LIST OF DRUGS (PHARMACOLOGY) TYPE NAME M/A @ CHARS Commonly used anti-hypertensive drug Diuretic -Can be used alone

or Combination with Loop (renal ACEI, ARB, b-blockers insufficiency) & CCB Thiazide ( normal renal) -thiazides -amiloride/ hydrochlorothiazide -Indapamine SR -Indapamine -Triamterene/ hydrochlorothiazide Calcium Channel Decreasing of Blockers (CCB) intracellular Nifedipine availability of Ca2+ Verapamil Diltiazem EFFECTS Antihypertensive Lower BP Decrease preload ~ reduce circulating volume BAD EFFECTS High dose~ -Serum cholesterol , glucose, uric acid & Ca levels -Decrease K, Na & Mg levels -Erectile dysfunction CONTRAINDICATION *patient with gout *renal insufficiency

Smooth muscle relaxation Vasodilator action

b- blocker (-lol) ~ propanolol

Inhibit adrenergic (adrenalin=NE/E) response ~means block sympathetic act.

-Decrease heart rate -Reduce rennin release -local anasthetics

ACE inhibitors (pine/verapamil) Amlodipine Diltiazem Felodipine Isradipine Lacidipine Nicardipine Nifedipine verapamil Angiotensin Receptor Blockers (ARBs) (-tan) -losartan -candesartan -irbesartan

Cause arteriolar and venodilation

Lowering BP

-initial tachycardia -hypotension --headache -flushing -ankle oedema -nausea -constipation Bradycardia Heart block Peripheral vascular disease Sick-sinus syndrome Asthma/COPD Enhance coronary artery disease tiredness -cough -angioedema -increase foetal n neonatal mortality

Use of sublingual nifedipine

Patient with Impaired CHO tolerance in prediabetic patients Partial & complete heart block

-renovascular disease - pregnant mother

-Block only Lowering BP thromboxane A2 receptor, -Block action of A-II (vasoconstricyion, central & peripheral sympathetic stimulation, relez of aldosterone, salt n water reabsortion, vasopressin relez) Anti-anginal drug (stable angina/angina pectoris: unstable angina: variant angina) Angina pectoris: coronary blood flow inadequate to meet myocardial oxygen demand Result from: artherosclerosis & spasm of coronary artery Nitrates Venodilator/ Short acting: vasodilator -Nitroglycerine Long acting:

hypotension hypokalemia headache dizziness weakness

pregnancy

-Isosorbide mononitrate -Isosorbide dinitrate -blockers cardiac Non-selective: contractility -Propanolol Cardioselective blockers (1) -Atenolol -Metoprolol Ca2+ channel blocker Inhibit Ca2+ entrance (CCB) into cardiac & Dihydropyridine: Smooth muscle -Nifedipine -Amlodipine Non-dihydropyridine: -Verapamil -Diltiazem Sedatives & Hypnotics Sedative: reduces anxiety and has calming effect Hypnotic: produce drowsiness, encourage onset and maintenance of sleep Benzodiazepines -bind to BZ receptor -sedative-hypnotic site on GABA -anxiolytic - increase receptor -anticonvulsant affinity for GABA -muscle relaxant -increase the frequency of opening of the chloride channels *GABA is the major inhibitory neurotransmitter in the CNS Barbiturates -promote GABA -cause sedative and (induced increase in promote sleep chloride conductance -anticonvulsant actions at GABA synapse) -anaesthesia -can directly cause in increase chloride conductance at higher doses Action are nonspecific and other excitable tissue are also inhibited at high doses (e.g.cardiovascular) Buspirone -acts on 5 HT 1 -relieves anxiety without receptors(partial marked sedation agonist) -no hypnotic or -suitable for anticonvulsant activity generalized anxiety Other (older) sedative hypnotic drugs -glutethimide -chloral hydrate -Similar action to -paradehyde barbiturate

-dependence -drowsiness and confusion -ataxia -cognitive impairment -tolerance

-drowsiness -CNS depression -paradoxical excitement -can precipitate acute porphyria in susceptible individuals

Acute porphyria in susceptible individuals *affect the nervous system or skin, or both. porphyria is due to the deficiency of heme.

