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143 Cards in this Set
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Hydralazine
|
MOA: Increase cGMP--> smooth muscle relazation ... vasodilates arterioles. After Load Reduction
USES: Severe HTN, 1st line for HTN in pregnacy w/ Methyl dopa |
TOXICITY:
Compensatory Tachycardia (contraindicated angina and /CAD) Fluid retention Nausause headache... LUPUS LIKE SYNDROME |
|
CLonidine
|
MOA: alpha 2 stimulation: Decrease sympathetic outflow
Decrease TPR but also HR |
TOX: CNS Depression
EDEMA |
|
Methyldopa
|
MOA: alpha 2 stimulation: Decrease sympathetic outflow
Decrease TPR but also HR USed: in HTN with Pregnancy |
TOX: Autoimmune Hemolysis (20% patients)
CNS Depression EDEMA |
|
Guanethidine
|
MOA: Accumulated in nerve ending by reuptake. binds vesicle inhibits Nor Epi Release
|
Adverse Effects :
Diarrhea EDEMA |
|
Prazosin
Doxazosin Terazosin alpha 1 blockers |
MOA: Decrease arteriolar venous resistance.
Reflex tachicardia... USES: HTN& BPH |
Adverse Effect:
First Dose Syncope Orthostatic Hypotension Urinary incontenence GOOD EFFECT ON LIPIDS |
|
Calcium Channel Blockers:
Verapamil, Diltiazem (NON DHP) DHP - Nifedipine (-- dipines) |
MOA: Block voltage dependent L- Type caclium channels of cardiac and smooth muscle thereby reducing muscle contractility.
USES; HTN, Angina, Arrhythmia (not dipinines) Prinzmetal Angina Raynauds |
Adverse effect:
Cardiac Depression, AV Block Periphereal edema Flushing Dizziness Constipation Dipines --> Reflex Tachy |
|
Nitroglycerin
Iso Sorbide Dinitrate |
MOA:
Vasodilate by releaseing NO into Smooth muscle causeing Increase in cGMP and smooth Muscle relaxation. Dilate veins >> Arteries Decrease Preload USE: Angina, Pulm Edema |
Adverse effects:
Reflex Tachycardia, hypotension, flushing, headache |
|
Nitroprusside
|
MOA: Short acting (titrate effect.) Increase cGMP via release of NO
USES: MALIGNANT HTN |
Adverse effects:
Cyanide Toxicity (co admininster with nitrites and Thiosulfate to prevent CN tox) |
|
Fenoldopam
|
MOA :Dopamine Receptor Agonist
Relaxes Vascular smooth muscle Uses: MALIG HTN |
Adverse Reactions:
Hypotension, SEVERE Tachycardia CHF MI HypOkalemia leukocytosis elevated intra ocular pressure |
|
Diazoxide
|
MOA: K+ channel opener--> hyperpolerizes and relaxes vascular smooth muscle
USES: MALIGNANT HTN (EMERGENCY) |
Adverse Effects :
Hyperglycemia (reduces insulin release) edema reflex Tachycardia |
|
Minoxidil
|
MOA: Opens K+ Channel cuase hyperpolarization of smooth muscle results in arteriolar vasodialation
USES; SEVERE HTN BALDNESS(TOPICAL) |
Adverse Effects:
Hypertrochosis- good for baldness EDEMA Reflex tachycardia |
|
-STATINS
Lovastatin Atorvostatin(lipitor) simvistatin Pravistatin |
MOA; HMG-COA reductase inhibitor. Inhibits cholesterol Prechurse Mevalonate (Decreases)
This cuases an Increase in LDL receptors and more is removed |
Adverse Effects RHABDOMYALYSIS--> muscle break down, decrease excercise tolerance muscle pain.
