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Prescribing Basics: 2 questions Prescriptive authority regulated by the state BON in each state. Tall man lettering to highlight dissimilaries with look-alike names *Prescription contains… Physicians Name, Address, and telephone number are required to be included in the prescription. DEA number (two letters, five numbers) if the prescription is for controlled substance, Patient name and DOB (also may include address and weight), Date Rx is written (expires 1 year after date issued), Name of drug and strength- avoid trailing zeroes, use leading zeroes, Directions with indications/route of administration and frequency, write out number of refills, quantity of drug, signature, NPI number (9 or 11 numbers), sign as A-PNP or role recognized by the BON Drug schedules – one is most addictive, up to schedule 5.
- heroin, LSD, marijuana.
- oxycodone, hydrocodone, methamphetamines.
- codeine, ketamine, testosterone.
- Xanax, valium, ambien, tramadol.
- antidiarrheal, antitussives, Lomotil, lyrica. *calculation question Pharmacology Principles: 3 questions Pharmacodynamics – effect of drugs on body. Works by receptors. Usually proteins that interact with drugs. Agonist – produce receptor stimulation, conformational change every time they bind. Partial agonist – properties between agonists and antagonists. Submaximal effect. Stimulate only some of the receptors. Antagonist – affinity for receptor but NO intrinsic activity. Affinity allows antagonist to bind to receptors, but lack of intrinsic activity prevents receptor activation. Blocks action of drugs (example Narcan). Therapeutic range – between minimum effective concentration and toxic concentration. Working effectivity with no toxicity or adverse effects. Wider therapeutic range is better! Easiest to control. Bioavailability – percentage of dose of drug that survives first pass through liver and reaches blood stream. Half life – time required for amount of drug to decline by 50%. Shorter half life admin more frequently. 4.5-5 half lives to get to steady state and to eliminate from body.
Pharmacokinetics – what body does to drug. Absorption, distribution, metabolism, elimination. (ADME) Parenteral (bypass first pass), then oral, then lungs, then skin, eye and ears for best absorption. Distribution affected by lipid/water solubility, PH, protein binding, size of molecule. Protein binding – unbound drug is free drug which is active. When 2 highly bound drugs are given it increases the level of one of the drugs, leading to toxicity. IE warfarin and phenytoin are both highly protein bound. Low plasma protein result in more free drug. May be in elderly, so decrease dose of medication. T3 and T4 both highly protein bound. 1% of drug is powerful. Distribution – BBB (only lipid soluble will pass) – these such as narcotics, only work because they do cross BBB. Some meds we do not want to pass. Placental barrier (many drugs can pass) so be careful with drugs in pregnancy. Metabolism – liver. Chemical change of a drug structure to enhance excretion, inactivate drug, increase therapeutic action, activate prodrug, increase or decrease toxicity. Substrate – agent that is metabolized by an enzyme into a metabolite and product and eventually excreted. *Inhibitors – compete with other drugs for a particular enzyme affecting the metabolism (decreases) of the substrate and decreases the excretion of the substrate and increasing the circulating drug. Need to decrease dose of substrate if start on an inhibitor. INH increases substrate. *Inducer – competes with other drugs for a particular enzyme affecting metabolism of the substrate (increases) decreasing the efficacy of the drug. Need to increase dose of substrate if start on an inducer. IND decreases substrate. Renal excretion – passive glomerular filtration, active tubular secretion, tubular reabsorption. Pharmacogenomics: 1 question Pharmacogenomics - the study of the influence of hereditary factors on the response of individual organism to drugs, and the study of variations of DNA and RNA characteristics as related to drug response. Pharmacogenetic tests mentioned on drug labels can be classified as “test required”, “test recommended”, and “information only”. Currently there are 4 drugs requiring to have pharmacogenetic testing performed before they are prescribed: Cetuximab, Trastuzumab, Maraviroc, and Dasatinib. No genetic testing is required by the FDA for the initiation of medications such as warfarin, carbamazepine, valproic avid and abacavir are currently in place, such tests are recommended prior to initial dosing. BBW initiated in December 2007- on carbamazepine label – testing recommended for HLA-B 1502 in patient with Asian ancestry due to high risk of developing SJS or toxic epidermal necrolysis (TEN). Drugs across the lifespan: 3 questions