-tachycardia -nervousness -palpitations -GIT distress

Not effective in panic disorder

-meprobamate -similar to barbiturate Anti-Psychotics Psychosis: loss of contact with reality + delusions & hallucinations Positive symptoms (delusion, hallucination) Negative symptoms (social withdrawal, blunted effect) Overactivity of dopamine at D2 receptors (limbic system & 5HT (serotonin) overactivity at 5HT2A

neocortex) Typical Antipsychotics *Phenothiazines (chlorpromazine) *Butyrophenones (haloperidol) *Thioxanthenes (flupentixol) *Other heterocyclics: sulpiride, pimozide

Alleviate +ve symptoms Bind & block D2 receptors Dopamine receptor D2 type (D2,D3,D4) D1 type (D1,D5)

USES: Psychosis Mania Organic brain syndrome Anxiety Antiemetics Mesolimbic-mesocotical: relieve behavioural manifestations of shizo.

Atypical Antipsychotics *Clozapine *Olanzapine *Risperidone

Alleviate +ve & -ve symptoms Block D2 (potency) & 5HT2A (potency)

agitated aggressive Withdrawn patients become more responsive & communicative Hallucination, delusion, disorganized incoherent thinking disappear gradually Less EPS

Basal ganglia (nigrostriatal pw) extrapyramidal effects Acute: parkinsonism Akathisia Dystonia Malignant neuroleptic syndrm Chronic: Tardive dyskinesia P.gland (tuberoinfundibular) Hyperprolactinemia menstrual irregular gynaecomastia galactorrhea Block muscarinic r: dry mouth, urinary retention,memory impairment Block 1-adrenergeic & H1-receptor: reflex tachycardia, hypotension, sedation Cardiovascular: Ventricular arrhythmias (thioridazine) Metabolic: Weight gain (olanzapine,clozapine Diabetes mellitus Cardiovascular: Ventricular arrhythmias

ADVERSE EFFECTS: Cholestatic jaundice Skin eruptions Agranulocytosis (clozapine) Cataract (chlorpromazine) Retinal deposit (thioridazine)

Anti-depressants persistent lowering mood, inability to experience pleasure in usual activities Classification: -reactive depression -endogenous depression * -bipolar effective disorder depression PATHOGENESIS: Monoamine hypothesis Neurotrophic Hypothesis functional amine dependent Loss of neurotrophic support neurotransmission (5HT & NA) (neurogenesis & synaptic connectivity) Selective serotonin reuptake inhibitors (SSRI) -fluoxetine -citalopram -escitalopram -fluvoxamine Inhibit NE and/or 5HT reuptake (acting on transporter) Clinical uses -major depression -severe anxiety disorders -Panic disorder (TCAs) -Phobic disorder (TCAs) -obsessive compulsory disorder (TCA,SSRI)

Neuroendocrine factors Abnormality hypothalamo-pituitaryadrenal axis cortisol , corticotrophine RH

Selective serotonin noradrenaline reuptake inhibitors (SNRI) -venlafaxine -desvenlafaxine -duloxetine -milnacipran Tricyclic antidepressants (TCA) -imipramine -clomipramine -desipramine -amitriptyline

-post-traumatic stress disorder (TCA,SSRI) -enuresis(bedwetting) in children & old pts -attention deficit hyperactivity disorder -psychosomatic disorder -chronic pain states

Low risk of interaction

TCA + *phenytoin,aspirin, phenothiazines TCA protein binding TCA effects *barbiturates TCA metabolism *SSRI (fluoxetine) TCA to toxic

Serotonin antagonist -trazadone -nefazodone Tetracyclic & unicyclic antidepressants -mirtazapine -bupropion -amoxapine -maprotiline Monoamine oxidase inhibitors Irreversible: -phenelzine -isocarboxazid -tranylcypromine Reversible: -Seligiline -Moclobemide