Hepatotoxic- (inc.LFTs) |
|
NIACIN
|
MOA: Inhibits lipolysis in adipose tissue reduces hepatic VLDL secretion into circulation
|
ADverse EFFECTs:
Red Face Flushed Face (decrease by asprin) Hyperglycemia (acanthosis nigricans) Hyper Urecemia (GOUT exacerbation) |
|
Bile Resins
Cholestyramine, colestipol, colesevelam |
MOA: Prevent intestinal reabsortionof bile acid
Liver must use cholesterol to make more |
ADVERSE EFFECTS:
pt. Hate it. tastes bad and causes GI discomfort . Decrease absorption of fat soluble vitamins Cholesterol gall stones |
|
Ezetimibe
|
Prevent cholesterol reabsorption at small intestine brush boarder
|
AE:
RARE (inc. LFTs) |
|
FIBRATES
Gemfibrozil Clofibrate Bezafibrate fenofibrate |
Upregulate LPL
Inc. Triglyceride clearance |
AE:
Myositis Hepatotoxicity (Inc. LFTs Cholesterol Gall stones |
|
Digoxin
|
MOA:
Direct inhibition of NA+/K+ ATPase leads to indirect inhibition of NA/Ca exchanger Increase [Ca]--> + inotropy Stimulates vagus |
AE:
Cholinergic- N/V/D, yellow vision, EKG- Inc. PR interval Decrease QT, scooping (digbowls), t wave inversion, Arrhythmia, HypERkalemia Antidote: Slowly Normalize K Lidocane Cardiac Pacer, Anti DIG FAB, Mg2+ |
|
Class 1a Anti-arrhythmic
Quinidine |
MOA: Block Fast Na+ channels, Preferentially in the open or activated state (state dependent blockade)
also Blocks alittle k+ (prolongs repolarization) Cause Muscarinic Receptor Blockade which can inc. Heart and AV conduction USES: A fib (need to use DIGOXIN first) |
AE:
Cinchonissim- (GI, Tinnitus, Occular dysfn, CNS ExcitatioN) Hypotension Prolongation QRS and Increas QT interval associated with syncope and Torsades Displaces Dig from plasma protein... Cuases increase tox of Dig |
|
Class 1a Anti arrhythmic
PROCAINAMIDE |
MOA: Block Fast Na+ channels, Preferentially in the open or activated state (state dependent blockade)
also Blocks alittle k+ LEss muscarinic (acetylated) |
SLE (with Slow acetylators)
Hematotoxicity (Thrombocyto, agranulocytosis) CV: TORSADES Pericardial Tamponade severe Hypotension |
|
Class 1a Anti arrhythmic
DYSOpyramide |
Block Fast Na+ channels, Preferentially in the open or activated state (state dependent blockade)
also Blocks alittle k+ |
AE:
AV block Edema NEG. Inotrope Urinary Retntion |
|
Class 1b Anti-arrhythmic
Lidocaine |
MOA: Block Fast Na+ channels. Innactivated channel blocking prefference for tissue partly depolarized (slow conduction) Hypoxic or ischemic. This result in ncrease threshold for excitation and less ecitability of hypoxic tissue
|
AE:
CNS Tox (seizure) least cardiotoxic of other antiarrythmic |
|
Class 1b Anti-arrhythmic
Mexiltine |
MOA: Block Fast Na+ channels. Innactivated channel blocking prefference for tissue partly depolarized (slow conduction) Hypoxic or ischemic. This result in ncrease threshold for excitation and less ecitability of hypoxic tissue
|
ORAL Formulation
|
|
Class 1 C Anti-arrhythmic
FLecainide |
Block fast Na Channels especially his perkinge tissue
|
AE: Proarrhythmic, Incr. Post MI and when used prophylactically in VTAC
|
|
Class II Anti- arrythymic
Beta Blockers Propranolol, Acebutolol, Esmolol |
MOA; Decresae SA and AV nodal Activity.
Decrease slope of Phase 4 depolarization current . USED: SVT, AFIB A FLUTTTER |
AE:
CV Depression Fatigue Sexual Dysfunction Increase LDL and TG |
|
Class III Anti-Arrythmic
K+ Channel Blocker AMIODARONE |
MOA;
Decrease Ik (rectifier channel) slowing phase 3 (repolarization) of AP Increase ADP and ERP epespecially in his Perkinje fibers. Mimics Class 1,2,3&4 Blocks Na, Ca, Beta,Ca+ |
AE; 1/2 life 80 days
Pulmonary Fibrosis Blue Pigment of skin Phototoxicity Corneal Deposits Hepatic necrosis Thyroid Dysfunction--Iodine |
|
Class III Anti-Arrythmic
K+ Channel Blocker SOTALOL |
