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Therapeutic dosing and monitoring of warfarin (Coumadin) Treatment with warfarin should be initiated with standard doses of 5–10 mg. The initial adjustment of the prothrombin time takes about 1 week, which usually results in a maintenance dosage of 5–7 mg/d. The prothrombin time (PT) should be increased to a level representing a reduction of prothrombin activity to 25% of normal and maintained there for long-term therapy. When the activity is less than 20%, the warfarin dosage should be reduced or omitted until the activity rises above 20%. Inherited polymorphisms in 2CYP2C9 and VKORC1 have significant effects on warfarin dosing; however, algorithms incorporating genomic information to predict initial warfarin dosing were no better than standard clinical algorithms in two of three large randomized trials examining this issue. The recommended INR for prophylaxis and treatment of thrombotic disease is 2–3. Patients with some types of artificial heart valves (eg, tilting disk) or other medical conditions increasing thrombotic risk have a recommended range of 2.5–3.5. Types of anticoagulants- mechanisms of action and indications for use

• Vitamin K antagonists.
• Direct Oral Anticoagulants (DOACs)
• Low molecular weight heparins (LMWH) What is the mechanism of action for anticoagulants?
• Anticoagulants achieve their effect by suppressing the synthesis or function of various clotting factors that are normally present in the blood. Such drugs are often used to prevent the formation of blood clots (thrombi) in the veins or arteries or the enlargement of a clot that is circulating in the bloodstream. What are the indications for anticoagulants?
• Anticoagulation is an important component of the management strategy for several common medical conditions. It is indicated for the prevention of recurrent thrombosis in patients with venous thromboembolism (VTE) , which includes deep venous thrombosis and pulmonary embolism, and ischemic stroke. Understand Starling’s law The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction. This assumes that other factors remain constant. The Frank–Starling law of the heart (also known as Starling's law and the Frank–Starling mechanism) represents the relationship between stroke volume and end diastolic volume.[1]^ The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant. [1] (^) As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibers, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length,[2]^ without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality. Medications which increase and decrease preload and afterload For heart failure, ACE inhibitors and ARBs reduce workload on the myocardium by reducing both preload and afterload.

Preload: When some measure of left ventricular performance such as stroke volume or stroke work is plotted as a function of left ventricular filling pressure or end-diastolic fiber length, the resulting curve is termed the left ventricular function curve (Figure 13–4). The ascending limb (<15 mm Hg filling pressure) represents the classic Frank-Starling relation described in physiology texts. Beyond approximately 15 mm Hg, there is a plateau of performance. Preloads greater than 20–25 mm Hg result in pulmonary congestion. As noted above, preload is usually increased in heart failure because of increased blood volume and venous tone. Because the function curve of the failing heart is lower, the plateau is reached at much lower values of stroke work or output. Increased fiber length or filling pressure increases oxygen demand in the myocardium, as described in Chapter 12. Reduction of high filling pressure is the goal of salt restriction and diuretic therapy in heart failure. Venodilator drugs (eg, nitroglycerin) also reduce preload by redistributing blood away from the chest into peripheral veins. Afterload: Afterload is the resistance against which the heart must pump blood and is represented by aortic impedance and systemic vascular resistance. As noted in Figure 13–2, as cardiac output falls in chronic failure, a reflex increase in systemic vascular resistance occurs, mediated in part by increased sympathetic outflow and circulating catecholamines and in part by activation of the renin- angiotensin system. Endothelin, a potent vasoconstrictor peptide, is also involved. This sets the stage for the use of drugs that reduce arteriolar tone in heart failure.

