CARDIOVASCULAR SIDE EFFECTS OF DRUG : ADVERSE EFFECT PART 1

#1)PERICARDITIS : (PGI DEC 01,PGI DEC 06).

SHIP Me Minor Problem.
S- sulphonamide.
H- hydralazine.
I- isoniazid.
P- procainamide.
Me – methysergide.
Mi- minoxidil.
P- phenytoin &penicillin.

NOTE : First 4 drugs ie SHIP also causes SLE (AIIMS NOV 2010, DPG 2011)

#2) HYPERTENSION(AIIMS MAY 07). READ: Any sympathomimetic can cause hypertension natable eg being cocaine. if we increase epinephrine or norepinephrine level in body by inhibiting their metabolism MAO INHIBITORS or by inhibiting uptake TCA they may also lead to hypertension. Fluid & water retension may lead to hypertension as by GLUCOCORTICOIDS, OCP,NSAIDS, COXIBS. If hematocrit is increased then blood becomes more viscous eg erythropoitin. one other important cause of hypertension being CYCLOSPORINE.

so we may summarise it as;
cocaine* &symphathomimetics.
MAO inhibitors & TCA.
Steroids, ocp, NSAIDS, coxibs ERythropoitin*
CYclosporine*

#3)CARDIOMYOPATHY(AI2010). ALCOHOL*: causes dialated cardiomyopathy(robbins 7e page 603).

Adriamycin (doxorubicin)* & daunorubicin* causes dialated cardiomyopathy (robbins 7e pg603).

TRASTUZUMAB, IMATINIB causes dialated cardiomyopathy( harrison manual 18e pg823).

other drugs are Li, sympathomimetics, emetin, phenothiazine.

NOTE: Radiation exposure to mediastinum causes restrictive cardiomyopathy.*

#4)METHMOGLOBINEMIA (AIIMS MAY 2004, KA 2004)
Nitrogen related drugs as :
Aniline derivatives.
Nitrates.
Nitrites.
Nitroglycerine etc
sulphonamide &dapsone.

Prilocaine can cause methmoglobinemia( AIIMS MAY 2009,2010 Ka 2004). It is due to its metabolite O- toulidine.

NOTE : bupivacaine is most cardiotoxic LA. It is best drug for regional blocks but it shouldnot be used for bier`s block. Prilocaine is most suitable LA for bier`s block.

#5) PROLONGED QTc INTERVAL(torsades de’pointes).
*class Ia antiarrythmics ie quinidine, procainamide.

*class III antiarrythmics (bretylium, ibutilide, defetilide, amiodarone, sotalol).

*some 2nd gen antihistamines : ie terfenadine & astemizole.

*some fluroquinolones ie gatifloxacin, sparfloxacin, grepafloxacin).

*some antipsychotics as thioridazine & ziprasidone.

*antiprotozoal ie efloquine & pentamidine.
*cisapride.

so try to remember it as broad heading with example.

Add on information: most arrythmogenic antiarrythmic group of drugs are class Ic eg flecainide, propafenone.

PART 2 COMING SOON

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CYCLOSPORINE : CALCINEURIN INHIBITOR

CALCINEURIN INHIBITOR : these drug inhibit the gene transcription of IL 2 by inhibiting calcineurin pathway ( AI 2007  ) or we can say that it acts by decreasing the production of IL 2 ( DPG 2005).

eg 1) cyclosporine  2) tacrolimus .

NOTE : SIROLIMUS( rapamycin) binds to mTOR and inhibits the ACTION of IL2 without affecting its transcription.(AI2007).

cyclosporine and tacrolimus act through inhibiting T helper cells / CD 4 lymphocytes selectively (DPG 2006 ,DNB 2004 , AIIMS 97, TN 2000 ,MH 2007).

These agents are used as immunosuppresive agents in organ transplantation, GVHD and some autoimmune disease as rheumatoid arthritis and psoriasis. ( AI 2007).

ADVERSE EFFECT OF CYCLOSPORINE: (DPG 2002) : nephrotoxicity, hepatotoxicity ,hypertention , hyperkalemia , hyperlipidemia , hyperglycemia ,hyperuricemia , hirsutism , gum hyperplasia ,neurotoxicity ( tremors ) .

Note that it cyclosporine doesnt cause bone marrow suppression as compared to sirolimus which causes thrombocytopenia(DPG 2002). Sirolimus is not a calcineurin inhibitor.

TACROLIMUS  VS CYCLOSPORINE

TACROLIMUS IS MORE POTENT THAN CYCLOSPORINE

HIRSUTISM , GUM HYPERPLASIA , HYPERURICEMIA , HYPERLIPIDEMIA IS NOT CAUSED BY TACROLIMUS ( AI 2008).

Hyperglycemia and neurotoxicity os more prominent with tacrolimus.

Tacrolimus is a macrilide antibiotic ( AI2004). Rifampicin being an enzyme inducer decrease tacrolimus efficacy (AI 2009).

Both r nephrotoxic so to be used carefully with other nephrotoxic drug. cyclosporine do not require dose adjustment in renal failure.

REFERENCE : katzung pg 913  10 edition )