MOA: Slowing phase 3
Beta 1 blockade leading to Decrease in HR and Av Conduction |
AE;
Proarrhthmetic- TORSADES |
|
Adenosine
|
MOA: Adenosine Receptors
causes Gi coupled Decreas in cAMP Antagonised by Methylxanthines |
AE:
Flushing Sedation Dyspnea transient Asystole |
|
Magnesium Sulfate
|
USE:
TORSADES |
|
|
Bosentan
|
USE: Pulmonary HTN
Endothelin-1 is a powerful vasoconstrictor through ET-a and B receptors. MOA- ETA recpetor Antagonoist |
Contraindicated; Pregnancy
AE: Headache flushing, hypotension) |
|
Sildenafil
|
MOA; Inhibits
Phosphodiesterase 5 Leads to Pulmonary artery Relaxation. Decrease in Pulmonary artery hypertension USE also for Male enhancement |
MI
Stroke Sudden Death Vent Arrhythmias Pulmonary hemorrhage non arteritic Anterior Ischemic Optic neuropathy |
|
Drugs that Improve Mortality with CHF/MI
Inhibit Cardiac Remodeling |
ACEI, ARB, Spironolactone,Metoprolol/carvedolol
|
|
|
Mannitol (IV)
Osmotic Diuretic |
MOA: inhibits water reabsorption throught the tubule. Increase Urine volume
Uses: Decrease IOP In Glaucoma Decrease Inctra Cerebral Pressure Oligure states rhabdomyolysis |
AE:
Acute HypOvolemia |
|
Acetazolamide
- Dorzolamide |
MOA: carbonic Anhydrase inhibition. Results in Dec. H+ formation in Proximal Convolute
decrease Na+/H+antiport Inc. Na and HCO3 in lumen Increase Diuresis Use For Metabolic alkalosis. Treat Acute Mountain Sickness |
AE;
Bicarbonaturia(HCO3 in urine) HypERchloremia HypOkalemia Paresthesias Renal Stones Sulfonamide Hypersensitivity |
|
Ethacrynic Acid
(LOOP) |
MOA: Block
Na+/K+ / 2 Cl- Transporter Decrease Intracellular K (TAL) Dec. back diffusion of K+ into lumen Decrea Positive potential Dec. Reabsorption of Ca and Mg Increase Diuresis |
OTOTOXIC
NO SULFA REACTION Sulfonamide Hypersensitivity HypOkalemia ALKalosis Hypocalcemia Hypomagnesemia Hyperurecemia |
|
Furosemide (lasix)
Torsemide Bumetanide |
MOA: Block
Na+/K+ / 2 Cl- Transporter Decrease Intracellular K (TAL) Dec. back diffusion of K+ into lumen Decrea Positive potential Dec. Reabsorption of Ca and Mg Increase Diuresis |
Sulfonamide Hypersensitivity
HypOkalemia ALKalosis Hypocalcemia Hypomagnesemia Hyperurecemia Ototoxic(enhanced with Amino Glycosides) Lithium decrease clearance Dig (inc Tox due to electrolite imbalance |
|
Hydrochlorothiazide
|
MOA: Na+/Cl- transporter inhibition
Result Inc. luminal NA and Cl in DCT Increase Diuresis USES;Nephrolithiasis, Nephorogenic Diabetes Insipitis |
AE:
Sulfa Hypersensativity HypOKalemia ALKalosis HypERCALCEMIA HyPERUrecemia HyperGlycemia Hyperlipidemia(not indampamide) AVOID IN Diabetics patinetis |
|
Spironolactone
|
MOA: Aldosterone Receptor Antagonist
UseS: Hyperaldosteronic state Adjunct to K wasters Antiandrogenic use(femal hersuiT) |
HypERkalemia
Acidosis Antiandrogen |
|
Amiloride
Tramterene |
Na+ channel blocker
Adjunct to K+ wasting diurentics .. lithimium induced Nephogenic DI. |
Hyperkalemia
Acidosis |
|
Angiotension Converting Enzyme Inhibitor
-Prils lisinopril Captopril |
Inhibit angiotension converting enzyme reducing levels of angiotensin II
Prevent bradykynin Degradation Renin Release Is Increase due to loss of feedback inhibition |
Angioedema
Dry Cough Hyper Kalemia Acute renal failure in pt with renal artery stenosis Contra indicated Pregnancy (fetal renal damage) |
|
Angiotension Receptor Blocker
(Sartans) Valsartan Losartan |
block At ! receptor
Resulst stame as ACEI not interfere with Bradykin activity |
HyperKalemia
Acute renal Failure In Pt with Renal Artery Stenosis |
|
Aliskerin
|
Renin Inhibitor
Blocks Formation of Ang 1 Preotective in Diabetic Nephropathy CHF |
Fetal Morbidity and Mortality
Angiedemia Hyptoension Teratogenic/ Kill fetus olighydramnios GERD Hyperkalemia |
|
Epinepherine
|