~~ Antidote therapies for benzodiazepines Flumazenil is approved for use in reversing the CNS depressant effects of benzodiazepine overdose and to hasten recovery following use of these drugs in anesthetic and diagnostic procedures. Although the drug reverses the sedative effects of benzodiazepines, antagonism of benzodiazepine-induced respiratory depression is less predictable. When given intravenously, flumazenil acts rapidly but has a short half-life (0.7–1.3 hours) due to rapid hepatic clearance. Because all benzodiazepines have a longer duration of action than flumazenil, sedation commonly recurs, requiring repeated administration of the antagonist. Adverse effects of flumazenil include agitation, confusion, dizziness, and nausea. Flumazenil may cause a severe precipitated abstinence syndrome in patients who have developed physiologic benzodiazepine dependence. In patients who have ingested benzodiazepines with tricyclic antidepressants, seizures and cardiac arrhythmias may follow flumazenil administration. Antiarrhythmic drug classes-mechanisms of action, indications for use, side effects, and be able to identify by name **Antiarrhythmic drug classes:** - Class I - Sodium-channel blockers. - Class II - Beta-blockers. - Class III - Potassium-channel blockers. - Class IV - Calcium-channel blockers. - Miscellaneous - adenosine. - electrolyte supplement (magnesium and potassium salts) - digitalis compounds (cardiac glycosides) Diuretic (thiazide, loop, potassium-sparing) classes- mechanism of action, indications for use, side effects, contraindications, and be able to identify by name **THIAZIDES Subclass, Drug Mechanism of Action Effects Clinical Applications Pharmacokinetics, Toxicities, Interactions THIAZIDES** - Hydrochlorothia zi Inhibition of the Modest increase inHypertension, mild Oral • duration 8–12 h de (^) Na/Cl NaCl excretion • heart failure, • _Toxicity:_ Hypokalemic transporter in some K wasting • nephrolithiasis, metabolic alkalosis, the distal hypokalemic nephrogenic hyperuricemia, hyperglycemia, convoluted metabolic alkalosis • diabetes insipidus hyponatremia tubule decreased urine Ca - _Metolazone: Popular for use with loop agents for synergistic effects_ - _Chlorothiazide: Only parenteral thiazide available (IV)_ - _Chlorthalidone: Long half-life (50–60 h) due to binding to red blood cells_ **LOOP DIURETICS** **Subclass, Drug Mechanism of Action Effects Clinical Applications Pharmacokinetics, Toxicities, Interactions LOOP DIURETICS** - Furosem i Inhibition of the Marked increase in Pulmonary edema, Oral and parenteral preparations de Na/K/2Cl NaCl excretion, some peripheral edema, heart - duration of action 2–4 h transporter in the K wasting, failure, hypertension, - _Toxicity:_ Ototoxicity, ascending limb hypokalemic acute hypercalcemia, hypovolemia, K wasting, of Henle’s loop metabolic alkalosis, anion overdose hyperuricemia, hypomagnesemia increased urine Ca and Mg - _Bumetanide, torsemide: Sulfonamide loop agents like furosemide_ - _Ethacrynic acid: Not a sulfonamide but has typical loop activity and some uricosuric action_ **POTASSIUM-SPARING DIURETICS Subclass, Drug Mechanism of Action Effects Clinical Applications Pharmacokinetics, Toxicities, Interactions POTASSIUM-SPARING DIURETICS** - Spironolact o Pharmacologic Reduces Na retention and K Aldosteronism Slow onset and offset of ne antagonist of wasting in kidney • poorly from any cause • effect • duration 24–48 h aldosterone in understood antagonism of hypokalemia • _Toxicity:_ Hyperkalemia, collecting tubules aldosterone in heart and due to other gynecomastia - weak vessels diuretics • post– (spironolactone, antagonism of myocardial not eplerenone) • additive androgen infarction interaction with other K- receptors retaining drugs - Amiloride Blocks epithelial Reduces Na retention and K Hypokalemia Orally active • duration 24 h sodium channels wasting • from other • _Toxicity:_ Hyperkalemic in collecting increases lithium clearance diuretics • metabolic acidosis tubules reduces lithium- induced polyuria - Liddle syndrome - _Eplerenone, finerenone, esaxerenone: Like spironolactone, more selective for aldosterone receptor_ Medications indicated to prevent cerebral vasospasm **Nicardipine** has similar effects and is used by intravenous and intracerebral arterial infusion to prevent cerebral vasospasm associated with stroke. Verapamil, despite its lack of vasoselectivity, is also used—by the intra-arterial route—in stroke. Antipsychotic medications- mechanisms of action, indications for use, side