ALL drugs

L-dopa












• Treat Parkinson’s In form of


(L-dopa + Carbidopa 'or Benserazide' + Entacapone' or Tolacapone


• Dopaminergic Drug


• Side effects :


Central  Dyskinesia + psychosis


Peripheral  nausea, vomiting & anorexia +tachycardia and

arrthymia +Postural hypotension +Brown saliva and Urine +
Mydriasis in high doses



• Contraindications:


1-Acute angle closure glaucoma


2)Psychosis

* Drug interactions:


1) V.B6 ( pyridoxine) ---> Inc. Peripheral decarboxylation of L-Dopa -

--> Inc. Peripheral Dopamine ---> Dec. efficacy of L-dopa

2) MAO inhibitors (Phenelzine, antidepressants) ----> Inc.

Catecholamine Accumulation ---> Inc. BP ---> Hypertensive crisis


3) Anti-psychotics (D2-blockers) ---> cause Parkinson's syndrome

4) Cardiac patients ---> Due to risk of cardiac arrhythmias as a result

of activation of B1 receptors

Amantadine









• Dopamine releaser
• Antiviral against influenza virus

• Use : TTT early disease of Parkinson’s, especially in younger
patients and as an adjunct to l-dopa

• Mechanism:
1.Inc. DA release

2.Inh. DA reuptake and
3.Inh. Ach by blocking M receptors


• Contraindications :

Patients with renal failure  because 95% of drug is
eliminated by kidneys


• Side effects :
Same a L-Dopa + Urinary retention + Xerostomia

Selegiline










(Deprenyl)









• irreversible Selective MAOB inhibitors.


• Uses :single drug in early or mild PD, combined with l-dopa -->
Inc.DA / Dec. dose of L-dopa / Improve motor function in

patients with On and OFF phenomena



• Mechanism:
Inhibit MAOB irreversibly -->inhibit dopamine breakdown --->

Inc.DA in brain


Side effects :


insomnia, & anxiety if the drug is administered later than mid-
afternoon---->as Deprenyl is metabolized into amphetamine &

methamphetamine



Contraindications :


• Since it is selective it does not suffer from hypertension crisis
when it is combined with tyramine containing food.


• At large dose = 6times normal therapeutic dose it loses it's

selectivity and affect both MAOB and MAOA which lead to
hypertensive crisis

Rasagiline









• irreversible Selective MAOB inhibitor.
• Doesn't cause the side effects of Selegiline .. Why ?


*Because It is not metabolized to an amphetamine like

substance


• 5 times more potent than Selegiline ( Deprenyl )

Benztropine, Trihexyphenidyl,


Procyclidine, Orphenadrine, & Biperiden




• Anticholinergics.

• used as adjuvant therapy to L-Dopa in Parkinson’s.. Why
1)Because it reduces Tremors and rigidity only

2).It's effect is much lower than L-dopa


*Drug of choice for PD caused by D2 blockers  Because it does
not cause Inc, in DA so does not induce psychosis


• Side effects : Atropine like side effects: mydriasis, blurred

vision, urinary retention, xerostomia, decreased GIT motility
(constipation) & decreased memory and concentration,
confusion with visual hallucination



• Contraindications:
glaucoma, prostatic hypertrophy

Bromocriptine








(Ergot alkaloid)











• Dopamine receptor agonists (ergot alkaloid)

• TTT of Parkinson’s :
1)used as initial therapy in patients who have mild PD and a

younger age of onset


2)adjuncts to levodopa in patients with severe motor
fluctuations (on–off phenomena, wearing off)


3)They decrease the dose of l-dopa in advanced PD


• Mechanism : Stimulate D2 receptors in the striatum


• Side effects :
-Nausea, Vomiting, Anorexia ---> Due to Inc dopamine in CTZ

in medulla
-Tachycardia=arrhythmia.
-Postural hypotension.

-Psychosis (centrally) ---->Neuropsychiatric disorders are more
frequent than with levodopa monotherapy.


• Drug interactions:

Worsening of patient with peripheral vascular disease due
to vasoconstriction as it is ergotamine derivative.

2)Patients with cardiac problems
3)psychiatric illness

Apomorphine, Pramipexole,


Ropinirole. Rotigotine



Mechanism , side effects and uses are same as Bromocriptine


• Apomorphine is used as an S.C injection ----> is used for acute
management of ‘off’ periods

• Apomorphine must be followed by antiemetic- Because it
causes sever nausea

VitaminK1






(phytonadione)





Uses
Treat bleeding


Mechanism :


Stop bleeding problems due to warfarin by increasing the supply of
active vitaminK1 ,there by inhibiting the effect of warfarin




• Administered via the oral ,subcutaneous ,or intravenous
route.
•

• Response to vitamin K1 is slow ,requiring about 24 hours to
reduce INR (time to synthesize new coagulation factors).