MOA: Decrease Aqueous Humor synthesis due to vasoconstriction
|
AE:
Mydriasis, Stinging DO NOT USE IN CLOSED ANGLE GLAUCOMA |
|
Brimonidine
|
MOA; Decrease Aq. Humor Synthesis
|
No pupilary or vision changes
|
|
Timolol
Betaxolol Carteolol |
Decrease Aq. Humor secretion
|
No Pupillary or vision changes
|
|
Acetazolamide
|
Decrease aq humor secretion due to decrease bicarb (via inhibition of Carbonic andhydrase)
|
No Pupillary or vision changes
|
|
Pilocarpine
Carbachol |
Inc. outflow of aqueous humor contract ciliary muscle and open trabecular meshwork
Pilocarpine for Closed angle emergency open Canal of Schlem |
AE:
Miosis and Cyclospasm (blurry vision) |
|
Latanoprost
|
Inc outflow of Aqueuos Humor
|
AE; Browning of Iris
|
|
Opiods
Morphine Fentanyl Codeine Heroin Methadone Meperidine |
MOA: act as agonist on Opiod receptor (Mu= Morphine) Delta enkephlin. to modulate synaptic transmission
Open K+ channels close Ca+ and modulate decreas synaptic transmission Inhibit substance p, glutamate, AcH, NE |
AE:
Addiction Respiratory Depression Constipation Miosis (pinpoint pupils) CNS depression with other drugs Tolerance not develop miosis and constipation. Toxicity treated with Naloxone |
|
Butorphanol
|
MOA: Partial agonist at Mu receptor agonist at Kappa
Use: pain causes less resp depression |
AE: causes withdrawl if on full opiod agonist
|
|
Tramadol
|
MOA:
very weak opiod agonist Inhibits Seritonin and NE uptake |
AE: similar to opiods
Decrease Seizure threshold (easier to throw siezure) |
|
Phenytoin (dilantin)
|
MOA: Increase Na Channel Inactivation ..Increase Refractory period inhibiton of glutamate release from excitatory presynaptic neuron
USE; ALL Seizure (EXCEPT ABSENT) |
AE:
Gingival Hyperplasia SLE like reaction nystagmus, ataxia, diplopia, sedation induction of P-450, Peripheral Neuropathy, Hirsuitism, Megaloblastic anemia (Dec. Folate absortion) Teratogenic : FETAL HYDANTOIN Syndrome |
|
Carbamazepine
|
Increase Na Channel Inactivation ..Increase Refractory period inhibiton of glutamate release from excitatory presynaptic neuron
USE; ALL Seizure (EXCEPT ABSENT) |
AE:
Diplopia, ataxia, blood dyscrasias(agranulocytosis, aplastic anemia) Hepatotoxic Teratogenic SIADH Steven Johnson Sydrome |
|
Lamotrogine
|
Blocks Votake gated Na Channels
|
Steven Johnson Syndrome
|
|
Gabapentin
|
MOA: Gaba analog...
primarily inhibits HVA calcium channels USed for Peripheral Neuropathy as well as seizure |
Sedation, Ataxia
|
|
Topiramate
|
MOA
Blocks Na channels Increase GABA Action |
AE:
Sedation Mental Dulling Kidney stones Weight loss |
|
Phenobarbitol (barbiturates)
|
MOA: facilitate action of GABA a action by Inc.duration of Cl- channel opening. thus decrease nueron firing
|
AE:
Dependence, additive CNS depression effect with alcohol, respiratory or cardiovascular depression (can lead to death) drug interation increase P450 |
|
Valproic Acid (valproate
|
Increase Na Channel Inactivation, Increase Gaba Concetration by inhibiting Gaba transaminase, Blockade of T type CA 2+ Channels
|
AE:
Gi Distress Rare but fatal Hepatotox (measure ur LFTs) Neural tube defects on fetus(spina bifida) Tremor, weight gain, PANCREATITIS, ALOPECIA (HAIRLOSS) DONT USE IF PREGNANT |
|
Ethosuximide
|
Blocks Thalamic L type calcium channels
1st Line for absent seizures |
Gi Distress, Fatigue , Headache, urticaria, Steven Johnson syndrome
|
|
Diazepam
Or Lorazepam |
Increase GABA A action
Status EPileptiocus |
AE;
Sedation, Tolerance, Dependence |
|
Vibagatrin
|
MOA:
Irreversible inhibits Gaba Transaminase (increase GABA |
|
|
Benzodiazepines
Alprozolam, Diazepam, Lorazepam, Triazolam, Temazepam, oxezepam, Midazolam, Chlodiazepoxide |
MOA: Facilitate GABAa action by increaseing frequency of Cl- channel opening.