effects, contraindications, and be able to identify by name Antihypertensive drug classes- mechanisms of action, indications for use, side effects, contraindications, and be able to identify by name Insulin classes, mechanisms of action, and be able to identify by name **Subclass, Drug Mechanism of Action Effects Clinical Applications Pharmacokinetics, Adverse Effects INSULINS** - Rapid-acting: Lispro, aspart, glulisine, inhaled regular, aspart + niacinamide - Short-acting: Regular - Intermediate- acting: NPH - Long-acting: Detemir, glargine, degludec Activate insulin receptor Reduce circulating glucose Type 1 and type 2 diabetes Parenteral [SubQ or IV (regular)] • duration varies (see text) • _Adverse effects:_ Hypoglycemia, weight gain, lipodystrophy (rare) - _Triamterene: Mechanism like amiloride, much less potent, more toxic_ ### SULFONYLUREAS - Glipizide Insulin secretagogues: Close Reduce circulating Type 2 Oral • duration 10–24 h • _Adverse_ - Glyburid e K+^ channels in beta cells • increase insulin release glucose in patients with functioning beta cells diabetes _effects:_^ Hypoglycemia,^ weight gain - Glimepi ri de - Gliclazid e^1 - _Tolazamide, tolbutamide, chlorpropamide, acetohexamide: Older sulfonylureas, lower potency, greater toxicity; rarely used_ **MEGLITINIDE ANALOGS;** D **-PHENYLANALINE DERIVATIVE** - Repaglinide, nateglini de - Mitiglinide^1 Insulin secretagogue: Similar to sulfonylureas with some overlap in binding sites In patients with functioning beta cells, reduce circulating glucose Type 2 diabete s Oral • very fast onset of action • duration 5–8 h, nateglinide • 4 h - _Adverse effects:_ Hypoglycemia **BIGUANIDES** i n - Metfor m Activates AMP kinase - reduces hepatic and renal gluconeogenesis Decrease s circulatin g glucose Type 2 diabete s Oral • maximal plasma concentration in 2–3 h • _Adverse effects:_ Gastrointestinal symptoms, lactic acidosis (rare) • cannot use if impaired renal/hepatic function • heart failure (HF), hypoxic/acidotic states, alcoholism ### ALPHA-GLUCOSIDASE INHIBITORS o l - Acarbose, miglit - Voglibose^1 Inhibit intestinal α- glucosidases Reduce conversion of starch and disaccharides to monosaccharides • reduce postprandial hyperglycemia Type 2 diabete s Oral • rapid onset • _Adverse_ _effects:_ Gastrointestinal symptoms • cannot use if impaired renal/hepatic function, intestinal disorders **THIAZOLIDINEDIONES** - Pioglitazone, rosiglitazo Regulate gene Reduce insulin resistance Type 2 Oral^ •^ long-acting^ (>24^ h)^ • _Adverse_ ne expression by diabetes _effects:_ Fluid retention, edema, binding to PPAR- γ anemia, weight gain, macular edema, and PPAR-α bone fractures, especially in women • cannot use if CHF, hepatic disease **GLUCAGON-LIKE POLYPEPTIDE-1 (GLP-1) RECEPTOR AGONISTS** e - Dulaglutide, exenatid Analogs of GLP-1: Bind to GLP- receptors Reduce post-meal glucose excursions: Increase glucose- mediated insulin release, lower glucagon levels, slow gastric emptying, decrease appetite Type 2 diabete s, liraglutid e only: obesit y Parenteral (SubC), (Oral: semaglutide only) • _Adverse effects:_ Nausea, headache, vomiting, anorexia, mild weight loss, pancreatitis, C-cell tumors in rodents (and exenatide ER), liraglutide, lixisenatide, semaglutide **DIPEPTIDYL PEPTIDASE-4 (DPP-4) INHIBITORS** - Alogliptin, linaglipti n, Block degradation of Reduces post-meal glucose excursions: Increases glucose- Type 2 diabete s Oral • half-life ~12 h • 24– h duration of action • _Adverse_ saxagliptin, sitagliptin, vildagliptin^1 GLP-1, raise circulating GLP- 1 levels mediated insulin release, lowers glucagon levels, slows gastric emptying, decreases appetite _effects:_ Rhinitis, upper respiratory infections, headaches, joint pain, pancreatitis, rare allergic reactions **SODIUM-GLUCOSE CO-TRANSPORTER 2 (SGLT2) INHIBITORS** - Canagliflozin, dapagliflozi n, Block renal glucose Increase glucosuria, lower plasma Type 2 Oral • half-life ~10–14 h • _Adverse effects:_ Genital and urinary tract infections, empagliflozin, ertugliflozin resorption glucose levels diabetes polyuria, pruritus, thirst, osmotic diuresis, constipation **ISLET AMYLOID POLYPEPETIDE ANALOG** - Pramlin ti de Analog of amylin: Binds to amylin receptors Reduces post-meal glucose excursions: Lowers glucagon levels, slows gastric emptying, decreases appetite Type 1 and type 2 diabete s Parenteral (SC) • rapid onset • half- life ~48 min • _Adverse effects:_ Nausea, anorexia, hypoglycemia, headache **BILE ACID SEQUESTRANT** - Colesevelam hydrochlori de Bile acid binder: Lowers glucose