Cholesterol (166 – 170) Normal Findings: Adult: <200 mg/dL Child: 120-200 mg/dL Newborn: 53-135 mg/dL -Needed for production of steroids, sex hormones, bile acids, and cellular membranes -The main lipid associated with arteriosclerotic disease -Metabolized by the liver -75% bound inside LDL and 25% is in HDL - Main component of LDL (minimal in HDL and VLDL) - Testing is typically part of a lipid profile (by itself is not an accurate predictor of heart disease) - Individual cholesterol levels can vary daily by 15% -Positional changes affect levels (15% decrease seen in lateral recumbent position, often seen in hospitalized patients) -Repeat tests should be done for abnormal values and an average will be established -Used to predict risk of CHD within the Framingham Coronary Prediction algorithm (determines overall risk of ischemic event)
Creatine kinase, pp. 199-202 Adult/elderly (values higher after exercise): 55-170 units/L (males); 30-135 units/L (females) Newborn: 68-580 units/L Isoenzymes: CK-MM: 100%, CK-MB: 0%, CK-BB: 0% This test is used to support the diagnosis of myocardial muscle injury…it can also be used to indicate neurologic or skeletal muscle diseases. CK is predominantly found in heart muscle, skeletal muscle, and brain…CK levels elevate when muscles or nerve cells are damaged: Rise within 6 hrs. after damage Levels peak at 18 hours (if damage is not persistent) Return to normal in 2-3 days Interfering Factors: IM injections, strenuous exercise, early pregnancy, muscle mass Drugs that cause increased CK levels: alcohol, amphotericin B, ampicillin, anesthetics, anticoagulants, aspirin, colchicine, dexamethasone, lithium, lidocaine, morphine, statins.
Creatine kinase, pp. 199-202 Electrophoresis is used to detect the 3 CK isoenzymes: CK-BB (CK1): Found predominantly in the brain and lung CK-MB (CK2): specific for myocardial cells. Rise 3-6 hrs. post-infarction, levels peak at 12-24hrs., return to normal in 12-48 hrs. Do not usually rise with transient chest pain cause by angina, PE, or CHF. Will see a rise in patients with shock, malignant hyperthermia, myopathies, or myocarditis. CK-MB levels used to determine the appropriateness of thrombolytic therapy (MI) CK-MM (CK3): makes up almost all of the circulatory total CK enzymes in healthy people. Increases in CK-MM suggest skeletal muscle damage. *See Chart p. 201—levels of Troponin, CK-MB, and Myoglobin post-MI*
Creatine kinase, pp. 199-202 CK is the main cardiac enzyme used to detect MI…others used include: Lactic dehydrogenase (LDH), and aspartate amino transferase (AST) *See Chart p. 201—levels of Troponin, CK-MB, and Myoglobin post-MI* AVOID IM injections in patients with cardiac disease (they cause elevated CK levels) Interfering Factors: IM injections, strenuous exercise, early pregnancy, muscle mass Drugs that cause increased CK levels: alcohol, amphotericin B, ampicillin, anesthetics, anticoagulants, aspirin, colchicine, dexamethasone, lithium, lidocaine, morphine, statins.
D-dimer, pp. 215-216 Normal Findings: <0.4 mcg/mL ELISA and ELFA test, (Enzyme-linked fluorescent immunoassay is faster and more reliable) D-dimer is used to identify intravascular clotting by assessing both thrombin and plasmin activity. (Disseminated intravascular coagulation). D-dimer is a fibrin degradation fragment that is made through lysis of cross-linked (d-dimerized) fibrin. The D-dimer assay provides a highly specific measurement of the amount of fibrin degradation that occurs…normal plasma does not have detectable amounts of d-dimer fragments.
D-dimer, pp. 215-216 D-dimer may be used in combination with the Fibrin Degradation Products assay for high sensitivity and specificity of disseminated intravascular coagulation (DIC). Levels of D-dimer will increase during thrombolytic therapy of fibrin clots and can be used to determine the duration of anticoagulant therapy in patients with DVT. High D-dimer levels are associated with PE, DVT, sickle cell anemia, and thrombosis of malignancy.