Decrease REM sleep Most have long half lives and Active Metabolites EXCPET Lorazepam and Oxazepam |
AE:
Dependence, additive CNS depression. Less risk of Respiratory depression and coma than with barbiturates Treat OD with FLUMAZENIL |
|
ZOLPIDEM (AMBIEN)
ZALEPLON ESZOPICALONE |
MOA: Act via BZD1 receptor subtype reverse by Flumazenil
USE: INSOMNIA |
AE:
Ataxia, headache, confusion, short duration rapid metabolism only modest day after psychomotor depression ...few amnestic effects. lower risk dependence then benzos |
|
Halothane, ENflurane,
Sevoflurane, Methoxyflourane NOxide |
MOA;
unknown |
AE:
Halothane- Hepatotox Nephro- Methoxyflourane Proconvosultant (enflouane Malignant hyperthermia Expansion of trapped gas (NO) |
|
Arylcyclohexylamine
Ketamine |
MOA:
PCP analog that acts as dissociative anesthetic. Blocks NMDA RECEPTOR |
AE:
Cardiovascular stimulant Cuase disorentation, Hallucinations and bad dreams. Incr. Cerebral blood flow |
|
Propofol
|
Rapid Iduction of anesthesia
short Procedures Potentiates GABA a |
Less Post operative Nausease then Thoiopentatl
|
|
Local Anesthetics
ESTERS Procaine, Cocaine,Tetracaine Amide Lidocaine, Mepivicane,bupivicane |
Blocks Na Channels by binding to specific receptors on inner portion of channel preferentially bind to activaterd NA channes so most effective in rapidly firind Neurons . Local anesthentics
|
AE:
CNS excitation, severe cardiovascular toxicity (bupivicaine), Hypertension Hypotension and arrythmias |
|
SuccinylCholine
|
Depolarizing Neuromuscular blocking drug
MOA; Motor Nicotinic Receptors |
MALIGNANT HYPERTHERMIA
|
|
Tubocurarine, Atracuriaum,Mivacurium, Pancuronium,vecuronium
|
NON depolarizing Neuromuscular Blockers
Competitive inhibition with ACh for receptors |
Malignant Hyperthermia
Reversal with Neostigmine,Edrophonium, Cholinesterase inhibitors |
|
Dantrolene
|
TREAT Malignant Hyperthermia, Neuroleptic Malignant Syndrome.
MOA Prevent release of Ca2+ frpm the sarcoplasmic reticulum of skeletal muscle |
|
|
Tolcapone
|
MOA: COMT Inhibitors and enhance levodopa uptake and efficacy
|
AE;
Hepatotoxic |
|
Seligiline
|
MOA;
MAO-B selective inhibitor (no tryamine transactions |
AE:
Dyskinesias, Psychosis, Insomnia, Metabolized to apmetamine |
|
Memantine
|
MOA: NMDA receptor antagonist helps prevent excitotoxicity
|
AE:
Dizziness confusion, Hallucinations |
|
Donepezil
Galantamine Rivastigmine |
ACh Esterase Inhibitiors
|
Naussea Dizzyness and Insomnia
|
|
Sumatripan
(-Triptan's) |
MOA: 5HT 1b/1d agonist causes vasoconstriction inhibition of trigeminal activation and vasoactive peptide release
|
AE
coronary Vasospasm(Contraindicated in Pt with CAD and Prinzmetals angina Mild Tingling) |
|
Typical Antipsychotics
-Haloperidol -Trifluoperazine -Fluphenazine -Thioridazine -Chlorpromazine |
MOA: All Typical Antipsychotics
block dopamine(D2) receptors (increase cAMP) |
AE: NEUROLEPTIC MALIGNANT SYNDROME
TARDIVE DYSKINESIA Highly lipid soluble, slow removal from body - EXtrapyramidal Side Effects Hyperprolactinemia, galactorrhea, amenorhea? -Drymouth constipation. Hypotension, |
|
Atypicals:
Olanzipine, Clozapine,Quetapine, Risperidone, Arriprozole,ziprasidone |
Block 5HT2, Dopamine, alpha and H1 recetoprs
OLanznipine for OCD |
AE:
Fewer Extrapyrimal and anticholinergic side effects than traditional antipsychotics olanzapine, clozapine, Wt gain ... Clozapine (agranulocytosis) weekly CBC |
|
Lithium
|
MOA: related to inhibition of Phosphoinositol Cascade
Mood Stabilizer BIPOLAR, Treat SIADH |
AE:
Tremor, Sedation, Edema, Nephrogenic DIabetes insipidus, hypothyroidism Teratogenisis Fetal Cardiac defects malformation of Great vessels Narrow theraputic... excreted by kidneys. |
|
TricyclicS
