Lipitor

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Alan Cheng, MD

  • Assistant Professor of Medicine
  • Doctor, Arrhythmia Device Service
  • Johns Hopkins University School of Medicine
  • Baltimore, Maryland

Advise patient to read the Medication Guide prior to first dose and with each Rx refill in case of changes cholesterol levels when not fasting generic lipitor 40 mg line. Inform patient that side effects may not appear until several days cholesterol screening ratio cheap lipitor 40 mg mastercard, weeks cholesterol medication equivalent chart generic 10 mg lipitor fast delivery, or yr after initiation of therapy and may persist for several mo after withdrawal unesterified cholesterol definition buy lipitor online pills. Advise patients that photosensitivity reactions may occur through window glass cholesterol levels high generic 20 mg lipitor with mastercard, thin clothing low cholesterol food indian order lipitor 5mg with visa, and sunscreens. Protective clothing and sunblock are recommended during and for 4 mo after therapy. Inform patients that bluish discoloration of the face, neck, and arms is a possible side effect of this drug after prolonged use. Instruct male patients to notify health care professional if signs of epididymitis (pain and swelling in scrotum) occur. Contraindications/Precautions Contraindicated in: Angle-closure glaucoma; Canadian drug name. Availability (generic available) Tablets: 10 mg, 25 mg, 50 mg, 75 mg, 100 mg, 150 mg. Concurrent use of other drugs that inhibit the activity of the enzyme, including cimetidine, quinidine, amiodarone, and ritonavir, may result inqeffects of amitriptyline. Concurrent use with clonidine may result in hypertensive crisis and should be avoided. Concurrent use with levodopa may result in delayed or pabsorption of levodopa or hypertension. Adrenergic and anticholinergic side effects may beqwith other agents having anticholinergic properties. Pain: Assess intensity, quality, and location of pain periodically during therapy. Geri: Geriatric patients started on amitriptyline may be at an increased risk for falls; start with low dose and monitor closely. Lab Test Considerations: Assess leukocyte and differential blood counts, liver function, and serum glucose before and periodically during therapy. If a dose is missed, take as soon as possible unless almost time for next dose; if regimen is a single dose at bedtime, do not take in the morning because of side effects. Orthostatic hypotension, sedation, and confusion are common during early therapy, especially in geriatric patients. Advise patient, family and caregivers to look for suicidality, especially during early therapy or dose changes. Therapy for depression is usually prolonged and should be continued for at least 3 mo to prevent relapse. Emphasize the importance of follow-up exams to monitor effectiveness, side effects, and improved coping skills. Advise patient and family that treatment is not a cure and symptoms can recur after discontinuation of medication. Antihypertensive effects may bepby concurrent use of nonsteroidal anti-inflammatory agents. Potential Nursing Diagnoses Ineffective tissue perfusion (Indications) Acute pain (Indications) Implementation Do not confuse amlodipine with amiloride. If 12 hrs since missed dose, skip dose and take next dose at scheduled time; do not double doses. Instruct patient on importance of maintaining good dental hygiene and seeing dentist frequently for teeth cleaning to prevent tenderness, bleeding, and gingival hyperplasia (gum enlargement). Advise patient to notify health care professional if irregular heartbeats, dyspnea, swelling of hands and feet, pronounced dizziness, nausea, constipation, or hypotension occurs or if headache is severe or persistent. Advise patient to contact health care professional if chest pain does not improve or worsens after therapy, if it occurs with diaphoresis, if shortness of breath occurs, or if severe, persistent headache occurs. Caution patient to discuss exercise restrictions with health care professional before exertion. Increase in activity tolerance and sense of well-be- (cross-sensitivity exists to cephalosporins and other beta-lactams). Contraindications/Precautions Contraindicated in: Hypersensitivity to penicillins ing. Spectrum: Active against: Streptococci, Pneumococci, Enterococci, Haemophilus influenzae, Escherichia coli, Proteus mirabilis, Canadian drug name. Dual therapy- 1000 mg amoxicillin three times daily with lansoprazole 30 mg three times daily for 14 days. Availability (generic available) Chewable tablets (cherry, banana, peppermint flavors): 125 mg, 200 mg, 250 mg, 400 mg. Powder for oral suspension (strawberry [125 mg/5 mL] and bubblegum [200 mg/5 mL, 250 mg/5 mL, 400 mg/5 mL] flavors): 125 mg/5 mL, 200 mg/5 mL, 250 mg/5 mL, 400 mg/5 mL. In combination with: clarithromycin and lansoprazole in a compliance package (Prevpac). Suspension may be given straight or mixed in formula, milk, fruit juice, water, or ginger ale. Persons with a negative history of clock and to finish the drug completely as directed, even if feeling better. Advise patient to report the signs of superinfection (furry overgrowth on the tongue, vaginal itching or discharge, loose or foul-smelling stools) and allergy. Instruct patient to notify health care professional immediately if diarrhea, abdominal cramping, fever, or bloody stools occur and not to treat with antidiarrheals without consulting health care professional. Instruct female patients taking oral contraceptives to use an alternate or additional nonhormonal method amoxicillin/clavulanate of contraception during therapy with amoxicillin and until next menstrual period. Use Cautiously in: Severe renal insufficiency (dose