Factor V-Leiden, pp. 244-245 Normal: Negative FVL The test is used to diagnose factor V-Leiden thrombophilia Factor V is an important factor in reaction 4 (common pathway) of normal hemostasis. The term “factor V-Leiden” refers to an abnormal form of factor V in which there is a specific glutamine to arginine substitution at nucleotide 1619 in the gene of factor V. FVL is inactivated 10 times slower than regular factor V due to a mutation in the site where protein C normally binds to deactivate and breakdown factor V. Result: increased thombin generation and a mild hypercoagulable state. FVL is the most common hereditary blood coagulation disorder in the US.(5% of Causcasian, 1.2% of Black Americans). Only about 10% of patients with FVL experience a thrombotic event. Testing for FVL is sometimes preceded by a screening coagulation test called the activated protein C (APC) resistance test, used to identify the resistance of factor V to activated protein C.
Factor V-Leiden, pp. 244-245 Individuals who are candidates for FVL testing include those who have: Experienced a thrombotic event without any predisposing factors A strong family history of thrombotic events Experienced a thrombotic event before 30 years of age Experienced DVT during pregnancy or while on birth control pills Had venous thrombosis at usual sites Experienced an arterial clot
Lipoproteins, pp. 356-361 Lipoproteins Should be collected after a 12-14 hour fast. Measured and classified by their density. Interfering Factors: smoking and alcohol ingestion decrease HDL, binge eating alter lipoproteins, HDL values are age and sex- dependent, HDL values (similar to cholesterol) decrease for 3 months post-MI, elevated HDL in hypothyroid, high triglyceride levels make LDL calculations inaccurate. General Categories: Chylomicrons-carry TAGs from the intestine à liver, skeletal muscle, adipose tissue VLDLs- carry newly synthesized TAGs from liver adipose tissue. VLDLs are the predominant carriers of triglycerides. To a lesser degree, VLDLs are also associated with increased risk of CAD because they can be converted to LDL by lipoprotein lipase in skeletal muscle. IDLs- intermediates between VLDLs and LDLs, not detectable in blood LDLs- carry cholesterol from liver cells of the body. “bad cholesterol” HDLs- collects cholesterol from the body’s tissues and brings it back to the liver, protective effect against heart disease. Out of the 5 subclasses of HDL, only 2b is cardioprotective
Lipoproteins, pp. 356-361 Risk for Coronary Heart Disease Based on Ratio of Cholesterol to HDL High levels of LDLs are atherogenic…target levels vary according to risk profile of patient (see p. 359). LDL= total cholesterol- ((TGs/5)- HDL). SGGE divides LDL into 7 classes based on particle size. IIIa and IIIb are the most commonly elevated forms, IVa and IVb are associated with aggressive arterial plaques (nearly all patients with IVa and IVb levels greater than 10% of total LDL have a cardiovascular events within months!) LDL patterns have been identified to assess risk of CAD: (LDLs can be lowered with diet, exercise, and statins) LDL Pattern A: mostly large LDL particles, no increased risk for coronary artery disease (CAD) LDL Pattern B: mostly small LDL particles associated with increased risk for CAD Intermediate pattern: small and large LDL molecules, carries an intermediate risk.