Block postsynaptic specific receptors

Inhibit degradation of monoamine (inhibit MAO) Excess neurotransmitter diffuse into synaptic cleft availability of monoamines binding Transcription of protein & inhibition of others Mood elevation

Drug interaction wif: SSRI & TCA -serotonin syndrome (too much 5HT) *hyperthermia *tremor *convulsions Agents + indirect sympathomimetics, amphetamine *bp Pethidine *severe respiratory *depression Cheese,wine ( tyramine= Sympathomimetic amine displace NA) *hypertensive crisis

Snippets: serotonin regulate mood, appetite, sleep muscle contraction 7 5HT receptors

Anesthesia: blocking sensation of one small part of the body to total unconsciousness General anesthesia: affect brain cells Lose of consciousness (reversible) analgesia muscle relaxation loss of reflexes Pre-anesthetic medication *to reduce anxiety *Benzodiazepines (anxiolysis) *to reduce pain (analgesia) *Morphine & NSAIDs *prevent bronchial *Antihistamines/ secretion anticholinergic drug *reduce gastric secretion *H2 receptor blockers / Proton pump inhibitor *to prevent nausea *Antihistamine (Promethazine) During surgery ST bind with GABA r Anesthesia (induction) Disadvantages: Inducing agent (I.V) Short duration

*Allergic to barbiturate

Sodium thiopental *ultra-short acting barbiturate *rapid & smooth onset * lipophilic Propofol Ketamine, Etomidate Inducing agent (inhale) Nitrous oxide

Open Cl- channel Hyperpolarization depress CNS anesthesia Induction & maintainance cation conductance in ion-channel Block excitatory neurotransmitter in brain X activity neuronal nicotinic AcH receptor Inhibit conduction of AP Neuromuscular blocker ability of Ach to open ligandgated ion channelparalyse Non-irritant Rapid induction of anesthesia Short recovery time Good analgesic effect X depress respiratory center /vasomotor center (VMC) Very potent anesthetic agent Smooth induction Non-irritant Pleasant to inhale

Anti-analgesic respiratory centr ( response to CO2 / hypoxia) BP myocardial actvty

*Acute intermittent porphyria *cardiovascular instability

potent anesthetic Oxidize components of Vit B12 Always used with halothane Combine wif O2 *Slow induction *Slow recovery *Lack analgesic efct *Depress cardio,respiratiory *Cause severe hepatic toxicity

Halothane (liquid)

Muscle relaxants Tubocurarine Gallamine Atracurium Pancuronium After Surgery: neostigmine

Produce muscle relaxation

Recover muscle paralyse Recover from unconscioucness Local Anesthetic numbing small local area, X unconsciousness analgesic Lidocaine Block AP propagation Cocaine in nociceptive neuron Procaine Block Na channels (inactivate) K Regional anethesia channel open K -spinal efflux -epidural repolarization

Toxicity: CVS: cardiac activity Hypotension CNS: Restleness Visual & auditory prob Convulsion Allergy: Insulin shock: Hypoglycaemia - Excess level of insulin - Weak - Drowsy - Confused - Hungry - Dizzy - Coma

Drugs Diabetes Mellitus Insulin [subcutaneous@IV]

Rapid acting: Humalog - 15 min b4 meal - Onset : < 30 min - Peak: 30 min 1 h - Duration: 2 4 h Short acting: Regular - Onset: 30 min 1 h - Peak: 2 5 h - Duration: 5 10 h Intermediate acting: Lente - Onset: 1 3 h - Peak: 6 14 h - Duration: 18 24

h Long acting: Ultralente - Onset: 4 6 h - Peak: 16 24 h - Duration: 24 28 h Oral Antidiabetic Agent 1. Secretagogues Sulphonylureas Tolbutamide Glipizide Glyburide Glipemiride

Stimulate insulin release from cell Block ATP sensitive channel Depolarization 2+ Ca influx hepatic glucose production peripheral insulin sensitivity Sama ngan sulphonylureas More rapidly absorbed and eliminated