pnecessary); Infectious mononucleosis (qrisk of rash); Hepatic impairment (dose cautiously, monitor liver function). Action Binds to bacterial cell wall, causing cell death; spectrum of amoxicillin is broader than penicillin. Clavulanate resists action of beta-lactamase, an enzyme produced by bacteria that is capable of inactivating some penicillins. Metabolism and Excretion: 70% excreted unchanged in the urine; 30% metabolized by the liver. Recurrent/persistent acute otitis media due to Multidrug-resistant Streptococcus pneumonia, H. Elderly men and patients receiving prolonged treatment are atqrisk for hepatic dysfunction. Administer at the Availability (generic available) Tablets: 250 mg amoxicillin with 125 mg clavulanate, 500 mg amoxicillin with 125 mg clavulanate, 875 mg amoxicillin with 125 mg clavulanate. Powder for oral suspension (125 mg/5 mL is banana flavor; 200 mg/5ml is fruit flavor; 250 mg/5 mL is orange flavor; 400 mg/5 mL is fruit flavor; 600 mg/5 mL is orange or strawberry-creme flavor): 125 mg amoxicillin with 31. Two 250-mg tablets are not bioequivalent to one 500-mg tablet; 250-mg tablets and 250-mg chewable tablets are also not interchangeable. Pedi: Do not administer 250-mg chewable tablets to children 40 kg due to clavulanate content. Reinforce importance of using measuring device supplied by pharmacy or with product, not household items. Instruct female patients taking oral contraceptives to use an alternate or additional method of contraception during therapy and until next menstrual period; may decrease effectiveness of hormonal contraceptives. Therapeutic Effects: Increased motor activity, mental alertness, and decreased fatigue in narcoleptic patients. Drugs that alkalinize urine (sodium bicarbonate, acetazolamide)pexcretion,qeffects. Drugs that acidify urine (ammonium chloride, large doses of ascorbic acid)qexcretion,peffects. Tricyclic antidepressants mayqeffect of amphetamine but may qrisk of arrhythmias, hypertension, or hyperpyrexia. Drug-Food: Foods that alkalinize the urine (fruit juices) canqeffect of amphetamine. If starting therapy with extended-release capsules, start with 10 mg once daily andqby 10 mg/day at weekly intervals (up to 40 mg/day). Availability (generic available) Amount is expressed in total amphetamine content (amphetamine dextroamphetamine). If exertional chest pain, unexplained syncope, or other cardiac symptoms occur, evaluate promptly. Advise patient and parents to read the Medication Guide prior to starting therapy and with each Rx refill in case of changes. Inform patient that the effects of drug-induced dry mouth can be minimized by rinsing frequently with water or chewing sugarless gum or candies. Advise patient to use caution when driving or during other activities requiring alertness until response to medication is known. Pedi: Children should be given a drug-free holiday each year to reassess symptoms and treatment. Doses will change as children age due to pharmacokinetic changes such as slower hepatic metabolism. Advise patient and/or parents to notify health care professional of behavioral changes (new or worse behavior and thought problems, bipolar illness, or aggressive behavior or hostility; new psychotic symptoms such as hearing voices, believing things that are not true, are suspicious, or new manic symptoms). Advise patient to notify health care professional if symptoms of heart problems (chest pain, shortness of breath, fainting), nervousness, restlessness, insomnia, dizziness, anorexia, or dry mouth becomes severe. Pedi: If reduced appetite and weight loss occur, advise parents to provide high calorie meals when drug levels are low (at breakfast and or bedtime). Instruct patients to notify health care professional of any new numbness; pain; skin color change from amphotericin B 155 pale, to blue, to red; or coolness or sensitivity to temperature in fingers or toes, and call if unexplained wounds appear on fingers or toes. Caution patients to inform health care professional if they have ever abused or been dependent on alcohol or drugs, or if they are now abusing or dependent on alcohol or drugs. Spectrum: Active against: Aspergillosis, Blastomycosis, Candidiasis, Coccidioidomycosis, Cryptococcosis, Histoplasmosis, Leishmaniasis (liposomal formulation only), Mucormycosis. The lipid complex, and liposome formulations should be considered for patients who are intolerant. Toxicity (especially acute infusion reactions and nephrotoxicity) is less with lipid formulations. Therapeutic Effects: Can be fungistatic or fungicidal (depends on concentration achieved and and hypotension with antineoplastics. Concurrent use with flucytosineqantifungal activity but mayqthe risk of toxicity from flucytosine. If respiratory distress occurs, discontinue infusion immediately; anaphylaxis may occur. Premedicating with antipyretics, corticosteroids, antihistamines, meperidine, and antiemetics may decrease these reactions. May be diluted in 250 mL of D5W if being administered via a central venous catheter. To obtain test dose, withdraw 1 mg (10 mL) from 500 mL infusion and further dilute with D5W to a total volume of 20 mL. Intermittent Infusion: Diluent: Reconstitute and dilute 50-mg vial as per the directions above. Y-Site Compatibility: aldesleukin, aminocaproic acid, argatroban, carmustine, dactinomycin, diltiazem, etoposide, hydromorphone, ifosfamide, lorazepam, nesiritide, octreotide, oxaliplatin, tacrolimus, teniposide, thiotepa, zidovudine, zoledronic acid. Y-Site Incompatibility: acyclovir, alemtuzumab, alfentanil, allopurinol, amifostine, amikacin, ampi- amphotericin B 157 cillin, ampicillin/sulbactam, anidulafungin, atropine, azithromycin, aztreonam, benztropine, bivalirudin, bleomycin, bumetanide, butorphanol, calcium