Lipoproteins (356 – 360) Lipoproteins- accurate predictor of heart disease -Proteins in the blood whose main purpose is to transport cholesterol, triglycerides, and other insoluble fats -Used as markers to indicate the levels of lipids Risk for Heart DiseaseMaleFemale High60 mg/dL70 mg/dL Moderate45 mg/dL55 mg/dL Low25 mg/dL35 mg/dL Risk of CHDMaleFemale ½ the average3.43.3 Average (3:1)5.04.4 2x average (moderate)10.07.0 3x average (high)24.011.0
Prothrombin time (448-451) Adequacy of extrinsic system and common pathway Activation of factor X in the presence of factor V and phospholipid and calcium Stimulates platelet aggregation and converts fibrinogen to fibrin in clot stabilization Tests: Factors I (fibrinogen), II (prothrombin), V, VII, and X
PT Hepatocellular liver disease (cirrhosis, hepatitis, neoplastic invasive processes) Factors I, II, V, VII, IX, X Obstructive biliary disease bile necessary for fat absorption decreases A,D,E and K are all fat soluble. II, VII, IX, X all dependent on vitamin K, differentiate from liver disease because it responds to vitamin K Coumarin ingestion (warfarin) interfere with vitamin K associated factors; effects long lasting, can be fixed by vitamin K. Monitors warfarin tx.
PT and INR Evaluate extrinsic and common pathway Fibrinogen, prothrombin, V, VII, X Decreased levels: hepatocellular disease affect factors I, II, V, VII, IX, and X Obstructive biliary disease causes fat malabsorption A, D, E, and K affected Coumarin (warfarin) ingestion INR is a stardardized ratio to correct for laboratory, environmental variations in clotting time, unrelated to sample quality. Warfarin interferes with vitamin K may be enhanced by aspirin, quinidine, sulfa, and indomethacin Barbituates, chloral hydrate and oral contraceptives cause increased coumarin drug binding decreasing the effects Alcohol can prolong Diet high in fat or leafy vegetables may shorten OT Diarrhea or malabsorption can prolong
Partial thromboplastin time (PTT) Assess the intrinsic system and common pathway of clot formation and to monitor heparin therapy First phase of reactions is intrinsic system: factor XII forms complex on subendothelial collagen Extrinsic factors include thromboplastin Prothrombin becomes thrombin converts fibrinogen to fibrin Plasmin degenerates Evaluates fibrinogen II (prothrombin, V, VIII, IX, X, XI, and XII If any of these exist in inadequate quantities then PTT is prolonged
PTT Vitamin K deficiency can prolong PTT II, IX, and X are dependent Coag factors are made in the liver so hepatocellualr disease will prolong Heparin inactivates prothrombin (II) not thromoplastin Monitor heparin whose effects are short-lived if too much is given protamine sulfate can reverse
PTT Assess the intrinsic and common pathway of coag Evaluates fibrinogen, prothrombin, V, VIII, IX, X, XI, and XII Hepatocellular disease prolongs PTT and obstruction which precludes GI absorption of fat soluble vitamins prolongs time Heparin prolongs PTT so it is used for therapy monitoring Antihistamines, ascorbic acid, chlorpromazine, heparin and salicylates prolong PTT Early DIC and extensive cancer causes decreased levels
Triglycerides (521 – 522) Adult: Male 40-160 mg/dL Female 35-135 mg/dL Critical: >400 mg/dL -Produced in the liver using fatty acids and glycerol -Transported by VLDL and LDL -When levels are high, triglycerides are deposited in fatty tissues -Constitute most of the fat of the body -Measured as part of a lipid profile Indications: TGs identify the risk of CHD. This test, along with Lipoproteins and Cholesterol create the lipid profile for the patient. This test may also be used to detect fat metabolism disorders. Test explanation: TGs are circulating fats in the blood that are attached to VLDL or LDL, act as a storage source for energy. When TG levels in the blood are high, TGs are deposited in the fatty tissues.
Triglycerides (521 – 522) Increased levels: ingestion of fatty meals, alcohol, pregnancy, glycogen storage disease, apoprotein CII deficiency, hyperlipidemias, hypothyroidism, high carb diet, nephrotic syndrome, chronic renal failure Drugs that may increase levels: cholestyramine, estrogens, and oral contraceptives Decreased levels: malabsorption, malnutrition, abetalipoproteinemia, hyperthyroidism Drugs that may decrease levels: ascorbic acid, asparaginase, clofibrate, colestipol, fibrates, and statins Interfering factors: ingestion of fatty meals can cause elevated TG levels ingesting alcohol causes increased VLDL levels, which increases TG Pregnancy causes increased levels Drugs causing increased TG levels: estrogen, oral contraceptives, cholestyramine Drugs causing decreased TG levels: ascorbic acid, asparaginase, clofibrate, fibrates, statins.