1st Gen Imipramine, Amytriptilyne, Desipramine Second cheneration Noreytrypitalin, Clomipramine, doxepen |
Blocks NE Reuptake and sodium
Major depression bdeeeting and ocd |
AE;
Dedation Apha blocjkoin atropine like effects tachicardia. urniary rententioin Despirpamine is least sedating and lower has seizure threshold |
|
SSRI
Fluoxteine Fluvoxamine Paroxetine Sertaline Citolpram |
MOA Seritonin specific reuptake inhibitors
Depression, OCD, Bulimia, social fobias |
AE; Seritonin Syndrome
With an drung that increase serotionin. IE MAO inhibitors -- hyper thermia muscle rigidity Seizure Treat Cycroheptadine |
|
SNRI
Ventafaxine, Duloxetine |
MOA:
Inhibit 5HT and NE Reuptake |
Increase BP most common and Stimulant effect , sedation and Nausea
|
|
MAO I
Phenylzine, Tranylcypromine, Isocarboxazid, |
MOA:
Non selective MAO inhibition increaselevels of amine NT (NE ,5HT, DA) |
AE:
Hypertensivie crisis with Tyramine ingestion (wine Cheese ) CNS Stimulation CONTRAINDICATED WITH SSRI and MEPERIDINE & Triptans |
|
Buproprion
|
Cigarette cessation
|
NE and Dopamine via unknown Mechanism Tocicity stimulat sideeffects (tachycardia, Insomnia) Headache, seizure in bulemics
|
|
Mirtazipine
|
MOA: Alpha 2 Antagonist ( Increase releasse of NE and 5HT) potent 5HT2 and 5HT3 recetpor antagonist
|
AE;
Sedation, Increase Apetite Weight gain, drymouth, |
|
Trazadone
|
Inhibits 5HT reuptake
Uses Insomnia |
AE: Priapism
Sedation, Nausea, Postural Hypotension |
|
WARFARIN
|
USE : Longterm Anticoagulation
MOA: ↓ Hepatic Synthesis of Vitamin K dependent clotting factors II,VII,IX,X Prevent the γ-carboxylation by inhibiting vitamin K-epoxide reductase. No effect on factors already present. Invivo effects only Monitor PT (INR) |
Toxicity:
Bleeding, skin Necrosis( if low protein C Hypercoagulable state) Teratogenic(bone dysmorphogenesis) DRUG Interactions: ↓ oral absorbtion by cholestyrimine(acid) Displaced from plasma proteins by PHENYTOIN,ASA, SULFONIMIDES (↑ PT) Cimetidine, Macrolides, Azoles (↑ PT) Barbs,carbamazepine,rifampin (↓PT) |
|
Digoxin
|
MOA: Direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger ↑ [Ca]--> Positive Inotropy Stimulates the vagus
antidote: Slowly Normalize K lidocaine, Cardiac pacter and Anti Dig- Fab |
Adverse Effects :
Cholinergic- N/V/D BLURRY YEllow vision, ECG--> ↑PR interval, ↓QT interval, Scooping(digbowl) T wave inversion, HypERkalemia Renal Failure (↓ exrection) HypOkalemia Quinidine displaces digoxin from tissue binding sites |
|
Beta Blockers
-olol |
MOA: Block β adrenergic receptors
|
ADVERSE EFFECTS:
Impotence, Exacerbation of asthma, Bradycardia, AV block, CHF, CNS adverse effects (Sedation and Sleep ateration... ) Mask Hypoglycemia in DIABETICS |
|
Phenytoin
|
MOA: Use-dependent blockade of Na+ channels (↑refractory period) inhibition of glutamate release from excitatory presynaptic neuron
|
Adverse Effects:
GINGIVAL HYPERPLASIA in kids, SLE like syndrome Nystagmus, ataxia, diplopia, sedation, induction of P450 Peripheral Neuropathy, Osteomalacia, Hirsutism Megaloblastic anemia (↓ Folate absorption) TERATOGENIC: FETAL HYDANTOIN SYNDROME : IUGR, Mental Retardation,Cleft Lip/ palate, under/poor developed fingers and toes, Microcephaly. |
|
Phenelzine
tranycypromine, Isocarboxazid |
CLASS: MAOi
MOA: Inhibits MAOa and MAOb |
AE: Hypertensive Crisis (inc. NE) Symptoms : ↑BP arrhythmia, excitation, hyperthermia
Drugs that cause (tyramine wine and CHeese, TCA, alpha1 agonist, Levodopa) Serotonin Syndrome:(SSRI, MEPERIDINE) Sweating Rigidity myclonus, Hyperthermia,ANS instability Seizures |
|
Lithium Carbonate
(lithium) |
MOA: Prevents Recycling of Inositol (↓PIP2) ↓cAMP
|
Adverse Reactions:
Narrow theraputic index; requires monitoring, Tremor, flu-like symptoms - Life threating seizures, Hypothyroidism w/ goiter (↓TSH effects and inhibition of 5'deiodinase) Nephrogenic Diabetes Insipidus (↓ ADH effect) Manage with amiloride Teratogenicity: Ebstein annomaly (malformed tricuspid valve. and malformation of the great vessels |
|
Cimetidine
Rinatidine, famotadine, nizaditidne |
CLASS: H2 blocker
MOA: reversibly blocks histamine (H2) receptors (↓H+) secretion by parietal cells |
Adverse EFFECTs:
Potent inhibitor of P-450: it also has anti androgenic effects(prolactin release) gynecomastia, ↓ libido (Males) Cross BBB, (confusion, diziness, headaches) Placenta crossing too |
|
Asprin
|
MOA: Irreversibly inhibits COX in platelets--> ↓activation
Covalent bond via acetylation of serine hydroxyl group near the active site LOW DOSES ↓tubular secretion- Hyperurecemia High Doses--> Inc. Secretion-->Uricosuria |
Adverse EFFECTS:
GI irritation, gastritis, ulcers, bleeding, Salicylism- Tinnitus, vertigo, ↓ hearing- 1st sign of tox Bronchoconstriction: Exacerbation of asthma Hypersensitivity - Asthma, Nasal Polyps rhinitis Reyes Syndrome: Encephalopathy, liver problems ↑ bleeding time chronic associated with renal dysfunction, Alcohol ↑ gi bleeding ↑warfarin effects Manage OD: Gastric Lavage vent support symptomatic manage of ACid base ALKALINIZE urine to facilitate removal TOXICITY: High doses: mild uncoupling of Oxidative phosphorylation-->↑ respirations-->↓PCO2--> Resp. Alkalosis--> Renal compensation ↑bicarb elimination---> Compensated Respiratory Alkalosis TOXIC: ↓respirations--> ↑pCO2--> Respiartory acidosis plus inhibition of Krebs cycle and severe uncoupling of oxidative phosphorylation (↓ATP) --> metabolic Acidosis, Hyperthermia, HypOkalemia |
|
ACETOMENOPHEN
|
MOA: reversibly inhibits Cyclo Oxygenase) MOstly in CNS
Inactivated peripherally |
Adverse Effects:
OD produces Hepatonecrosis, Metabolite Depletes Glutathione and forms toxic tissue adducts in liver MANAGE with N-acetylcystine - which is a precursor to glutathione |
|
THEOPHYLLINE
|
Class : Methyl Xanthine
MOA: cuase bronchodilation by inhibiting phosphodiesterase there by ↓ cAMP hydrolosis |
Adverse Effects:
Cardiotoxicity and Neurotox Blocks action of adenosine |
|
Cromolyn
|
MOA : helps prevent asthma attacks by inhibiting mast cell degranulation.
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asprin induced asthma
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Inhibition of enzyme
Wheezing after the ingestion of aspirin is due to inhibition of COX which increases leukotriene synthesis and results in bronchoconstriction. |
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Furosemide
Side effects? |
Common side effects for furosemide include: hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia, hypomagnesemia, allergic reactions, and hypercalciuria.
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A 6-month-old boy is brought in for a well-child visit. The mother says she has been trying to wean him from breast milk to formula, but since doing so, he has been vomiting, sweating, and fatigued. Serum glucose is found to be 37 mg/dL.
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This child has hereditary fructose intolerance, which is associated with a deficiency of aldolase B. Aldolase B is the enzyme responsible for splitting fructose-1-phosphate into glyceraldehyde and DHAP. Thus, in its absence, fructose-1-phosphate accumulates at the expense of the glyceraldehyde-3-phosphate, normally made from glyceraldehyde and DAP. Without this essential molecule gluconeogenesis and glycogen breakdown are impaired thus causing hypoglycemia whenever fructose is ingested. Treatment with a fructose free diet allows the patient to live a normal life.