chloride, calcium gluconate, cangrelor, carboplatin, caspofungin, cefepime, cefotetan, ceftaroline, chloramphenicol, chlorpromazine, cisplatin, clindamycin, cyanocobalamin, cyclophosphamide, cytarabine, dacarbazine, dantrolene, daptomycin, daunorubicin, dexamethasone, dexmedetomidine, dexrazoxane, diazepam, digoxin, diphenhydramine, dobutamine, docetaxel, dolasetron, dopamine, doxorubicin, doxorubicin liposome, doxycycline, ephedrine, epinephrine, epirubicin, epoetin alfa, eptifibatide, ertapenem, erythromycin, esmolol, etoposide phosphate, famotidine, fenoldopam, filgrastim, fluconazole, fludarabine, fluorouracil, foscarnet, fosphenytoin, ganciclovir, gemcitabine, gentamicin, glycopyrrolate, granisetron, haloperidol, hetastarch, hydralazine, hydrocortisone, hydroxyzine, idarubicin, irinotecan, isoproterenol, ketorolac, labetalol, leucovorin, levofloxacin, lidocaine, linezolid, melphalan, meperidine, mechlorethamine, meropenem, mesna, methotrexate, methylprednisolone, metoclopramide, metoprolol, metronidazole, midazolam, milrinone, mitomycin, mitoxantrone, morphine, mycophenolate, nafcillin, nalbuphine, nicardipine, nitroprusside, norepinephrine, ondansetron, oxacillin, paclitaxel, palonosetron, pamidronate, pancuronium, pantoprazole, papaverine, pemetrexed, penicillin G, pentamidine, pentazocine, phenylephrine, phenytoin, piperacillin/tazobactam, potassium acetate, potassium chloride, prochlorperazine, promethazine, propofol, propranolol, protamine, pyridoxine, quinupristin/dalfopristin, rituximab, rocuronium, sodium acetate, sodium bicarbonate, succinylcholine, telavancin, thiamine, tigecycline, tirofiban, tobramycin, topotecan, trastuzumab, trimethoprim/sulfamethoxazole, vancomycin, vasopressin, vecuronium, verapamil, vinblastine, vincristine, vinorelbine, voriconazole. If administering through an existing line, flush line with D5W before infusion or use a separate line. Y-Site Compatibility: acyclovir, allopurinol, aminocaproic acid, aminophylline, amiodarone, anidulafungin, argatroban, azithromycin, aztreonam, bumetanide, buprenorphine, busulfan, butorphanol, carboplatin, carmustine, cefazolin, cefepime, cefotaxime, cefotetan, cefoxitin, ceftazidime, ceftriaxone, cefuroxime, chloramphenicol, chlorpromazine, cisatracurium, clindamycin, cyclophosphamide, cyclosporine, cytatabine, dactimomycin, dexamethasone, digoxin, diphenhydramine, docetaxel, doxorubicin liposome, enalaprilat, ephedrine, epinephrine, eptifibatide, ertapenem, etoposide, famotidine, fentanyl, fludarabine, fluorouracil, fosphenytoin, furosemide, ganciclovir, granisetron, heparin, hydrocortisone, hydromorphone, ifosfamide, insulin, ketorolac, lidocaine, linezolid, lorazepam, mannitol, melphalan, meperidine, methotrexate, methylprednisolone, metoclopramide, mitomycin, nafcillin, nesiritide, nitroglycerin, nitroprusside, octreotide, oxaliplatin, paclitaxel, pamidronate, pantoprazole, pemetrexed, pentazocine, pentobarbital, phenobarbital, piperacillin/tazobactam, procainamide, ranitidine, succinylcholine, sufentanil, tacrolimus, telavancin, teniposide, theophylline, thiopental, thiotepa, verapamil, vinblastine, vincristine, zidovudine, zoledronic acid. Replace needle from syringe filled with amphotericin B lipid complex with 5-micron filter needle. Solution Incompatibility: Do not dilute or admix with saline solutions, other medications, or solutions containing a bacteriostatic agent. Immediately shake vial vigorously for at least 30 seconds until all particulate matter is completely dispersed. Attach the 5-micron filter to the syringe and inject syringe contents into an appropriate volume of D5W. Infusion time may be shortened to 1 hr if patient tolerates infusion without any adverse reactions. May be administered through an in-line filter with pore diameter of at least 1 micron. Y-Site Compatibility: acyclovir, amifostine, aminocaproic acid, aminophylline, anidulafungin, argatroban, atropine, azithromycin, bivalirudin, bumetanide, buprenorphine, busulfan, butorphanol, carboplatin, carmustine, cefazolin, cefoxitin, ceftriaxone, cefuroxime, clindamycin, cyclophosphamide, cytarabine, dactinomycin, daptomycin, dexamethasone, dexmedetomidine, diphenhydramine, doxorubicin liposomal, enalaprilat, ephedrine, epinephrine, eptifibatide, ertapenem, esmolol, etoposide, famotidine, fenoldopam, fentanyl, fludarabine, fluorouracil, foscarnet, fosphenytoin, furosemide, granisetron, haloperidol, heparin, hydrocortisone, hydromorphone, ifosfamide, isoproterenol, ketorolac, lidocaine, linezolid, mesna, methotrexate, methylprednisolone, metoprolol, milrinone, mitomycin, nesiritide, nitroglycerin, nitroprusside, octreotide, oxaliplatin, oxytocin, palonosetron, pamidronate, pancuronium, pantoprazole, pemetrexed, pentobarbital, phenobarbital, phenylephrine, piperacillin/tazobactam, potassium acetate, potassium chloride, procainamide, ranitidine, sufentanil, tacrolimus, theophylline, thiopental, thiotepa, tigecycline, trimethoprim/sulfamethoxazole, vasopressin, vincristine, voriconazole, zidovudine, zoledronic acid. Unlabeled Use: Prevention of infection in certain high-risk patients undergoing cesarean section. Spectrum: Active against: Streptococci, nonpenicillinase-producing staphylococci, Listeria, Pneumococci, Enterococci, Haemophilus influenzae, Escherichia coli, Enterobacter, Klebsiella, Proteus mirabilis, Neisseria meningitidis, N. Distribution: Diffuses readily into body tissues and Bacterial Meningitis Caused by H. Powder for injection: 125 mg/vial, 250 mg/vial, 500 mg/vial, 1 g/vial, 2 g/vial, 10 g/vial. Obtain a history before initiating therapy to determine previous use and reactions to penicillins or cephalosporins. Assess skin for "ampicillin rash," a nonallergic, dull red, macular or maculopapular, mildly pruritic rash.