Weight gain Hyperinsulinemia Hypoglycaemia Renal hepatic insufficiency

Renal Insufficiency delayed excretion of drug Accumulation Hypoglycaemia

Meglitinides Repaglinide Nateglinide

Repaglinides: - Hypoglycaemia - Upper respiratory tract infection - Rhinitis - Bronchitis - Headache - Weight gain Nateglinide: - Nausea - Diarrhoea - Dizziness - Light headedness

2. Sensitizers Biguanides Metformin

hepatic glucose production inhibit hepatic gluconeogenesis skeletal muscle glucose uptake & metabolisme free fatty acids # PPAR involved in genes transcription regulating glucose and fat metabolism. Glitazones (bind) Peroxisome Proliferator Activated Receptor y (PPARy)

Nausea Vomiting Diarrhoea Stomach pain

Glitazones Rosiglitazone Pioglitazone

- Water retention - Tissue swelling - Weight gain

PPARs act on Peroxisome Proliferator Responsive Elements (PPRE) Influence insulin sensitive genes Enhance production of mRNAs of insulin dependent enzyme Better use of glucose by the cells

3. -glucosidase Inhibitors Acarbase Miglitol

-glucosidase inhibitors Inhibit enzyme [that breakdown polysaccharide sucrose] Slow down glucose absorption Cortisol binds to - Effect on metabolism (carb, glucocorticoid protein & fat metabolism. receptor in cytoplasm Clucocorticoid receptor activation TRANSLOCATION activated hormone receptor complex enter nucleus Interact with glucocorticoid response element (GREs) & other regulatory proteins. Modulate transcription - Anti-inflammatory

- GIT disturbance: Flatulence Diarrhoea Bloating Abdominal discomfort

Adrenocorticosteroids Cortisol (glucocorticoid)

- Immunosuppressive

Hypersecretion cause abnormal deposition of fat - Face (moon-face) - Shoulder (buffalo hump) - Pendulous abdomen *cushings syndrome Others : - Osteoporosis - Thinning of skin - Increase capillary fragility (pecah) - Bruising - Striae **due to protein catabolism

- No abrupt withdrawal, always gradual withdrawal abrupt withdrawal may lead to suppression of hypothalamic/ pituitary/ adrenocortical feedback system severe mental depression.

Aldosterone (mineralocorticoid)

reabsorption of sodium from renal tubule followed by reabsorption of water Increase in ECF volume, blood volume & Blood Pressure

- Increase the absorption of sodium and water - Increase the renal excretion of potassium.

- Excessive use in sodium - water retention - loss of potassium Muscle weakness symptoms : - edema Congestive heart failure - Hypertension - Sweating - Bruising - Allergic skin rash

Contraindicate if the patient already receiving a potassium-sparing diuretic.