Troponins, pp. 530-532 Normal Findings: Cardiac Troponin T: <0.2 ng/mL Cardiac Troponin I: <0.03 ng/mL This test is performed on patients experiencing chest pain to determine if the pain is caused by cardiac ischemia. It is a specific indicator of cardiac muscle injury. Cardiac troponins are biochemical markers for cardiac disease and can actually be used in patients with unstable angina to determine the likelihood of a cardiac event. Their sensitivity and specificity are similar to that of CK-MB (but troponins are even more sensitive)—Cardiac troponin levels become elevated as early as 3 hrs. post-myocardial injury and stay elevated for 7-14 days (7-10 days for troponin I, 10-14 days for troponin T) ELISA method w/monoclonal Abs—fast, can be done bedside.
Troponins, pp. 530-532 If reinfarction is suspected, troponins may not be as helpful because levels could still be elevated from the first ischemic event. [Stay elevated longer than CK-MB] Cardiac troponins are useful for the following situations: Evaluation of patient with unstable angina Detection of reperfusion associated with coronary recanalization Estimation of MI size Detection of perioperative MI Evaluation of severity of PE Congestive heart failure Interfering factors: Troponin T levels are falsely elevated in dialysis patient.
Oximetry (1173-1174) >95% is normal Monitors arterial oxygen saturation in patients at risk for hypoxemia. Surgery, cardiac stress testing, mechanical ventilation, heavy sedation, lung function testing or trauma Non-invasive measures how many hemoglobin have oxygen attached to them Fetal oxygen saturation monitoring: if heart is in distress but saturation is fine you can avoid c-section, placed on cheek between 30 and 70%
Radiology 101:Pages 16-23 Reading frontal chest x-ray Designed to look at lungs, not trauma to the ribs etc. R marker should be on your left side Glance over the image for any obvious abnormality always look at your four corners Anterior posterior and posteroanterior Start at top and make sure trachea is midline Move to heart, transverse diameter of cardiac silhouette should not be more than 50% transverse diameter of thoracic cage Greater the distance between and object and film, the greater the magnification
Radiology 101:Pages 16-23 Frontal chest X-ray (continued) Right heart convex, left cardiac border at the top should be concave Left ventricle makes up left heart SVC makes straight right border In enlargement left superior border becomes convex Left enlargement cardiac apex moves down and out Right enlarges right border is more protuberant Left and right pulmonary arteries form hilar shadows, left should be more cephalad Aorta forms knob Aortopulmonary window between knob and pulmonary artery shadow; should be concave or suspect mass or adenopathy
Radiology 101:Pages 16-23 Frontal chest X-ray (continued) Mediastinum shadow is caused by great vessels and vascular pedicle Pedicle extends from thoracic inlet to base of heart; right border is SVC left is aortic knob Divide lungs into horizontal thirds Domed diaphragm with right side higher than left Lateral costophrenic angles should be sharp and acute Look at lower cervical spine and ribs Ribs we see are posterior arcs anterior ribs are angled downward
Radiology 101:Pages 16-23 Lateral radiograph Right ventricle is anterior border Left ventricle is inferior-posterior cardiac border Left atrium forms superior-posterior cardiac border IVC can be seen as it enters from abdomen If left ventricle is 2 cm or more posterior to IVC then it is enlarged Evaluating hila left is posterior to line drawn down from tracheal air column and one third the size of the right Silhouette sign when two objects of similar density are in direct juxtaposition interface or borders are lost