The individual may have tried to complete this act several times in the past but the will to survive overpowered the will to end life cholesterol lowering foods list dr oz buy cheap lipitor 40mg. This will give the individual enough time to prevent himself from stopping the process cholesterol in eggs bad discount lipitor 10 mg free shipping. A ligature is something flexible that can encircle the neck cholesterol risk ratio buy 20mg lipitor visa, like a cord lowering cholesterol diet exercise buy lipitor master card, belt cholesterol levels normal values order 5 mg lipitor, or piece of clothing cholesterol in eggs yolk or white purchase lipitor online pills. Manual strangulation is usually characterized by multiple irregular, angulated, abraded contusions around the neck. Ligature strangulation is usually characterized by a horizontal furrow or mark pattern around the neck. The extent of these injuries depends on the type of ligature, how broad and soft it is, the amount of struggle, etc. The act of strangulation is often a very physically dominating, often non-premeditated, way of killing somebody. Often a sexual component to the assault exists and a rape kit should be performed in all cases of suspected strangulation. There are usually hemorrhages in the strap muscles of the neck, and there may be fractures of the laryngeal cartilages and/or hyoid bone. These fractures are more common in older victims because the cartilages are more calcified, brittle, and less elastic. Younger victims or children tend to have more flexible upper airways that often will stretch or collapse rather than fracture. Depending on how great the struggle, the amount of force used, and the type of neck compression, there may or may not be petechiae and/or hemorrhages above the ligature or region of neck compression. The presence of petechiae is less common when the force is very strong, consistent, and applied with a small surface area ligature. Victims of strangulation often have defensive-type injuries, including other abrasions and contusions to their bodies. It is possible to ligature strangle yourself; it is not possible to manually strangle yourself. If one is able to apply enough force to lose consciousness manually, revival occurs after the pressure is released. Someone murdered by ligature strangulation may die within a similar time frame as someone hanged; however, the time frame is usually longer. If there are multiple petechiae with hemorrhages and fractures of the neck structures, whether ligature or manual, the time frame may be much longer. If an individual is released shortly following loss of consciousness, revival may follow. Asphyxia 479 Proper autopsy technique dictates that the brain and visceral organs be removed prior to a layered neck dissection being performed. Drowning occurs when water is inhaled, filling up the alveolar spaces and preventing gas exchange. The manner of death will vary depending on how the individual came to be in the water. If the event is not witnessed, the manner often remains undetermined because it is unknown whether the individual was pushed, jumped, or slipped into the water. Also, with decomposition it may be impossible to tell whether the person died of drowning. Water in the lungs, or pulmonary edema and water within the paranasal sinus, is often present but neither is specific for only cases of drowning. These findings may also be found in cases with natural disease, including congestive heart failure with pulmonary edema. The degree of pulmonary edema may vary in a fraction of the cases due to the heart beating after respirations cease. As the heart beats, before eventual asystole, some of the fluid in the lungs will be absorbed and there may be little or no edema at the time of death. An adult may drown in a big pool or ocean but not in a small pool or bathtub unless neurologically compromised or intoxicated. Homicide victims are sometimes placed in a water-filled bathtub to wash away evidence. Note the black cord that matches the underlying furrow pattern at the superior aspect of the neck with upward extension on the left side of the face. This fixed lividity pattern is appropriate for an individual that remained in an upright position for many hours after death. If his lividity was fixed posteriorly and not inferior, this would indicate prior scene alteration. There were hesitation marks at the wrist with blood seeping downward due to gravity. They were left unattended for a short period of time by chronic care nursing staff, and got tangled in the cord from a window blind. This individual also took part of the cord and loosely wrapped his hands behind his back so he would not be able to reach up and prevent the hanging from being successful. It is not very unusual for people to hang themselves and loosely tie their hands in this fashion. There is also a moderate state of putrefactive change with skin slippage, bloating, and purging. Her clothing was discovered on the side of the building, after being thrown from a window. Each victim had multiple petechiae with areas of hemorrhage in the sclera and conjunctivae of each eye. The constellation of these findings is typical for a homicidal manual strangulation. As decomposition progresses, it may become more difficult to interpret these findings. Careful internal examination after the brain and visceral organs had been removed revealed areas of hemorrhage within the anterior strap muscles and posterior paraspinal muscles. This individual was found face down and the eye hemorrhages were initially thought by some to be associated with postmortem lividity. Therefore, there was no pressure release mechanism, leading to capillary rupture and hemorrhage. The absence of scleral or conjunctivae hemorrhages is more typical in hanging fatalities. Part of the undersurface of the platysma muscle is visible at the top of this image adjacent to the yellow subcutaneous tissue of the neck. The anterior strap muscles are visible directly above the label and are free of antemortem injury. Dissection should be done in a layer-by-layer fashion until the surface of bone is exposed. It is important