Analgesic-opioid (drug that relieve pain)-moderatesevere Pain: an unpleasant sensory & emotional experience associated with actual/potential tissue damage Nociceptive pain Neuropathic pain -tissue damage -damage/dysfunction of nerves (PNS/CNS) -acute: quick, excessive noxious stimulus /chronic: slow transmission Endogenous opioid (body synthesized) -somatic:localized visceral: internal organ Enkephalin, endorphin, dynorphin referred pain: sakit tmpt lain, rasa tmpt lain (endomorphin-1/-2)-new Opioid /narcotics Bind to opioid CNS: *histamine release asthmatic patient analgesic receptors (, ,,)*analgesia -urticaria Opiates (Morphine) coupled G-protein -exert effect at receptor -swearing -inhibit neuronal activity -bronchospasjm Less effective analgesia Inhibit adenylyl -inhibit release of cyclise neurotransmitter GIT: Codeine -activate descending motility Tramadol Activate receptorinhibitory system tone Methadone activated K+ currents *Sedation seretion K+ efflux doseconvulsion passage of fecal Antagonist: naloxone (hyperpolarization (muscles contract and relax mass Inhibit Ca2+ entry rapidly and repeatedly, water absorption resulting in an uncontrolled transmitter release shaking of the body) (anti-diarrheal effect) & excitability *euphoria -delay gastric (sense of well-being) emptying Inhibit transmission *respiratory suppression nociceptive impulse -depress respiratory center (overdose) CO2 sensitivity arterial PCO2 Cerebral vascular dilatation *cough suppression -anti-tussive -codeine,pholcodeine *nausea & vomiting -stimulate chemoreceptor trigger zone (CTZ) *miosis -pin-point pupil (constriction of pupil) NSAIDs (non-opioid) mildmoderate (inflammation) NSAIDs Inhibiting Non-selective COX *Anti-inflammatory #GIT #Renal COX-1>COX-2 (can inhibit both COX- *Analgesic effect -- peptic ulcer insufficenency 1,COX-2) inhibit *Antipyretic effect -nausea #hepatic Indomethacin prostaglandin # platelet dysfunction Sulindac synthesis aggregation #peptic ulcer Piroxicam #hepatic #renal failure Phospholipid (hepatoxicity) #NSAID allergy Phospholipase #renal #anticoagulant Arachidonic acid (glumorukopathy) #thrombocytopenia Cyclooxygenase #CNS (hallucinations) Prostaglandin #Hypersensitivity Salicylates (Aspirin) A:Well absorbed in + Anti platelet effect #Renal: derived from Salicylic GIT *PG (renal acid (SA) rectal absorption vasodilatior) M:Rapid hydrolysed * PG: blood flow SA *Na & H2O retention Glycine bp conjugateinactivate *GFR: renal failure ions #Salicylism: tinnitus, E:kidney headach, confuse #Allergy:urticaria #Reyes syndrome: detrimental effects

to organs NSAIDs Inhibiting COX-1 = COX-2 Ibuprofen Highly selective COX-2 Celecoxib Paracetamol (Acetaminophen) (not NSAIDs) Non-selective COX (can inhibit both COX1,COX-2) inhibit prostaglandin synthesis Selective COX-2 Inhibitors Inhibit PG synthesis in CNS (maybe via COX3) A:well absorb (GIT) M: conjugate as glucoronide & sulphate Brochial Asthma 2-receptor agonist Non-selective: Adrenaline Selective: *Short -salbutamol -terbutaline -fernoterol *Long -salmeterol -fomoterol Methylxanthine -Theophylline -Amophylline cAMP Stimulate adenyl cyclase [x] SM contraction [x] mast cell mediator release

#analgesic effect #anti-pyretic effect

-lack GIT effect -not produce Reyes syndrome Overdose: -hepatoxicity -slow death (liver damage) (B1 receptor-effects) -tachycardia -palpitation -peripheral vasodilation -hypokalemia

Relief acute attack of asthma

Anticholinergic (antimuscarinic) -ipratropium bromide -tiotropium Corticosteroid *systemic -hydrocortisone (IV) -prednisolone *inhaled -beclomethasone -budesonide Mast cell stabilizers -sodium cromoglycate -nedocromil Leukotrienes Pathway Inhibitors *Leukotriene synthesis inhibitor -zileuton *Leukotriene receptor antagonist -zafirlukast -montelukast Anti-IgE monoclonal ab Opioids

[x] phosphodiesterase enzyme cAMP Relax SM [x] adenosine receptor (X) AcH at muscarnic receptor (X) bronchoconstriction (X) phospholipase A2 (X) COX-2 arachidonic acid D inflammatory mediators (leukotrienes) (X) mast cell degranulation Arachidoic acid (X) 5-lipoxygenase Leukotrienes

Chronic treatment Nocturnal cough prophylaxis IV acute asthma Oral chronic asthma

Vomiting, nausea Headache, anxiety, tremor, seizures, dysrhythmmias

Effective in COPD

Prophylactic Prevent broncoconstriction Moderate asthma Maintenance prophylaxis Mild Git upset headache

-blockCysLT (leukotriene receptor) contraction of SM (x) igE binding (X) igE synthesis Block medullary -