Extended- Spectrum- Ticarcillin, Piperacillin Beta Lactamase Inhibitors- Clavulanic Acid, Tazobactam, Sulbactam Cephalasporins- binds to penicillin binding proteins (PBPs), disrupts cell wall synthesis, causing cell to lyse. First generation cephalosporins – gram positive cocci. Second and third generation more broad spectrum
- gram positive and gram negative. !st generation- prophylactic for surgery- never for active infection
- Cephazolin (do not give with alcohol)
- Cephalexin
- Cefadroxil 2 nd^ generation- works against URI- pneumonia from h. flu, klebsiella, pneumoniacocci, staphylococci
- Cefotetan (do not give with alcohol or drugs that promote bleeding)
- Cefprozil
- Cefoxitin
- Cefuroxime
- Cefactor 3 rd^ generation - preferred gram -, treats meningitis
- Ceftriaxone (do not give with drugs that promote bleeding, or calcium)
- Cefixime
- Cefditoren
- Cefotaxime 4 th^ generation- Used to treat HAP, pseudomonas aeruginosa
- Cefepime
- Ceftolozone 5 th^ generation- used to treat MRSA
- Ceftaroline *which can cause bleeding, which contraindicated with alcohol? If have an anaphylactic reaction, do not give PCNs or Cephalosporins. If not anaphylactic, can give cephalosporins. Vancomycin – active against MRSA, bacteriocidal, red man syndrome. Bacteriostatic inhibitors of protein synthesis: 1 question Tetracyclines - non-lethal inhibitors of protein synthesis- Broad Spectrum
Used to treat: Infectious Disease, Acne, Peptic Ulcer disease, Periodontal disease, RA, Mycoplasma Pneumoniae, helicobacter Pylori, lyme disease, anthrax, RMSF Do not give with calcium, iron, mag, aluminum, zinc, laxatives, antacids- decreases absorption- wait a couple of hours between Adverse reactions- GI irritation, staining of bones and teeth in children less than 8 years (only exception is with the infection of RMSF and doxycycline), superinfection, renal toxicity, photo sensitivity, caution of women in childbearing age. -Diarrhea may indicate potential life-threatening superinfection
- High dose may be associated with liver damage (tetracycline- Short acting, Doxycycline- long acting, Minocycline- long acting) Macrolides (Mycins)- Bacteriostatic or Bacteriocidal- inhibit protein synthesis, broad spectrum Used if: a patient is allergic to PCNs, whooping cough, active diptheria, coryne bacterium, diptheriae, chlamydia infections, m. pneumoniae, group A strep pyogens, may also be used as an alternative for PCN G if allergic. Drug interactions- CYP3A4, Cisapride, ergotamine or dihydroergotamine, terfenadine, astemizole, lovastatin, simvastatin Adverse Effects- GI, QT prolongation and sudden cardiac death, superinfection, thrombophlebitis, transient hearing loss Clindamycin- BBW- can cause C-diff. Example: Erythromycin, (Others: Clarithromycin, Azithromycin- prolong QT) Rifampin, Metronidazole, and Floroquinolones- inhibit synthesis of DNA or RNA by binding directly to nucleic acids or interacting with enzymes required for nucleic acid synthesis Aminoglycosides MOA – inhibit protein synthesis, can cause ototoxicity and nephrotoxicity. Gentamicin – continues to exert antibacterial effects even after plasma levels decrease below detectable levels – reaction will stay for a while. Erythromycin – can prolong QT interval, so pause simvastatin while taking erythromycin! Traveler’s diarrhea – ciprofloxacin for E.Coli (gram negative bacillus) Sulfonamides – most common SE is skin reactions. Allergy to sulfa – usually skin rx. Ciprofloxacin – tendonitis and tendon rupture may occur. Drugs used for UTIs: 2 question *Tx UTIs. 80% E.Coli, then Proteus and Klebsiella. Most UTI gram- d/t cause from intestinal bacteria. Prophylaxis -SMZ/TMP- 3x/wk for 6 months
Antifungals: 1 question Onychomychosis of toenail- Terbinafine x3 months ( check liver enzymes) Fluconazole – penetrates the BBB, not safe during pregnancy, eliminated renally. ***** Tx for fungal disease SEs of antifungal medications. Systemic mycoses: amphotericin B. SE infusion reaction, nephrotoxicity, hypokalemia, bone marrow suppression. Azoles are less toxic than amphotericin B and can be given orally. Itraconazole (Sporanox) can cause cardiosuppression (do not use in HF), liver damage, inhibitor of CYP450, GI. Many are inhibitors so increases effects of substrates. Teratogenicity. STD: 1 question Chlamydia trachomatis – azithromycin, doxycycline. Erythromycin in child <45kg. Neisseria gonorrhea – cephalosporins. Nongonococcal urethritis – azithromycin, doxycycline. Syphilis – penicillin G. Herpes Simplex – acyclovir, famciclovir, valacyclovir. Genital Herpes - Valacyclovir Herpes Labialis - Penciclovir HIV prophylaxis- Truvia Bacterial Vaginosis- Metronidazole applicator x5 days (AE- neurotoxicity, risk for Ca in mice and rats, unknown for humans, disulfiram reaction when given with alcohol for 3 days before or after) Faginal Candidas- Fluconazole x Trichamonas - Metronidazole x1, Tinedazole x *review treatment of STDs Non-HIV antivirals: 1 question
All antivirals either induce or inhibit CYP40 system, a lot of drug reactions. Flu meds have to be given w/in 48 hours of onset to be effective.