to dissect the arms as well, which may demonstrate contusions from being held during a struggle. It is often more difficult to externally visualize contusions in darker-skinned individuals. Note the large hemorrhage to the anterior neck structures including the left sternohyoid muscle. Fractures of the hyoid bone are often found in association with homicidal strangulation. The presence of a hyoid bone fracture does not indicate the case must be a strangulation, and the absence of fractures to the hyoid bone does not indicate the decedent was not strangled. As varied degrees of neck pressure continue after petechiae formation, hemorrhages progressively become larger and more confluent until death occurs. Note the areas of hemorrhage within the eyes and face associated with gravity-dependent settling of blood. Petechiae are more obvious on paler surfaces of the body such as the sclera and conjunctiva. Her head was wrapped in multiple layers of plastic, which covered her mouth and nose. Note the yellow to brown discoloration from mold and mildew forming on her face due to the moist environment from terminal breathing. This individual was found in a moderate to marked state of decomposition within her apartment. She was reportedly dealing drugs and was found tied up with a piece of cloth stuck down her mouth and throat. Note the lacerations with hemorrhage to the anal region and the abrasion, braided contusions to the thighs from rubbing. The large size of the hot dog piece caused it to get wedged in her throat leading to asphyxia. Children are susceptible to such events because they are impulsive and may gulp food. This typically happens in somebody who is intoxicated or neurologically compromised. One of these individuals was stuck in a box-folding machine, another trapped under a car, and another stuck under a single-person elevator lift. This individual also had numerous petechial hemorrhages of the upper trunk, face, eyes, and visceral organs including the heart. Note the extensive hemorrhage at the superior chest visible at the superior aspect of the Y-shaped incision during autopsy. This individual was punched, strangled, and then the perpetrator sat on her chest during the assault. This old-fashioned cooler had a locking mechanism that prevented the child from escaping after the lid closed. These individuals were markedly intoxicated and passed out in a position, which prevented them from breathing and obstructed blood circulation. Note the aggregates of platelets and blood cells extending into the lumen from the plague rupture site. Acute myocardial infarctions may present with rapid death due to fatal arrhythmia from myocardial irritability. Active myocarditis requires an inflammatory infiltrate with myonecrosis (arrow) as per the modified Dallas criteria. Many forensic pathologists believe fatal arrhythmia can occur without the presence of necrosis. Note the many artifactual empty vacuoles following processing leading to glycogen loss. One of the most common types of amyloid seen in the heart at autopsy is transthyretin. It may present as a restrictive cardiomyopathy and is X linked or autosomal recessive. This can result in sudden cardiac death through the same mechanism as marked coronary artery disease within epicardial vessels. Hypertrophic cardiomyopathy is also associated with fibromuscular dysplasia, causing marked narrowing of small coronary artery branches. Although usually considered a benign condition, it can result in myocardial ischemia and death. Since the coronary arteries supply blood to the heart during diastole, compression of this vessel during systole usually will not create significant blood flow obstruction. An exception to this can occur during strenuous exertion with increased oxygen demand and rapid left ventricular contraction which has, on occasions, been shown to have an exclusive effect leading to ischemia, myocardial irritability, and arrhythmia. Low- to high-power magnification showing hemorrhage in the myocardium of an individual who was in a motor vehicle collision and impacted his chest on the steering wheel. In cystic medial necrosis or degeneration, the tunica media of elastic arteries such as the aorta show loss of smooth muscle fibers and fragmentation of the elastic fibers with a cystic-like appearance, best seen on elastin stains. Although characteristic in Marfan syndrome, these changes are nonspecific and degenerative. This process is seen to varying degrees in patients with systemic hypertension and annuloaortic ectasia and is a risk factor for aortic dissection. This is associated with many different types of heart diseases and some drug toxicities including from opiates. Some degree of pulmonary congestion and edema are common findings at autopsy and associated with the terminal phases of death. Also associated with this is thrombotic microangiopathy with thrombi inside capillaries and arterioles, endothelial injury, and fibrinoid necrosis of the arterioles. A variety of mechanisms are possible for this type of "food" material to be introduced into the pulmonary arterial system such as peripheral venous injection, atrioesophageal fistula, or enterovascular fistula into the systemic venous nonportal circulation, possibly related to a diverticula or diverticulitis, or arteriovenous fistula introduction possibly related to dialysis. In the respiratory epithelium, the goblet cells and submucosal glands will be increased, with increase in the basement membrane thickness. In acute asthma the lungs are hyperaerated and expand to overlie the pericardial sac. The alveolar ducts and possibly bronchioles will be filled with loose fibromyxoid plugs, sometimes in a "butterfly" pattern. On the left side of each image, the dense collection of neutrophils destroys the liver, leaving collapse of the hepatocytes at the periphery. Liver abscess can occur as a result of infection with pyogenic bacteria (both aerobic and anaerobic), fungal with Candida species being most common, amoebic, Actinomyces, ascariasis, or Nocardia. Pseudomembranous colitis develops following treatment with broad-spectrum antibiotics such as clindamycin.