ANTI-TUSSIVE

-morphine -codeine -methadone H-receptor antagonist st -1 generation *promethazine *pheniramine

cough center cough reflex

-2 generatiomn

Expectorants

Mucolytics -Carbocysteine, mecysteine

-dornase alfa

-bromhexine, ambroxol

Peptic Ulcer -triple therapy for 14days is considered the treatment of choice. - 1 PPI + 2 antibiotics -can substitute Flagyl 500mg PO for 14d if allergic to PCN -in active peptic ulcer, continue qd PPI for additional 2 weeks - goal: complete elimination of H. Pylori Histamine/H2 receptor -Block the H2 Relieves heartburn and antagonist receptor of histamine functional dyspepsia pain -cimetidine(tagamet) in parietal cells and promotes ulcer healing -ranitidine (zantac) -Inhibit the cAMPby decreasing stomach acid -famotidine(peptid) dependent pathway -nizatidine (axid) from activating the proton pump -Inhibit HCl secretion Proton pump receptor (PPI) - omeprazole (prilosec) -lansoprazole (prevacid) -rabeprazole (aciphex) -Esomeprazole (nexium) Exist in inactive form prodrugs -readily converted to active form in low pH(acidic) -become thiolreactive - Inhibits H+/K+ ATPase enzyme irreversibly Results in more complete acid suppression in comparison to H2 blockers

-Headache -Dizziness -Diarrhoea..etc

Antibiotic -clarithromycin -amoxycillin -tetracycline

A single antibiotic is not sufficient, combination of 2 antibiotics are required (synergistic effect)

Elimination of H. Pylori

Antibiotic (AMA) B-lactam antibiotics *Penicillin *Cephalosporins *Carbapenems

Inhibition of cell wall synthesis -prevent cross-linkage (inhibit transpeptidase) -prevent cross-linkage (bind D-alanine) Disrupt cell membrane Bind to phospholipids Inhibit protein synthesis Change 30S rRNA shape mRNA read incorrectly Bind to 50S rRNA X movement on mRNA Interfere tRNA anticodon reading Bind to 50s rRNA X peptide bond form Inhibit N.A synthesis

Glycopeptide *Vancomycin *Teicoplanin Polymyxin

*Prophylaxis (prevention of serious infection) *Empirical therapy (therapy before lab result) *Directed therapy *Combine use of AMAs? -to achieve synergism effects (-cidal/-static) - adverse effect -X resistance -broaden spectrum of AMA action

*Toxicity (Local/Systemic) *Hypersensitivity *Superinfection (disruption of normal microflora) *Nutritional deficiencies

CHOICES OF AMA -PATIENT Age, drug allergy, immune status Eg: bacteriostatic immune system OK -ORGANISM Clinical diagnosis, culture & sensitivity, severity

Aminoglycosides *streptomycin

Drug Resistance 1. natural (lack of specific target site for the drug) 2.acquired (mutation) *X entrance of drug,change in CM permeability *alter drug binding site (acquire new gene) *pump out drug/efflux pump *inactive the drug *use alternative p/way:metabolite

-DRUG Spectrum (narrowgram +/-) (broadboth) Toxicity, route, pharmacokinetics

Macrolides *Erythromycin Tetracycline Chloramphenicol Rifampin Quinolones Nalidixic acids Rifamycin

Antifungal Polyene Amphothericin B (AMB) Liposomal Ampho B Ampho B in lipid delivery vehicle toxicity tolerability of infusion

Interact with ergosterol (fungi cell membrane) Produce hydrophilic channels(micropore) Electrolytes,cell contents move out

-for oral, vaginal, cutaneous candidiasis -otomycis -systemic mycoses #broad spectrum eg: (against candida spp,aspergillus,

Highly toxic a) acute reaction occur in each infusion: chills, fevers, hypotension,nausea #: add hydrocortisone