Cox 2- bad (increased risk for heart disease)- produced at sites of injury, and where mediates inflammation, and sensitizes to painful stimuli, and present in the brain so takes part in fever as well, in kidneys- supports renal function with renal vasodilation, and in colon- linked to colon cancer- blocking effects: suppression of inflammation, alleviation of pain, reduction of fever, protection again colorectal Ca. *NSAIDs – SE is GI ulcers/bleeds, prevent by giving PPIs (-prazole). Danger of PPIs include increased risk for fractures when given long term, increased risk for C.DIFF. ASA- nonselective inhibitor of cox- not recommended for primary prevention of MI and stroke, not worth the risk of GI bleed. Antipyretic, anti-inflammatory, decreases platelet aggregation, decreases risk for colon cancer, prevent Alzheimer’s. AE: GI (ulcers or GI bleed), can cause acute reversible impairment of renal function. Ductus arteriosus of fetus (do not give with pregnancy). Interaction with glucocorticoids, alcohol, warfarin, ibuprofen- reduces antiplatelet effects of asprin. ACEi, and ARBs- can increase risk for bleed 1 st^ generation NSAIDS - prevent Cox1 and Cox2- Used to alleviate mild-moderate pain, suppress fever, alleviate dysmenorrhea. Supress inflammation but pose risk of serious harm. can cause GI bleed and renal impairment Ibuprofen- tx RA and OA, don’t protect against MI and Stroke. SE- GI bleed. Check RFP, Check CBC for H&H, check occult blood, watch for tarry stools. 2 nd^ gen- only cox2 inhibitors- increase risk for heart problems. (Celebrex) Celebrex- decrease risk for GI bleed, but increased risk for MI and stroke. Drug interactions- can increase anticoag effects of warfarin, decrease diuretic effect of Lasix, can decrease the antihypertensive effect of ACEi, can increase levels of lithium, Celebrex levels can be increased with fluconazole. Acetaminophen- considered cox medication, but only has analgesic and antipyretic effects, doesn’t have any anti-inflammatory- works by inhibiting prostaglandin synthesis in the central nervous system AE: hepatotoxicity (alcoholics), if taking pain medication, some contain Tylenol- could overdose. Overdose: acetylcystine (mucomyst) Three main classes opioid receptors – mu, kappa, delta. Reverse effects caused by opioid agonists – naloxone (antagonist). Tolerance – increased doses needed to obtain same response. Opioid abuse – naltrexone. Naloxone for reversal.