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Patients taking vasoconstricting drugs are most susceptible cholesterol z frakcjami lipitor 40 mg with amex, and when the diagnosis is chemic colitis cholesterol over 200 purchase discount lipitor on-line, these medications are discontinued and supportive care is given cholesterol levels too high order lipitor with amex. Immediate surgical intervention is required for bowel infarctions and other complications cholesterol uk order lipitor 10mg mastercard. Shows a soft tissue mass on the lateral wall of the rectum containing a central ulceration (straight arrows) cholesterol levels and exercise order on line lipitor. Thickening of the perirectal fascia (curved arrow) cholesterol test how long do you fast order cheap lipitor on line, the presence of multiple lymph nodes (on the more cephalic images), and increased soft tissue density of perirectal fat were suggestive of tumor extension beyond the bowel wall, which was confirmed at surgery. Note the sharply defined proximal and distal margins of this relatively short, apple-core lesion (arrow). Annular carcinomas appear to arise from flat plaques of tumor (saddle lesions) that involve only a portion of the circumference of the colon wall. Unless meticulous care is taken to search for an area of minimal straightening or slight contour defects, the small and subtle, but lethal, saddle carcinoma can be easily overlooked. As the tumor grows, it characteristically infiltrates the bowel wall rather than forming a bulky intraluminal mass. This produces a classic bilateral contour defect with ulcerated mucosa, eccentric and irregular lumen, and overhanging margins. Progressive constriction of the bowel can cause complete colonic obstruction, most commonly in the sigmoid region. It can vary from an excavation within a large fungating mass to mucosal destruction within an annular apple-core tumor. A patient with carcinoma of the colon has a 1% risk of having multiple synchronous (occurring simultaneously) colon cancers. Therefore, it is essential to carefully examine the rest of the colon once an obviously malignant lesion has been detected. In addition, such a patient has a 3% risk of developing additional metachronous cancers later. Carcinoma causes asymmetrical or circumferential thickening of the bowel wall with narrowing and deformity of the lumen. Transrectal ultrasound produces the most accurate images for staging of local rectal cancer by demonstrating the depth of invasion within the bowel wall. Ultrasound also may determine the presence of a tumor in adjacent, normal-size lymph nodes. Large Bowel Obstruction Approximately 70% of large bowel obstructions result from primary colonic carcinoma. Colonic obstructions tend to be less acute than small bowel obstructions; the symptoms develop more slowly, and fewer fluid and electrolyte disturbances are produced. The radiographic appearance of colonic obstruction depends on the competency of the ileocecal valve. If the ileocecal valve is incompetent, there is distention of gas-filled loops of both colon and small bowel, which may simulate an adynamic ileus. If the ileocecal valve is competent, the colon behaves like a closed loop, and the increased pressure caused by the obstruction cannot be relieved. Because the cecum is spherical and has a large diameter, it is the most likely site for perforation. Volvulus of the Colon Volvulus refers to a twisting of the bowel on itself that may lead to intestinal obstruction. Because twisting of the bowel usually requires a long, movable mesentery, volvulus of the large bowel most frequently involves the cecum and sigmoid colon. The transverse colon, which has a short mesentery, is rarely affected by volvulus. A sigmoid volvulus, more commonly found in the elderly, results from a low-fiber diet causing constipation. Upper (A) and lower (B) abdominal radiographs in a 4-year-old illustrate a gas pattern indicating a large bowel obstruction. A low-pressure barium enema was performed to relieve the obstruction, as seen on the post-evacuation view. It should be stressed, however, that cecal volvulus develops in only a few patients with an extremely mobile cecum. In cecal volvulus, the distended cecum tends to be displaced upward and to the left, although it can be found anywhere within the abdomen. A barium enema examination is usually required for definite confirmation of the diagnosis. Sigmoid Volvulus A long, redundant loop of sigmoid colon can undergo a twist on its mesenteric axis and form a closed-loop obstruction. In sigmoid volvulus, the greatly inflated sigmoid loop appears as an inverted U-shaped shadow that rises out of the pelvis in a vertical or oblique direction and can even reach the level of the diaphragm. The affected loop appears devoid of haustral markings and has a sausage or balloon shape. A barium enema examination demonstrates an obstruction to the flow of contrast material at the site of volvulus and considerable distention of the rectum. Surgical detorsion is usually required for large bowel obstruction or volvulus, although a water-soluble enema may be therapeutic and resolve the obstruction. Hemorrhoids Hemorrhoids are varicose veins of the lower end of the rectum that cause pain, itching, and bleeding. Like varicose veins in the leg, hemorrhoids are caused by increased venous pressure. The most common cause of increased pressure is chronic constipation with resulting excessive muscular straining needed to empty the bowel. Increased venous pressure can also be produced by a pelvic tumor or a pregnant uterus. The proper diagnosis can easily be made by inspection, digital examination, or direct vision through the anoscope. The surgical intervention consists of circumferential mucosectomy, which is a stapled hemorrhoidectomy, a safe and effective procedure for advanced stages (third- and fourth-degree hemorrhoidal prolapse). Cholesterol stones are predominant (75%) in the United States, whereas pigment stones occur more frequently in the tropics and Asian countries. Genetic predispositions associated with higher incidence include family history of the disorder, age older than 40 years, excess weight, and female sex. Gallstones can develop whenever bile contains insufficient bile salts and lecithin in proportion to cholesterol to maintain the cholesterol in solution. This situation can result from a decrease in the amount of bile salts present (because of decreased reabsorption in the terminal ileum as a result of inflammatory disease or surgical resection), or it can be caused by increased hepatic synthesis of cholesterol. Because cholesterol is not radiopaque, most gallstones are radiolucent and visible only on contrast examinations or ultrasound. Gallstones can have a central nidus (or focus) of calcification, a laminated appearance (with alternating opaque and lucent rings), or calcification around the periphery. It is rarely used today because it has been replaced in most