Removing the upstream substrates, in this case sucrose, fructose, and sorbitol, can prevent downstream products from forming. Increased intake of ketogenic nutrients, or foods with a high fat content, is used to treat pyruvate dehydrogenase deficiency, as these foods will provide energy without using the citric acid cycle. |
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Overdose on phenobaribital, Asprin, Pens, Cephs, loops, thiazides, MTX
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Treat with BICARB
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OVERDOESE ON
Morphine, local anesthetics, Amphetamine, PCP... |
Treat with amonium Chloride
NH4CL |
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Atropine Like side effects
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TCA
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Coronary Vasospasm
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Cocaine, Sumatriptan
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Cutaneous Flushing
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Vancomycin, Adenosine, Niacin, Ca Channel blockers,
Isoproteranol, Histamine release, Morphine, Ampho B, |
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Dilated cardiomyopathy
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Doxirubicin, Daunorubicin
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Torsades de Pointes
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K+ channel Blockers (class 3)
Class 1 a(quinidine), Antipsychotics (thioridizine) TCA's |
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Agranulocytosis
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Clozapine,Carbamazepine, colchicine, Propylthiouracil, methimazole, Dapsone
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Aplastic anemia
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Chloramphenicol, benzene, NSAID, Propylthiouracil, Methimazole
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Direct coombs test
Positive Hemolytic anemia |
Methyldopa
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Gray baby
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Chloramphenicol
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Hemolysis in
G6PD deficinecy |
Isoniazid, Sulfonamides, Primaquine, Asprin, Ibuprofin Nitrofurantoin
fAva Beans |
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Megaloblastic Anemia
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Phenytoin, Methotrexate, Sulfa drugs
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Thrombotic Complications
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OCP's (estrogens and progestins)
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Cough
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ACE Inhibitors
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Pulmonary Fibrosis
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Amiodarone, Bleomycin, Busulfan
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Acute Cholestatic Hepatitis
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Macrolides
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prolonged QT interval
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Quinidine/Quinine
MACROLIDES (especially Erythromycin) |
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Focal -->Massive Hepatic Necrosis
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Halothane, Valproate, Acetominophen, Amanita, phalloides
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Hepatitis
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Isoniazid
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Pseudomembranous Colitis
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Clindamycin, Ampicillin
TREAT Metronidazole |
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Adrenocorcical insuficiency
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Glucocorticoid w/drawl
HPA suppression |
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Gynecomastia
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Spironolactone,nandrolone, digitalis, cimetidine, chronic alcohole use, estrogents. Ketoconazole
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Hot Flashes
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Tamoxifen, Clomiphene
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Hypothyroidism
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Lithium, Amiodarone
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Gingival Hyperplasia
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Phenytoin, Cyclosporine, Verapamil, Nifedipine
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GOUT
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Furosemide, thaizides
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osteoperosis
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Cortecosteroids, Heparin
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Photosensitivity
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Sulfonimides, Amiodarone, Tetracycline
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Steven Johnsons Syndrome
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Ethosuximide, Lamotrigine, carbamezepine, Phenobarbitol, Phenytoin, Sulfa's, Penicillin, Allopurinol
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Systemic Lupuse ERETHEMATOSIS Like Syndrome
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Hydralizine ,
Isoniazid, Procainamide Phenytion |
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Tendonitis/ tendon rupture
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Floroquinolones
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Fanconi Syndrome
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expired tetracyclines
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interstitial Nephritis
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Methicillin, Nsaids, Furosemide
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Hemorrhagic cystitis
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Cyclophosphamide,ifoshamide
(prevent by coadminister with MESNA) |
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Cincohonism flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes
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Quinine/Quinidine
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Diabetes Insipidus
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Lithium, Demeclocycline
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Parkinson-like syndrome
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Haloperidol, Chlorpormazine, Reserpine, Metoclopramide
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Siezures
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Bupropion, Imipenemim/cilastatin
Isoniazid, |
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Tardive Dyskinesia
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Antipsychotics, Metoclopramide
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Disulfram Like Reaction to alcohol
Sweating, Headache , Chills... |
Disulfram, Metronidazole, Cefoperpazone, Cefotetan, chlorpropamide, Grisofulvin, 1st gen sulfonylureas
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Nephro /Neurtox
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Polymyxins
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Nephrotox/ototoxic
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Aminoglycosides, Vancomycin, Loops, Cisplatin
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P450 Inducers ( reduce drug levels)
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Quinidine, Barbiturates, St. Johns wartt, phenytoin, Rifampin, Grisofulvin, Carbamazepine, Chronic alcohol abuse
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Inhibitors of P450 (more drug around)
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HIV Protease inhibitors (navirs)
Ketoconazole, Erythromycin, Grapefruit juice, Acute alcohol use, Sulfonamides Isoniasinde Cimetidine |
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