DrugUsesSide effectsContraindicationsTherapeutic considerations Aspirin (ASA) MOA-Inhibits synthesis of prostaglandin by cyclooxygenase; inhibits platelets aggregation; has antipyretic (anti- fever) and analgesic activity. Metabolized by the liver. Prophylaxis against transient ischemic attack, MI, acute coronary syndrome, prevent reocclusion, arthritis, mild pain or fever GI bleeding, acute renal insufficiency, thrombocytopenia, Reye dz, asthma, tinnitus, dyspepsia, occult bleeding, prolonged bleeding, rash NSAID induced sensitivity, chickenpox of flu like symptoms, G6PD deficiency Bleeding like hemophilia, von Willebrand thrombocytopenia Inhibit both Cox 1 and 2 Use cautiously with GI bleeds impaired renal function, vit K deficiency, purpura, hepatic impairment
DrugUsesSide effectsContraindicationsTherapeutic considerations Atenolol MOA: Blocks response to beta- adrenergic stimulation; cardio selective for beta 1 receptors at low doses with little to NO effect on beta two (safer in asthmatics) Limited metabolization in liver. Beta-blocker (B1 specific) HTN, angina, thyroid storm, HFAV block, bradyarrythmia, sedation, decreased libido, mask hypoglycemia, depression, dyspnea, wheezing Bronchial asthma, COPD, cardiogenic shock, decompensated heart failure, 2 nd and 3 rd degree AV block, severe sinus bradycardia Beta one selective adrenergic antagonists
DrugUsesSide effectsContraindicationsTherapeutic considerations Atorvastatin Pg 330 MOA: HMG-COA reductase inhibitor, inhibits rate-limiting step in cholesterol biosynthesis by competitively inhibiting HMG- COA reductase Class: Inhibitor of cholesterol synthesis (Statin) Mech: inhibits HMG-CoA reductase Indications: Hypercholesterolemia Familial hypercholesterolemia Coronary atherosclerosis Prophylaxis for coronary aterosclerosis Myopathy-increased risk Rhabdomyolysis Hepatotoxicity Abdominal pain (constipation, diarrhea, nausea) Headache Active liver disease Pregnancy and lactation Up to 60% dec. in LDL 10% HDL increase 40% Triglyceride dec. Drug of choice for lowering LDL, one of the most potent Metabolism by P450 3A4 Combo with bile acid sequestrant yields lower LDL Co-admin with Niacin-> inc. risk of myopathy Co-admin with gemfibrozil can induce rhabdomyolysis
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Atropine MOA: Antimuscarinic; inhibits action of acetylcholine at parasympathetic sites in smooth muscle, CNS, and secretory glands. Increases cardiac output and dries secretions. Metabolized: Liver Anticholinergic Agent, Anticholinesterase overdose, bradycardia, excessive salivation and mucus production during surgery “No See, No Pee, No Spit, No Sh*t” Blurry vision, xerostomia (dry mouth), constipation, urinary hesitancy, increased IOP, loss of taste, hypotension, confusion, coma, ataxia, insomnia, headache, Actions of PNS inhibited Narrow Angle glaucomamarginal nicotinic effect; more effective at reversal of exogenous rather than endogenous cholinergic activity
DrugUsesSide effectsContraindicationsTherapeutic considerations Clopidogrel (Plavix) MOA: Inhibitor of adenosine (ADP)- induced pathway for platelet aggregation. Metabolized in liver by CYP450 enzymes. ACS, recent MI, stroke, peripheral artery disease, CAD, cardioembolic stroke 1-10% URI, chest pain, headache, flu like syndrome, arthralgias, pain, dizziness, diarrhea, depression, rhinitis, rash, UTI <1% neutropenia, acute liver failure, TTP, hypotension, hepatitis, myalgia, eczema Active bleeding disorderNeeds loading dose. Less side effects tha ticlopidne
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Eptifibatide (integrelin)- antiplatelet agent MOA: blocks binding of fibrinogen & von willebrand factor of glycoprotein IIB/IIIA receptor on platelet surface. Acute coronary syndrome, percutaneous coronary intervention Major bleeding, intracerebral hemorrhage, hypotension, bleeding History of bleeding, recent major surgery, recent stroke, intracranial hemorrhage, uncontrolled hypertension Don’t give with second, second anti GIIb-IIIa agent, minimize arterial and venous puncture, synthetic peptide as parenteral