institutions by ultrasound (discussed later). Calculi (arrowheads) lie in common bile duct, some of which overlie the spine and are difficult to detect. Infrequently a gallstone is coated with tenacious mucus and adheres to the gallbladder wall. If these causes can be excluded, failure of the gallbladder to opacify after the administration of two doses of orally administered cholecystographic contrast material is highly reliable evidence of gallbladder disease. In addition to imaging the gallbladder, ultrasound can provide important additional information by effectively demonstrating the biliary tree and hepatic parenchyma. The mobility of free-floating gallstones may be demonstrated by performing the examination with the patient in various positions. Acute Cholecystitis Acute cholecystitis (inflammation of the gallbladder) usually (in 95% of cases) occurs after obstruction of the cystic duct by an impacted gallstone. Echogenic focus (white arrow) in otherwise sonolucent gallbladder (G) represents a large gallstone. B acute cholecystitis requires the demonstration of a distended gallbladder containing gallstones. Important additional findings include edema of the gallbladder wall and focal tenderness elicited directly over the gallbladder. A normal gallbladder ultrasound image virtually excludes the diagnosis of acute cholecystitis. Because many disorders may mimic acute cholecystitis, ultrasound can also be used to evaluate the remainder of the right upper quadrant for any other acute abnormality. Failure to accumulate radioactivity (after 4 hours) in the gallbladder is highly sensitive (98%) and specific for cystic duct obstruction. If associated with appropriate symptoms, this finding is virtually diagnostic of acute cholecystitis. Emphysematous Cholecystitis Emphysematous cholecystitis is a rare condition in which the growth of gas-forming organisms in the gallbladder is facilitated by stasis and ischemia caused by cystic duct obstruction (most often by stones). Emphysematous cholecystitis occurs most frequently in elderly men and in patients with poorly controlled diabetes mellitus. Plain abdominal radiographs demonstrate gas in the gallbladder lumen that dissects into the wall or pericholecystic tissues. For acute impaction and biliary colic, prompt treatment using an antispasmodic and an analgesic helps alleviate symptoms. The radiographer may be requested to obtain images during operative cholangiography to determine ductal blockage and identify remaining stones. Imaging must be performed at the appropriate medium-to-low kVp (70 to 80) at the completion of contrast injection. The contrast agent should be free of air bubbles, which would otherwise simulate stones. Because chronic cholecystitis produces a loss of wall function, the gallbladder becomes fibrotic and calcified. The term reflects the blue discoloration and brittle consistency of the gallbladder wall. The calcification in a porcelain gallbladder can appear as a broad continuous band in the muscular layers, or it may be multiple and punctate and occur in the glandular spaces of the mucosa. The detection of extensive calcification in the wall of the gallbladder should indicate the possibility of carcinoma. Because of the high incidence of associated carcinoma, patients with porcelain gallbladder usually undergo prophylactic cholecystectomy even if they are asymptomatic. Hepatitis A virus, previously known as infectious hepatitis, is transmitted in the digestive tract from oral or fecal contact. Hepatitis B virus, previously known as serum hepatitis, is contracted by exposure to contaminated blood or blood products, or through sexual contact. Healthcare workers are more susceptible to this virus and are usually required to have been vaccinated or to prove immunity. Hepatitis C virus, formerly known as non-A, non-B hepatitis, is the common cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Because it is contracted by blood transfusion or sexual contact, some authorities believe that healthcare workers are more susceptible; however, in the general population, the source of 40% of cases is unknown. Hepatitis E virus is self-limited and is acquired by the ingestion of food or water that has been contaminated with fecal material. Portal hypertension, due to enlargement or blockage of the portal system, can also be detected. In fatty liver, infiltrates of fat appear as discrete or diffuse areas of low density within the liver. Standard precautions for healthcare workers should include the use of personal protective equipment for all patients. The liver sonogram illustrates multiple nodules and has an internal coarse texture with increased echogenicity. On ultrasound images, the liver demonstrates an internal coarse texture (A) and a lobulated surface (B), which is consistent with severe cirrhosis. Because blood cannot flow through the obstructed portal vein, it must find an alternative route to bypass the liver. This leads to the development of collateral circulation, with large dilated veins becoming prominent on the abdominal wall in the area of the umbilicus. Destruction of liver cells substantially decreases the ability of the organ to synthesize proteins, such as albumin, and several of the factors required for blood clotting. A deficiency of albumin (hypoalbuminemia) results in fluid leaking out of the circulation and the development of generalized edema, which is evidenced by swelling of the lower extremities. When edema involves the wall of the intestinal tract, it can produce regular, uniform thickening of small bowel folds. One of the most characteristic symptoms of cirrhosis is the accumulation of fluid in the peritoneal cavity (ascites), which causes characteristic abdominal distention. The abdomen is tight and quite hard, and an increase in exposure factors is required if a large amount of fluid has accumulated. Ascites develops because of a combination of albumin deficiency and increased pressure within obstructed veins, which permits fluid to leak into the abdominal cavity. Smaller amounts of fluid (300 to 1000 mL) may widen the flank stripe and obliterate the right lateral inferior margin of the liver (the hepatic angle). Cirrhosis may lead to the development of jaundice, either from destruction of liver cells or from obstruction of bile ducts. Because the liver cannot perform its usual task of inactivating the small amounts of female sex hormones secreted by the adrenal glands in both men and women, men with cirrhosis often have breast enlargement (gynecomastia). The inability of necrotic liver cells to detoxify harmful substances leads to an accumulation of ammonia and other poisonous material in the circulation. The patient becomes confused and disoriented, demonstrates a typical flapping tremor or shaking, becomes abnormally sleepy (exhibits somnolence), and may lapse into a potentially fatal hepatic coma. Ascites occurs in advance stages of cirrhosis; of those afflicted, only 20% survive 5 years.