Euphoria induced by morphine – well-being exaggerated
■ Preparations, dosage, and administration Given IV infusion with loading dose Second generation Cox 2 inhibitors – suppress inflammation, less risk gastric ulceration, increase risk heart disease!!! Give for acetaminophen overdose – acetylcysteine. Antiinflammatory Drugs and Glucocorticoids: 5 questions *SEs of glucocorticoids – major SEs- GI bleeds, increased blood sugar, negative effect on protein metabolism, decrease muscle mass, decrease protein matrix of bone causing osteoporosis and thinning of skin. central adiposity, moon face, adiposity on cervical of the spine, psychosis. Can lead to Cushing’s syndrome. If diabetic, and on glucocorticoids, sugars can go up- may need to adjust diabetic meds. *steroids used to: suppress immune response and inflammation, reducing swelling, redness, warmth, and pain. Used to treat RA, SLE, Inflammatory Bowel Disease, misc inflammatory disorders (bursitis, tendonitis, synovitis, OA, gouty arthritis, disorders of the eye. Also used to treat allergic conditions, asthma, and dermatologic disorders. Used for neoplasms, suppression of allograft rejection, and Given to mother in preterm labor in maturation of the lungs of infant. If on long term, want to get to minimum dose= 5mg/day, Be aware of adrenal suppression, need to taper if over 7 days, except for asthmatic or COPD patients, can go up to 10 days without tapering. *Do not give glucocorticoids with ASA – BBW increased risk for GI bleeds. Nonendocrine uses for glucocorticoids – RA, SLE, IBS, OA, bursitis, gout, disorders of eye. Monitor adrenal glands and endocrine system. Prolonged use of glucocorticoids – adrenal insufficiency. Principles of Neuropharmacology/PNS Pathophysiology: 2 question PNS: Parasympathetic functions – constrict pupils and bronchial smooth muscle, decreases HR, increases gastric secretions, empties bladder and bowel, digestion of food, excretion of waste, control vision, conservation of energy – muscarinic agonists, cholinergic agonists, acetylcholine function Sympathetic functions – mostly acts on vascular- maintain blood flow to brain, redistribution of blood, and compensation for loss of blood (fight or flight)- increase HR and BP, shunting blood to vital organs, dilating bronchi and pupils, mobilizing stored energy. Agonist and antagonist
Sympathomimetic drugs: HTN, angina Cholinergic : acetylcholine. Nicotinic and muscarinic receptors. Adrenergic : epi and nonepi. Alpha, beta, dopamine receptors. Alpha1: vasoconstriction, ejaculation, contraction of bladder and prostate Alpha2: nonclinical Beta1: heart, kidney, conduction of AV node Beta2: bronchodilation, relaxation of uterine smooth muscle, vasodilation, glycogenolysis Sympatholytics are antiadrenergic drugs Muscarinic agonists and antagonists: 4 questions Muscarinic agonists: mimic acetylcholine at muscarinic receptors. Bethanechol: constricts bronchi, increases GI and bladder. Use for urinary retention. Adverse effects diarrhea, increased salivation, asthma exacerbation. Muscarinic poisoning: give atropine.
- Muscarinic antagonists: atropine: use in preanesthesia, eye disorders, tx bradycardia in codes, intestinal hypermobility, can help in asthma or worsen asthma, muscarinic agonist poisoning. Cholinergic side effects: urinary retention, constipation, tachycardia. Do not use in elderly patients- they get really bad side effects! Dry eyes, mouth, constipation, urinary retention. OAB: oxybutynine, darifenacin, solifenacin, tolterodine, (these three can prolong QT interval, watch for drug interactions), fsotarodine, trospium. Scopolamine: motion sickness. Ipratropium bromide (Atrovent): mostly in COPD pts. Cholinesterase inhibitors: neostigmine and physostigmine. Use in MG to strengthen muscles. Physo for reversal of toxicity. Irreversible are pesticides. Adrenergic agonists and antagonists and indirect acting adrenergic agents: 3 questions Adrenergic agonists: Alpha1: vasoconstriction, mydriasis. Use in hemostasis, nasal decongestion, delay absorption of anesthetic (can cause necrosis in areas with poor circulation!!), mydriasis for surgery. Adverse: HTN, necrosis, bradycardia. Alpha2: causes reduction in outflow to heart, relieves severe pain. Beta1: use in HF (+ inotropic effect), shock, AV heart block, cardiac arrest.