through unknown mechanisms Reduce s glucose levels Type 2 diabete s Oral • 24-h duration of action • _Adverse effects:_ Constipation, indigestion, flatulence **DOPAMINE AGONIST** e - Bromocript in D 2 receptor agonist: Reduces Type 2 Oral • 24-h action • _Adverse_ Lowers (^) glucose through unknown mechanism glucose levels diabete s _effects:_ Nausea, vomiting, dizziness, headache Antidiabetic agent classes- mechanisms of action, indications for use, side effects, contraindications, and be able to identify by name What are the classes of antidiabetic drugs? Currently, six classes of oral antidiabetic drugs (OADs) are available: **biguanides (e.g., metformin)** , sulfonylureas (e.g., glimepiride), meglitinides (e.g., repaglinide), thiazolidinediones (e.g., pioglitazone), dipeptidyl peptidase IV inhibitors (e.g., sitagliptin), and α- glucosidase inhibitors (e.g., acarbose). These agents work by **closing potassium channels on the surface of beta cells** , which causes an influx of calcium ions into the cells and a consequent outflow of insulin from cellular storage vesicles. The thiazolidinediones (e.g., pioglitazone, rosiglitazone) decrease insulin resistance. .Types of antibiotic classes- mechanisms of action, indications for use, side effects, contraindications, and be able to identify by name Best antibiotic choice to treat specific organism (i.e., aerobic gram-negative, etc.) Medications that effect contractility (inotropic), heart rate (chronotropic), and conductivity (dromotropic) **Inotropic** - Digitalis is the name of the genus of plants that provide most of the medically useful **cardiac glycosides,** eg, digoxin. The net result of the action of therapeutic concentrations of a cardiac glycoside in vitro is a distinctive increase in cardiac contractility. **Milrinone** is a bipyridine compound that inhibits phosphodiesterase isozyme 3 (PDE-3). It is active orally as well as parenterally but is available only in parenteral form. It has an elimination half-life of 3–6 hours, with 10–40% being excreted in the urine. An older congener, **inamrinone,** is no longer available in the USA. **_Dobutamine_** _- BETA-ADRENOCEPTOR AGONISTS - is the selective β 1 agonist that has been most widely used in patients with acute decompensated heart failure. Dopamine - BETA-ADRENOCEPTOR AGONISTS - has also been used in acute heart failure and may be particularly helpful if there is a need to raise blood pressure._ **Chronotropic** – **Dromotropic – Inotropic Chronotropic Dromotropic** Definition Affects the force of cardiac contraction Affects^ the^ heart^ rate Affects conduction velocity through the conducting tissues of the heart Positive Inotropic – strengthens the force of cardiac contraction Positive chronotropic - accelerates the heart rate Positive dromotropic – speeds up conduction Classification Negative Inotropic – weakens the force of cardiac contraction Negative chronotropic – slows down the heart rate Negative dromotropic - slow down conduction Examples Positive Inotropic – dopamine, adrenaline, etc. Positive chronotropic – Adernaline Positive dromotropic – phenytoin Negative Inotropic – labetalol and propanolol Negative chronotropic – digoxin Negative dromotropic - verapamil Origin of word From fiber or sinew)^ Greek^ in-,^ meaning time,^ From chrono-, meaning and tropos, "a turn" From the Greek word "dromos", meaning running, a course, a race Identify the difference between drug abuse, dependence, misuse, and tolerance Drug abuse - The use of illegal drugs or the use of prescription or over-the-counter drugs for purposes other than those for which they are meant to be used, or in excessive amounts. Drug abuse may lead to social, physical, emotional, and job-related problems. Drug dependence - Dependence on a drug means that your body has become so used to having that drug regularly that you need that particular drug to function normally, and if it were stopped you would feel unwell. Dependence, however, refers to the physical or psychological symptoms that occur that make someone feel like they must continue taking a substance. Misuse - the use of a substance for a purpose not consistent with legal or medical guidelines (WHO, 2006). It has a negative impact on health or functioning and may take the form of drug dependence, or be part of a wider spectrum of problematic or harmful behaviour (DH, 2006b). Drug tolerance - A condition that occurs when the body gets used to a medicine so that either more medicine is needed or different medicine is needed. Sedative-hypnotic