•

Protamine sulphate








Uses
Treat bleeding


Mechanism :


• Antagonizes the anti coagulant effects of heparin

• Positively charged protamine interacts with the negatively
charged heparin ,forming a stable complex without

anticoagulant activity.

• Adverse effects :hyper sensitivity as well as dyspnea ,flushing

,bradycardia , and hypotension when rapidly injected

Aminocaproic acid





and Tranexamic acid












Uses: Stop bleeding caused by fibrinolytic drugs



Mechanism :

•
• Inhibit plasminogen activation.





• Side effect is intra vascular thrombosis.



• Tranexamic acid is 10 times more potent than aminocaproic
acid.






• Tranexamic acid is used for heavy menstrual bleeding.

Streptokinase,






Alteplase,





Urokinase





• THROMBOLYTIC DRUGS = Fibrinolytic Drugs
• Mechanism:
Activate the conversion of plasminogen to plasmin , that

hydrolysis fibrin and thus dissolves clots.

• Side effects:
haemorrhage is a major side effect- thrombolytic agents do
not distinguish between the fibrin of an unwanted thrombus

and the fibrin of a beneficial haemostatic plug.

Warfarin









• Anticoagulant drug

• Mechanism :
1-Antagonize cofactor functions of Vitamin


2-Inhibit synthesis of coagulation factor II (prothrombin) ,VII , IX and X, whose
carboxylation is dependent on a reduced form of vitamin K.
3-blocks the reduction of oxidized vitamin (vitamin K epoxide ) and thereby
prevents vitamin k–dependent carboxylation of clotting factors

• Has narrow therapeutic index.

• Anticoagulant effects are overcome by Administration of Vitamin K
• Therapeutic uses :
Prevention and treatment of deep vein thrombosis (DVT) and
pulmonary embolism (PE) , stroke prevention ,stroke prevention in the
setting of atrial fibrillation and/or prosthetic heart valves


• Side effects:#

1) Haemorrhage


2) Teratogenic


• Contraindications :
Pregnancy - due to teratogenic activity  cause fetal warfarin
syndrome -- malformations result from antagonism of vitamin K–
dependent maturation of bone proteins during a process in which
these proteins are carboxylatd in the same manner as the clotting
factors .Warfarin and other vitamin K antagonists block this process
and can cause bone deformities and various birth defects
Heparin,

Low molecular heparin



(LMWH) enoxaparin,




Fondaparinux








• They are Anticoagulants.

• Heparin mechanism  Activates anti thrombin III (AT-III)→

complex→ rapid inactivation of coagulation factors.


• Enoxaparin mechanism Same as heparin but its complex
with AT-III has less affinity for thrombin (mainly inhibits

factor Xa).



• Fondaparinux mechanism  Similar to those of other
heparin-like drugs, more selective active factor X inhibitor.




• Therapeutic uses:
1)TTT of acute thrombi disorders
2)Prophylaxis of post operative venous thrombosis in patients

undergoing surgery
3)Drug of choice for TTT of pregnant women as they don’t cross the

placenta  due to their large molecular size and negative charge



• Adverse effects:
-Excessive bleeding which is managed by  Drug discontinuation

/ or treating with protamine sulphate

Cilostazol







• Vasodilator, Antiplatelet



• Mechanism  Inc. cAMP by inhibiting PDE - DEC. TXA2
synthesis

Dipyridamole










• Coronary vasodilator ,Weak antiplatelet
• Mechanism  Inc. cAMP by inhibiting PDE - DEC. TXA2

synthesis

• Used in stroke prevention and usually in combination with

aspirin


• Adverse effects  Headache / Orthostatic hypotension

Abciximab:







•
• Mono clonal antibody, Anti Platlet.


• Mechanism :

1) Inhibits the GP IIb / III a receptor complex.


2) Blocks the binding off ibrinogen and, consequently,

aggregation does not occur.

Ticlopidine and





Clopidogrel





• They are anti platelets

• Mechanism:
Inhibit the binding of ADP to its receptors on platelets and

,thereby ,inhibit the activation of the GP IIb / III a receptors
required for platelets to bind to fibrinogen and to each

other.

• Uses:

1) Prevent Atherosclerotic events
2) Prophylaxis of thrombotic events in acute coronary

syndromes
3) Percutaneous coronary intervention (PCI) with or without

coronary stenting


• Adverse effects:

1) Can cause prolonged bleeding with no Antidote.

2) Ticlopidine - can cause neutropenia
3) Clopidogrel cause less adverse effects and lower chances of

incidence of neutropenia.

Aspirin







• (NSAID) , Anti platelet

• Mechanism:

• Inhibits cyclo oxygenase enzyme - that catalyses

ThromboxaneA2 (TXA2) synthesis -- which promotes platelet
aggregation


• Suppression of platelet aggregation last for the life of the

platelet ,which is approximately 7 to 10 days (Irreversible
inhibitor)


• Side effect :


Bleeding time is prolonged- increased incidence of haemorrhagic
stroke & GI bleeding