Propranolol: adrenergic blocker Dobutamine: sympathomimetic Acetylcholine binds to muscarinic and nicotinic receptors. Atropine antidote for muscarinic agonist toxicity. Sympathomimetic is a adrenergic agonist. Muscarinic antagonist is anticholinergic. Cholinergic is muscarinic agonist and parasympathomimetic Toxicity of cholinergic: bradycardia, bronchoconstriction, pupil constriction, urinary urgency. Muscarinic antagonist toxicity opposite symptoms. Alpha1 agonists increase blood pressure. Alpha 1 antagonists decrease blood pressure. Beta 1 activation will cause bronchodilation, nonselective beta blocker causes bronchoconstriction Alpha 2 agonist (clonidine) decreases blood pressure Epinephrine in cardiac arrest, anaphylaxis, hypotension Parkinson’s: 1 question Parkinson’s: caused by low dopamine, high acetylcholine- characterized by dyskinesias(tremmors at rest, rigidity, postural instability, bradykinesia) and akinesia, motor symptoms (autonomic disturbances, depression, psychosis and dementia)- early symptoms include loss of smell, excessive salivation, clumsiness in hands, worstening handwriting, bothersome tremor, slower gait, and reduced voice volume. Treatment to cure does not exist, goal is to improve patients ability to carry out activities of daily life. Mild symptoms: MAO-B inhibitor- Selegiline or Rasagiline If respond to Levodopa, diagnosis is sure. Levodopa can also make dyskinesias worse, especially as it is given longer. Usually only good for five years, so wait to start on levodopa for as long as you can. Initially when mild start on dopamine agonist. Start to have off periods when levodopa levels drop, so combine with * MAOB inhibitor (selegilene, rosagiline) or COMT inhibitor (entacapone)- add for off periods of disease. Amantadine can also help with off periods. Shorten dosage interveral, give another drug listed above, give dopamine agonist. *Give levodopa with carbidopa, they work better together. Levodopa replaces depleted stores of dopamine Alzheimer’s Disease/Spasticity: 2 questions
Alzheimer’s: Progressive degeneration of the neurons- early in hippocampus- short term memory loss, and later in cerebral cortex difficulty in language begins such as speech perception, reasoning, and other high functions. no drugs cure it or reverse. Treatment goal slow memory loss and cognition and prolong independent function. Only keep from progressing as fast. Weight risk and benefit with family. Deonepezil, can add memantine. 4 drugs approved for treatment- Donepezil, Galantamine, Rivestigmone, and Memantine Muscle spasm: all meds can cause physical dependence. Can give benzodiazepines if also having insomnia, or give metaxalone or chlorzoxazone (no sedation). *treatment for alzheimer’s Epilepsy: 2 questions SZ meds: many side effects and drug interactions Carbamazepine: use in SZ, BPD. Can cause bone marrow suppression, aplastic anemia BBW. Ethosuximate: can cause blood dysgracias Lamotrigine: oral contraceptives lower effectiveness of lamotrigine, need increased dose. Lamotrigine for SZ: if starting on oral contraceptive, increase dose lamotrigine Gabapentin monitoring: record SZ frequency, duration, severity always *Phenytoin: side effect of gingival hyperplasia- give folic acid, good hygiene. Decreases effects of oral contraceptives, warfarin, glucocorticoids. Antipsychotic drugs/Schizophrenia: 1 question Psych drugs: Refer BPD, Schizo patients to psychiatrist. Antipsychotic drugs: first generation (haloperidol, fluphenazine) side effect of tardive dyskinesia, weight gain. Used for schizo, major depression, mania. Schizo: first generation APS, second generation, benzodiazepine, antidepressants *know difference in 1 st^ gen and 2 nd^ gen antipsychotic Tailor to person, if sexual dysfx from SSRI give bupropion. If fatigue during day, give bupropion. *Serotonin syndrome: altered mental status, myoclonus, hyperreflexia, fever, tremor, can cause death St.John’s wort: many drug interactions.