medications-mechanisms of action, indications for use, side effects, contraindications, and be able to identify by name Medications used for alcohol abuse and withdrawal Three drugs—naltrexone, acamprosate, and disulfiram—have FDA approval for adjunctive treatment of alcohol dependence. **DRUGS USED IN CHRONIC ALCOHOLISM** - Naltrexon e Nonselective competitive antagonist of opioid receptors Reduced risk of relapse in individuals with alcoholism Available as an oral or long-acting parenteral formulation • _Toxicity:_ GI effects and liver toxicity; will precipitate a withdrawal reaction in individuals physically dependent on opioids and will prevent the analgesic effect of opioids - Acamprosat e Poorly understood NMDA receptor antagonist and Reduced risk of relapse in _Toxicity:_ GI effects and rash GABAA agonist effects individuals with alcoholism - Disulfiram Inhibits aldehyde dehydrogenase, resulting in aldehyde accumulation during ethanol ingestion Deterrent to drinking in individuals with alcohol dependence; rarely used _Toxicity:_ Little effect alone but severe and potentially dangerous flushing, headache, nausea, vomiting, and hypotension when combined with ethanol **DRUGS USED IN ACUTE ETHANOL WITHDRAWAL** - Benzodiazepines (eg, chlordiazepoxide, diazepam, loraze pam) BDZ receptor agonists that facilitate GABA-mediated activation of GABAA receptors Prevention and treatment of acute ethanol withdrawal syndrome See Chapter 22 - (^) Thiamine (vitamin B 1 ) (^) Essential vitamin required for Administered to Administered synthesis of the patients suspected of parenterally coenzyme thiamine pyrophosp having alcoholism • _Toxicity:_ None hate (those exhibiting • _Interactions:_ No acute alcohol intoxicat ne ion or alcohol withdrawal syndrome) to prevent Wernicke-Korsakoff syndrome Adverse effects associated with medications to treat psychosis Alternative uses of antiseizure medications Medications indicated for seizure disorders Medications contraindicated in pregnancy Local anesthetics-mechanism of action, indications for use, and contraindications Rapid sequence intubation (RSI) agent classes- mechanisms of action, indications for use, side effects, contraindications, and be able to identify by name Amnestic medications used in the treatment of chronic pain Ketamine??? **SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIs)** - Duloxetine - Venlafaxin e - Levomilnacipr an Moderatel y selective blockade of NET and SERT Acute increase in serotonergic and adrenergic synaptic activity • otherwise like SSRIs Major depression, chronic pain disorders • fibromyalgia, perimenopausal symptoms _Toxicity:_ Anticholinergic, sedation, hypertension (venlafaxine) - _Interactions:_ Some CYP2D inhibition (duloxetine, desvenlafaxine) • CYP3A interactions with levomilnacipran - _Desvenlafaxine: Desmethyl metabolite of venlafaxine, metabolism is by phase II rather than CYP phase I_ - _Milnacipran: Approved only for fibromyalgia in the USA; significantly more selective for NET than SERT; little effect on DAT_ **TRICYCLIC ANTIDEPRESSANTS (TCAs)** - Imipramin e - Many others Mixed and variable blockade of NET and SERT Like SNRIs plus significant blockade of autonomic nervous system and histamine receptors Major depression not responsive to other drugs • chronic pain disorders • incontinence • obsessive- compulsive disorder (clomipramine) Long half-lives • CYP substrates • active metabolites - _Toxicity:_ Anticholinergic, α- blocking effects, sedation, weight gain, arrhythmias, and seizures in overdose - _Interactions:_ CYP inducers and inhibitors Medications indicated for general anesthesia-know mechanisms of action, indications for use, side effects, contraindications, and be able to identify by name General anesthetics have been in clinical use for more than 170 years, but their **mechanism of action** remains unknown. The principal effect that is common to all anesthetic agents is suppression of the normal activity of the central nervous system (CNS). Initial research focused on identifying a single biologic site of action for these drugs. This “unitary theory” of anesthetic action has been supplanted by a more complex model of molecular targets located at multiple levels of the CNS. Ongoing research has focused on cellular, molecular, ## and network sites to understand the mechanism of general anesthesia. Intravenous nonopioid anesthetics play an essential role in the practice of modern anesthesia. They are **used** to facilitate rapid induction of anesthesia and have replaced inhalation as the