotifen: the same mechanism of action plus also inhibition of H1histaminoreceptors.

II. exogen origin

III. synthetic origin:

Immunostimulants: these agents are envisaged to enhance bodys resistance against

Side effects of prescription immunomodulator medications

Cyclosporine More effective against

I group: Nonsteroidal anti-inflammatory drugs

A) non- selective NSAIDs

II group: steroidal anti-inflammatory drugs

III group: Slow-acting , anti-inflammatory drugs:

Mechanism of Action of NSAID

pharmacological actions of Nsaids

Mechanism of Action : non selective Nsaids

Pharmacokinetics: non-selective Nsaids

ionic inhibitors, which block the iodide transport mechanism

Actions: carbohydrate and protein metabolism

Action: lipid metabolism

Action: electrolyte and water balance