CNS stimulants: highly addictive. Decrease appetite, insomnia are side effects. Substance abuse: 1 question Alcohol abuse: overdose S/S are vomiting, respiratory depression, hypotension, aspiration, coma. Drugs to facilitate withdrawal: benzodiazepines and adjuncts. Drugs to maintain abstinence: disulfiram, naltrexone, acamprosate. Nicotine abuse: cardiac toxicity includes vasoconstriction, accelerated HR, increased force of contraction causing HTN, increase cardiac work. Can cause tremors and convulsions. Teratogen. Pharmaceutical nicotine is safer than tobacco smoke. Bupropion: decreases urge to smoke and decreases nicotine withdrawal symptoms of anxiety and irritability. Varenicline is an agonist at nicotinic receptors and is the most effective aid for smoking cessation. Diuretics/RAS:4 questions Loop diuretics: Lasix- acts on the ascending loop of henle to block reabsorbtion , bumatide. Block sodium and chloride reabsorption. Can cause hypoelectrolytes and increase lipids and increase glucose. Thiazide: *MOA: increase renal excretion of sodium, chloride, potassium, and water to decrease BP. HCTZ- works on the early segment distal convoluted tubule, metolazone (give with Lasix to diuresis much more, give prior to giving Lasix). Chlorthalidone – older diuretic that is coming back in use for HTN. Osmotic: mannitol- promotes diuresis by creating osmotic force within lumen of the nephron. To decrease ICP, given parenterally. Potassium sparing diuretics: spironolactone – blocks aldosterone in the distal nephron, causes retention of potassium and increased excretion of sodium. (decrease mortality in HF patients), triamterene, amiloride. ACE inhibitors (-pril): use in HTN, HF, MI, diabetic and nondiabetic nephropathy. Decrease mortality in HF and MI. Prevent MI and death in high risk patients. Give diabetics ACE inhibitors and ARBs to protect the kidneys. Can cause dry cough and angioedema (bradykinin increase). Can cause hyperkalemia, check potassium one week after starting. Can cause neutropenia. Help kidney until pt has CKD and creatinine is up to 2.5 then REMOVE medication. Can cause fetal injury, teratogenic. ARBs (-sartan): same uses, same side effects (except cough!). DRIs: aliskiren, tecturna. Same side effects. Renin inhibitors: inhibits angiotensinogen to angiotensin I ACE inhibit (-pril): constrict renal blood vessels, promote sodium and water excretion, keep potassium (can cause hyperkalemia) ARBs (-sartan): block angiotensin II, promote vasodilation
CCB, Vasodilators and other hypertensive drugs: 1 question CCBs (-dipine): decrease calcium in cell, promotes vasodilation. Two classes. Nifedipine one class (dihydropyridine), diltiazem and verapamil other group. Nifedipine used for HTN, migraine, angina. All cause constipation, edema of ankles and feet, gingival hyperplasia. Diltiazem and verapamil used for angina, HTN, cardiac dysrhythmias (Afib, Aflutter, PVT), migraine prevention. Same side effects. Can cause heart block. CCBs: same effect on heart as BB. Reduce force of contraction, slow HR, suppress conduction through AV node. Side effects of CCBs: constipation, leg edema, gingival hyperplasia CHF: 2 questions Starlings Law: force of ventricular contraction is proportional to muscle fiber length. In the failing heart, starling’s law breaks down. This is, the force of contraction no longer increases in proportion to increased ventricular filling. Digoxin and drug interactions- esp clonidine HF: aldosterone antagonist, ACE/ARBs, BBs all prolong life in HF. Not loop diuretics- treat symptoms only. Statins tx CAD. Hydralazine and isosorbite denodrite: reduce mortality in AA pts with HF. Class two for non-AA. When symptomatic and on other first line drugs. Then add these. ANRIs: ARB and neprolysin inhibitor. Salisartan/something. Prolongs life in HF pt. Only second line. New meds: ibrababrine, corlonele: EF of less than 35% when on maximum other first line drugs. Reduces hospitalization, not mortality. Inotropes: use in end stage HF. Increase risk for mortality! Given for symptoms. Digoxin: increase CO, blocks neurohormones. Narrow therapeutic index- high risk especially with elderly who may be noncompliant. Stages of HF A: no symptoms of HF, only risk factors. Tx is to reduce risk. Tx HTN, CAD. Lifestyle changes. B: known heart disease, high risk HF. No symptoms. Tx prevent development, start on ACE or ARB, add BB if any decrease in EF or if hx MI. C: symptoms of HF, structural HD. Tx improve fx of heart and quality of life, slow progression of disease, prolong life. Tx diuretic, ACE/ARB, aldosterone antagonist, digoxin, isosorbite, hydralazine (if maxed out on others and symptomatic or AA). Avoid antidysrhythmics (CCB) and NSAIDs, including ASA. Device therapy: pacemaker, biventricular cardioverter/defibrillator. D: marked S/S HF, advanced HD, repeated hospitalizations. Tx LVAD or transplant. Tx loop diuretics, inotropes (dopamine, dobutamine), remove BB (S/S worse).*