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Heparin- Anticoagulant MOA: Low dose: inactivates factor Xa and inhibits conversion of prothrombin to thrombin High dose: inactivates factor IX, X, XI, & XII and thrombin and inhibits conversion of fibrinogen to fibrin Also inhibits activation of factor VIII Prevent embolism, thrombosis, prevent systemic embolism with MI, unstable angina, open heart surgery, DIC, maintain patency IV cath Hemorrhage, heparin induced thrombocytopenia, hypersensitivity, prolonged clotting time, mucosal ulceration, hematoma Heparin induced thrombocytopenia, active major bleeding, bleeding tendencies, open ulcerative wounds, conditions that increase capillary permeability, severe HTN, bacterial endocarditis Unfractionated causes thrombocytopenia more than LMW, antihistamines, cardiac glycosides, nicotine and tetracycline affect ability Cephalosporins, penicillins, oral anticoagulants, platelet inhibitors may increase affects Don’t use ginger, garlic, ginkgo
DrugClinical appAdverse effectsContraindicationsTherapeutic considerations Isosorbide mononitrate Class: Nitrate MOA- Donate NO, which activates guanylyl cyclase and increase dephosphorylation of myosin light chain in vascular smooth muscle, causing vasodilation. Prophylaxis of angina, treatment of chronic ischemic heart disease Refractory hypotension, palpitations, tachycardia, syncope, flushing, headache Severe hypotension, shock or acute MI with low left ventricular filling pressure, increased intracranial pressure, angle closure glaucoma, co administration of phosphodiesterase inhibitor type V [These are viagra and it’s relatives ] venous dilation greater than arterial, can lead to tolerance
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Metoprolol (Lopressor) – Beta Blockers, Beta 1 selective MOA: Blocks response to beta-adrenergic stimulation; cardio selective for beta 1 receptors at low doses with little to NO effect on beta two (safer in asthmatics) [B2 are in bronchiole smooth muscle, blocking causes bronchoconstriction] Metabolized in liver by CYP2D6. AMI, CHF, HTN, Angina, Hyperthyroidism, Acute Tachy, Side Effects: 1-10% Dizziness, headache, tiredness, depression, diarrhea, pruritus, dyspepsia, heart failure, wheezing, nausea Asthma or COPD, cardiogenic shock, Decompensated cardiac failure, 2nd & 3rd degree AV Beta 1 selective adrenergic antagonists
DrugClinical appAdverse effectsContraindicationsTherapeutic considerations Nitroglycerin (Nitrostat) – Nitrate Nitrate enters vascular smooth muscle and converted to Nitric Oxide (NO) leading to activation of cGMP and vasodilation, thus also reducing preload. Short acting, short term treatment of acute anginal attacks Refractory hypotension, palpitations, tachycardia, syncope, flushing, headache Severe hypotension, shock or acute MI with low left ventricular filling pressure, increased intracranial pressure, angle closure glaucoma, co administration of phosphodiesterase inhibitor type V, transdermal contraindicated in patients allergic to skin tape, IV contraindicated in tamponade, restrictive cardiomyopathy, constrictive pericarditis Preferred due to longer half life, better absorption, nonsusceptibility to extensive first pass, less rebound angina, greater efficacy, venous dilation greater than arterial, can lead to tolerance shorter half life than isosorbide mononitrate