preferred method of anesthesia induction in most settings except for pediatric anesthesia. Intravenous agents are also commonly used to provide sedation during monitored anesthesia care and for patients in ICU settings. With the introduction of propofol, intravenous anesthesia also became a good option for the maintenance of anesthesia. However, similar to the inhaled agents, the currently available intravenous anesthetics are not ideal anesthetic drugs in the sense of producing all and only the five desired effects (unconsciousness, amnesia, analgesia, inhibition of autonomic reflexes, and skeletal muscle relaxation). Therefore, balanced anesthesia employing multiple drugs (inhaled anesthetics, sedative-hypnotics, opioids, neuromuscular blocking drugs) is generally used to achieve the desired combination of effects while minimizing unwanted effects. **Side effects -** An interesting and desirable side effect of propofol is its antiemetic activity. Pain on injection is a common complaint and can be reduced by premedication with an opioid or coadministration with lidocaine. Dilution of propofol and the use of larger veins for injection can also reduce the incidence and severity of injection pain. ketamine is considered to be a cerebral vasodilator that _increases_ cerebral blood flow, as well as CMRO 2. For these reasons, ketamine has traditionally not been recommended for use in (^) patients with intracranial pathology, especially increased ICP. **Contraindication – Dexmedetomidine, Diazepam, Etomidate, Ketamine, Lorazepam, Methohexital, Midazolam, Propofol, Thiopental** Medications indicated for thyroid disorders- know mechanisms of action, indications for use, side effects, contraindications, monitoring, and be able to identify by name **Subclass, Drug Mechanism of Action and Effects Indications Pharmacokinetics, Toxicities, Interactions** **_THYROID PREPARATIONS_** - (^) Levothyroxine (T 4 ) - (^) Liothyronine (T 3 ) Activation of nuclear receptors results in gene expression with RNA formation and protein synthesis Hypothyroidism See Table 38–1 • maximum effect seen after 6–8 weeks of therapy - _Toxicity:_ See Table 38– for symptoms of thyroid excess **_ANTITHYROID AGENTS_** **THIOAMIDES** - Methimazole Inhibit thyroid peroxidase Hyperthyroidism Oral • duration of action: 24 h **Subclass, Drug Mechanism of Action and Effects Indications Pharmacokinetics, Toxicities, Interactions** - Propylthiouracil (PTU ) reactions • block iodine organification - inhibit peripheral deiodination of T 4 to T 3 (primarily PTU) (methimazole), 6–8 h (PTU) • delayed onset of action - _Toxicity:_ Nausea, gastrointestinal distress, rash, agranulocytosis, hepatitis (PTU black box), hypothyroidism, teratogenicity (methimazole > PTU) **IODIDES** - Lugol solution - Potassium iodide Inhibit organification and hormone release • reduce the size and vascularity of the gland Preparation for surgical thyroidectom y Oral • acute onset within 2– days - _Toxicity:_ Rare (see text) **BETA BLOCKERS** - Propranolol, other β blockers lacking partial agonist activity Inhibition of β adrenoreceptors • inhibit T 4 to T 3 conversion (only propranolol) Hyperthyroidism, especially thyroid storm • adjunct to control tachycardia, hypertension, and atrial fibrillation Onset within hours • duration of 4–6 h (oral propranolol) - _Toxicity:_ bronchospasm, AV blockade, hypotension, bradycardia **RADIOACTIVE IODINE 131 I (RAI)** Radiation destruction of thyroid parenchyma Hyperthyroidism • patients should be euthyroid or on β blockers before RAI • avoid in pregnancy Oral • half-life 5 days • onset in 6– 12 weeks • maximum effect in 3– months • _Toxicity:_ Sore throat, sialitis, hypothyroidism **Subclass, Drug Mechanism of Action and Effects Indications Pharmacokinetics, Toxicities, Interactions** and in nursing mothers **GENERIC NAME AVAILABLE AS THYROID AGENTS** Oral levothyroxine (T 4 ) Generic (also IV), Euthyrox, Levoxyl, Levo-T, Levolet*, Novothyrox, Synthroid (IV also), Tirosint, Tirosint-SOL, Unithroid Oral liothyronine (T 3 ) Generic, Cytomel, Triostat (IV) Oral Liotrix (a 4:1 ratio of T 4 :T 3 ) Thyrolar Oral Thyroid desiccated (USP) Generic, Armour, Nature-Throid, Westhroid **ANTITHYROID AGENTS** Radioactive iodine (^131 I) sodium Iodotope, Sodium Iodide I 131 Therapeutic Oral methimazole Generic, Tapazole Potassium iodide Oral solution (SSKI) ThyroShield Oral solution (Lugol solution) Lugol solution **GENERIC NAME AVAILABLE AS** Oral potassium iodide tablets IOSAT, Thyro-Block, Thyro-Safe Oral propylthiouracil [PTU] Generic **DIAGNOSTIC AGENT** Thyrotropin; recombinant human TSH Thyrogen Medications indicated for shock IVF – 30ml/kg/hr Broad spectrum ATB – Zoysn and Vancomycin Vasopressin Alternative indication for glucagon use besides hypoglycemia Intravenous glucagon is commonly used in the endoscopic retrograde cholangiopancreatography procedure to facilitate the relaxation of the sphincter of Oddi. Glucagon is sometimes used in the treatment of beta blocker overdose because of the drug’s ability to increase cAMP production in the heart independent of β-receptor function. Glucagon should not be given to patients with pheochromocytoma in whom it can cause release of catecholamines and increase blood pressure; it also should not be given to patients with insulinoma where it can cause rebound hypoglycemia. Medications indicated for myocardial infarction **Aspirin.** The 911 operator might tell you to take aspirin, or emergency medical personnel might give you aspirin immediately. Aspirin reduces blood clotting, thus helping maintain blood flow through a narrowed artery. **Thrombolytics.** These drugs, also called clotbusters, help dissolve a blood clot that's blocking blood flow to your heart. The earlier you receive a thrombolytic drug after a heart attack, the greater the chance you'll survive and have less heart damage. **Antiplatelet agents.** Emergency room doctors may give you other drugs known as platelet aggregation inhibitors to help prevent new clots and keep existing clots from getting larger. **Other blood-thinning medications.** You'll likely be given other medications, such as heparin, to make your blood less "sticky" and less likely to form clots. Heparin is given by IV or by an injection under your skin. **Pain relievers.** You might be given a pain reliever, such as morphine. **Nitroglycerin.** This medication, used to treat chest pain (angina), can help improve blood flow to the heart by widening (dilating) the blood vessels. **Beta blockers.** These medications help relax your heart muscle, slow your heartbeat and decrease blood pressure, making your heart's job easier. Beta blockers can limit the amount of heart muscle damage and prevent future heart attacks. **ACE inhibitors.** These drugs lower blood pressure and reduce stress on the heart. **Statins.** These drugs help control your blood cholesterol. Insulin infusion In the United States, Medtronic MiniMed, Insulet, and Tandem make battery-operated pumps for continuous subcutaneous insulin infusion (CSII). The externally worn pumps are about the size of a pager and they deliver short- acting insulin throughout the day and night. The catheter connecting the insulin reservoir to the subcutaneous cannula can be disconnected, allowing the patient to remove the pump temporarily (eg, for bathing). Omnipod (Insulet Corporation) is a disposable waterproof electronic patch pump in which the insulin reservoir and infusion set are integrated into one unit (pod), so there is no catheter. The pod, placed on the skin, delivers subcutaneous basal and bolus insulin based on wirelessly transmitted instructions from a personal digital assistant. A major advantage of an insulin pump is that it allows for establishment of a basal profile tailored to the patient allowing for better overnight, between-meals glucose control, and management of glycemic excursions that occur with exercise. Software assists the patient in calculating boluses based on glucose reading and carbohydrates to be consumed. They keep track of the time elapsed since the last insulin bolus and reduce the risk of overcorrecting and subsequent hypoglycemia. CSII therapy is appropriate for patients with type 1 diabetes who are motivated, mechanically inclined, educated about diabetes (diet, insulin action, treatment of hypoglycemia and hyperglycemia), and willing to monitor their blood glucose four to six times a day. Known complications of CSII include ketoacidosis, which can occur when insulin delivery is interrupted, and skin infections. Another disadvantage is its cost and the additional time needed by the clinician and staff to initiate therapy. Almost all patients use rapidly acting insulin analogs in their pumps. V-Go (Valeritas) is a mechanical patch pump designed specifically for people with type 2 diabetes who use a basal/bolus insulin regimen. The device is preset to deliver one of three fixed and flat basal rates (20, 30, or 40 units) for 24 hours (at which point it must be replaced) and there is a button that delivers two units per press to help cover meals.