Pharmacokinetics * I.V administration *poor CSF absorbintrathecal *slow release *slow excrete *protein-bound Nystatin Azoles: Imidazole -Ketoconazole -Miconazole -Clotrimazole Triazoles affinity toxic *topical Lanoesterol (14-demethylase/ P450 enzyme) (-) Ergosterol Abnormal fungi membrane Superficial candidiasis Less toxic than ampho B Broad: Candida sp., c. Neoformans, aspergillus

b) chronic reaction -nephrotoxic -electrolyte disturbance -CNS toxicity

-nausea -bad taste in mouth -GIT Upset -hepatitis

Drug interaction: Affect mammalian P450

-flucanazole -itraconazole -voriconazole Flucytosine (5-FC) (narrow spectrum) Griseofulvin Echinocandis -caspofungin -micsfungin -anidulafungin Antivirals Anti-Herpes virus (HPV-1,HPV2,CMV,EpsteinBarr,Varicella zoster) Acyclovir

Pharmacokinetics: Oral & i.v Good absorption Inhibitor of thymidylate synthesis P/kinetic: oral Mitotic inhibitor Block synthesis 1,3--D-glucan (cell wall p/kinetic: i.v Deoxyguanosine analog Acyclovir v.l thymidine kinase Acyclovir monophosphate Acyclovir triphosphate x viral DNA pol x lengthening DNA strands

Chromoblasto Mycosis Synergestic with AMB Dermatophyte Protect skin For Resistant infection

Marrow suppression hepatitis Headache, git disturbance Not much side effects

Foscarnet

Inhibit v. DNA pol, reverse transcriptase

Anti-CMV Gancyclovir (analogue Acyclovir, more active)

Pharmacokinetics: I.V, oral, intraocular

Anti-influenza virus Adamantanamine -amantadine -rimantadine Sialic acid Oseltamavir (oral) Zanamivir (inhaler) Anti-hepatitis Interferon

Inhibit replication of influenza A virus Prevent uncoating of viral RNA Inhibit neuraminidase enzyme (for viral release) Inhibit all steps of viral infection (i.v / i.m) PEGylated interferon Slow absorb Sustained effects Guanosine analogue Inhibit GTP synthesis Reverse transcriptase inhibitor (X) viral RNADNA

Low toxicity on normal host cell Preferentially taken up by virus infected cell Active aginst all herpes v. except CMV Uses: -genital herpes simplex (HPV2) -mucutaneous H. Simplex (HPV1) -H.simplex encephalitis (HPV1) -H.simplex I keratitis -Herpes zoster -Chicken pox *CMV retinitis & other CMV infections *Acyclovir-resistant mucocutaneous Active aginst all HPV Congenital & severe CMV -delay progession of retinitis risk of Karposis sarcoma i n HIV CMV infection -prophylaxis of influenza A2 (epidemic) -treatment Prophylaxis & treatment of Influenza A, B, H5N1 -chronic hepatitis B,C -Kaposis sarcoma -chronic myeloma leukemia

Headache Nausea Rashes Low BP Reduce GFR

Toxicity: Damage kidney Anemia Convulsions,tremor Rash, fever Bone marrow depression Retinal detachment Neuro psychiatric probs. Nausea, anorexia, insomnia, dizziness, nightmares Nausea, abdominal pain, headache, diarrhoea,cough Flu-like symptoms, fatigue, aches, anorexia, neurotoxicity, myelosuppression, hypotension, thyroid dysfunction Haemolytic anemia Psychiatric problem Toxicity: Anaemia, neutropenia Epilepsy, CNS disease, gastric ulcer, pregnancy

Ribavirin

Antiretrovirals Nucleoside RTI -Zidovudine -Didanosine -Lamivudine

-chronic hepatitis C -severe Respiratory Syncytical Virus (RSV) Combination therapy -reduce vertical transmission -symptomatic AIDS -infants with HIV

Non-nucleoside RTI -Nevirapine -Efavirenz -saquinavir -indinavir -ritonavir Enfuvirtude

-low CD4

Protease Inhibitors (X) aspartyl transferase Inhibit fusion of viral and cell membrane