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Ramipril (Altace) – ACE Inhibitor “End in pril” MOA: Competitively inhibits angiotensin- converting enzymes, resulting in decreased plasma angiotensin II concentrations; BP may be reduced in part through decreased vasoconstriction increased renin, activity, and decreased aldosterone secretion; increases renal blood flow Hypertension, heart failure, diabetic nephropathy, myocardial infarction > 10% Cough (if cough switch to an ARB), hypotension, 1-10% headache, angina, dizziness, N/V, postural hypotension, syncope, vertigo, <1% angioedema Hx of angioedema, bilateral renal artery stenosis [They depend on RAA axis for renal perfusion], renal failure, pregnacny 3 patterns of metabolism: 1) active drug --> active metabolite 2)prodrug -- >active drug 3) active drug and excreted unchanged. Cough and angioedema are caused by bradykinin action: potentially life- threatening. Delay progression of cardiac contractile dysfunction in heart failure and after MI, and delay progression of diabetic nephropathy
DrugClinical appAdverse effectsContraindicationsTherapeutic considerations Simvastatin (Zocor) – Lipid Lowering Agent, Statin MOA: HMG-COA reductase inhibitor, inhibits rate- limiting step in cholesterol biosynthesis by competitively inhibiting HMG-COA reductase Hypercholesteremia, familial, coronary atherosclerosis, prophylaxis for coronary atherosclerosis Myopathy, rhaddomyolysis, hepatotoxicity, dermatomyositis, abdominal pain, constipation, diarrhea, nausea, headache Active liver disease pregnancy and lactation Lowering LDL metabolized by P450, 3A4 inhibitors increase risk of myopathy, combo with bile acid sequestrant or cholesterol absorption inhibitor additive decrease in LDL, combo with niacin maybe used in high LDL and low HDL increases risk of myopathy, gemfibrozil decreases statin clearance induce rhabdo
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Tissue plasminogen activator (t-PA) (Alteplase, Activase) – Thrombolytics MOA: Recombinant human tissue-type plasminogen activator (t- pa); produces local fibrinolysis. Promotes thrombolysis by converting plasminogen to plasmin which degrades fibrin and fibrinogen. AMI = acute MI, PE, Acute Ischemic Stroke pulmonary edema, arterial embolism, bleeding, DVT, hypotension, intracranial hemorrhage, stroke, fever, chills, N/V, sepsis, shock Internal bleeding, intracranial/spinal trauma, surgery, masses, recent stroke, uncontrolled hypertension Binds to newly formed thrombi with high affinity, causing fibrinolysis at the site of a thrombus Can generate a systemic lytic state and cause unwanted bleeding
DrugClinical appAdverse effectsContraindicationsTherapeutic considerations triamterene/ Hydrocholorothiazide (Maxide,Dyazide) – Thiazide Combos, HTN Triamterene – Direct effect on renal distal tubule to inhibit Na reabsorption. Inhibits Na/K- ATPase, decreases Ca and MG and hydrogen excretion =Postassium sparing diuretic HCTZ- inhibits Na reabsorption in distal renal tubules; results in increased excretion of Na and water also K and H ions. -is a sulfa drug HTN, adjunct in edema states associated with HF, cirrhosis, renal dysfunction, corticosteroid and estrogen Arrhythmia, stevens-johnson, pancreatitis, hepatotoxicity, SLE, hypotension, alkalosis, vasculitis, photosensitivity, electrolyte abnormalities, impotence, restlessness, blurrred vision, headache, hyperglycemia, hyperuricemia Anuria, hypersensitivity to sulfonamides, co administration with agents that prolong QT First line in treating HTN, diminish hypercalcuria in patients at risk for nephrolithiasis, decreases glucose tolerance may unmask diabetes, don’t use with antiarrhythmic
DrugClinical appAdverse affectsContraindicationsTherapeutic considerations Warfarin (Coumadin) – Anticoagulants MOA: Interferes with hepatic synthesis of vitamin K dependent clotting factors II, VII, IX, & X as well as proteins C and S. Venous Thrombosis, DVT, Afib, Cardiac Valve Replacement, Post MI 1-10% Intraocular Hemorrhage, UNK Freq – abd pain, rash, pruritus, tissue necrosis, headache, lethargy, anemia, hemorrhage, fever, purple toe syndrome, Pregnancy, Hemorrhage, Bleeding tendency, uncontrolled Hypertension Monitor with PT/INR. Many drug-drug interactions, never give to pregnant woman, can cause skin necrosis, receive fresh frozen plasma if hemorrhaging occurs