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The components of blood are also a major defense against infection does cholesterol medication help lose weight order cheap lipitor on line, toxic substances cholesterol levels triglycerides normal order discount lipitor line, and foreign antigens cholesterol medication safe in pregnancy generic lipitor 20mg overnight delivery. Red bone marrow (found in vertebrae is there cholesterol in quail eggs discount lipitor 10mg, proximal femurs cholesterol levels for 60 year old woman cheap lipitor online mastercard, and flat bones such as the sternum cholesterol medication pfizer purchase lipitor overnight delivery, ribs, skull, and pelvis) and lymph nodes are the blood-forming tissues of the body. If a bone marrow puncture is necessary for diagnostic testing, the iliac rim and sternum are good sites. The amount of hemoglobin per deciliter is approximately 14 g in women and 15 g in men. Neutrophils (polymorphonuclear leukocytes), which make up 55% to 75% of white blood cells, defend the body against bacteria by ingesting these foreign organisms and destroying them (phagocytosis). The number of polymorphonuclear leukocytes in the blood increases enormously in acute infections because the bone marrow rapidly releases into the bloodstream the large numbers of these cells kept in reserve. Eosinophils (1% to 4%) are red-staining cells whose number greatly increases in allergic and parasitic conditions. The third type of leukocyte is the basophil (0% to 1%), which contains granules that stain blue. These three types of cells are formed in the sinusoids of bone marrow, and they, like red blood cells, go through immature stages before reaching the adult form. They play a major role in the immune system and aid in the synthesis of antibodies and the production of immunoglobulins. The final type of white blood cell is the monocyte, which is actively phagocytic and plays an important role in the inflammatory process. Monocytes are formed in the bone marrow and represent approximately 2% to 8% of white blood cells. Normally, there are approximately 150,000 to 400,000 platelets in every cubic millimeter of blood. This reduction can be attributable to improper formation of new red blood cells, an increased rate of red blood cell destruction, or a loss of red blood cells as a result of prolonged bleeding. Regardless of the cause, a hemoglobin deficiency causes the anemic person to appear pale. This is best appreciated in the mucous membranes of the mouth and conjunctiva, and in the nail beds. A decrease in the oxygen-carrying hemoglobin impairs the delivery of an adequate oxygen supply to the cells and tissues, leading to fatigue and muscular weakness and often to shortness of breath on exertion (dyspnea). It most frequently results from chronic blood loss, such as from an ulcer, a malignant tumor, or excessive bleeding during menstruation (menorrhagia). Other causes of iron deficiency anemia are inadequate dietary intake of iron and increased iron loss caused by intestinal parasites. If chronic blood loss causes the iron deficiency, the cause must be determined and treated. The first choice of treatment is for the patient to change dietary habits to include more foods rich in iron. When a patient is taking an iron supplement, it is important to remember that other products influence iron absorption. Most hemolytic anemias are caused by a hereditary defect that may produce abnormal red blood cells or abnormal hemoglobin. Less commonly, hemolytic anemia is acquired and related to circulating antibodies from autoimmune or allergic reactions. Spherocytosis, sickle cell anemia, and thalassemia are the major hereditary hemolytic anemias. In spherocytosis, the erythrocytes have a circular rather than a biconcave shape, making them fragile and susceptible to rupture. In sickle cell anemia, which is generally confined to African Americans, the hemoglobin molecule is abnormal and the red blood cells are crescentic or sickle shaped and tend to rupture. A defect in hemoglobin formation is also responsible for thalassemia, which occurs predominantly in persons living near the Mediterranean Sea, especially those of Italian, Greek, or Sicilian descent. The breakdown of hemoglobin produces bilirubin, a pigmented substance that is normally detoxified by the liver and converted into bile. The accumulation of large amounts of this orange pigment in plasma causes the tissues to have a yellow appearance (jaundice). Hemolytic anemia of the newborn (erythroblastosis fetalis) can result when the mother is Rh negative and the fetus has Rh-positive blood inherited from the father. The mother thus becomes sensitized to the Rh factor of the fetus and makes antibodies against it. Any antibodies reaching the fetal blood through the placenta in future pregnancies cause hemolysis of the fetal red blood cells. Although the radiographic findings are similar in the various types of hemolytic anemia, they tend to be most severe in thalassemia and least prominent in spherocytosis. As the fine secondary trabeculae are resorbed, new bone is laid down on the surviving trabeculae, thickening them and producing a coarsened pattern. Normal modeling of long bones does not occur because the expanding marrow flattens or even bulges the normally concave surfaces of the shafts. In the skull, there is widening of the diploic space and thinning or complete obliteration of the outer table. When the hyperplastic marrow perforates or destroys the outer table, it proliferates under the invisible periosteum, and new bone spicules are laid down perpendicular to the inner table. Note the absence of normal modeling caused by the pressure of expanding marrow space. Localized radiolucencies simulating multiple osteolytic lesions represent tumorous collections of hypoplastic marrow. Note the normal appearance of the calvaria inferior to the internal occipital protuberance, an area in which there is no red marrow, and poor pneumatization of the visualized paranasal sinuses. A lateral projection of the chest demonstrates lobulated posterior mediastinal masses of hematopoietic tissue (arrows) in the lower thoracic region. Extramedullary hematopoiesis is a compensatory mechanism of the reticuloendothelial system (liver, spleen, and lymph nodes) in patients with prolonged erythrocyte deficiency resulting from the destruction of red blood cells or the inability of normal blood-forming organs to produce them. This is most often caused by circulatory stasis and ischemia, which retard growth in the central portion of the vertebral cartilaginous growth plate. The periphery of the growth plate, which has a different blood supply, continues to grow at a more normal rate. Bulging of the abnormally shaped red blood cells in sickle cell anemia typically causes focal ischemia and infarction in multiple tissues. They most frequently involve the small bones of the hands and feet, producing an irregular area of bone destruction with overlying periosteal calcification, which may be indistinguishable from osteomyelitis. In older children and adults, bone infarction may initially appear as an ill-defined lucent area that becomes irregularly calcified. Acute osteomyelitis, often caused by Salmonella infection, is a common complication in sickle cell disease. Throughout their lives, patients with sickle cell anemia are plagued by recurrent painful crises. These episodes are attributable to recurrent vaso-occlusive phenomena and may appear with explosive suddenness and attack various parts of the body, especially the abdomen, chest, and joints. It is often difficult to distinguish between a painful sickle cell crisis and some other type of acute process, such as biliary colic, appendicitis, or a perforated viscus. In the extremities, a sickle cell crisis may mimic osteomyelitis or an acute arthritis, such as gout or rheumatoid arthritis. The most common extraskeletal abnormality in the hemolytic anemias is cardiomegaly caused by severe anemia and increased cardiac output. Increased pulmonary blood flow produces engorgement of the pulmonary vessels, giving a hypervascular appearance to the lungs. Pulmonary infarction, pulmonary edema with congestive failure, and pneumonia are frequent complications. Renal abnormalities can be demonstrated by excretory urography in approximately two-thirds of patients with sickle cell disease. The cause and type of hemolytic anemia must be determined to successfully begin treatment. Diffuse lytic destruction of the proximal humerus can be seen along with extensive periosteal reaction (arrows). Mottled areas of increased and decreased density reflect osteonecrosis without collapse. Trabeculae in the neck and intertrochanteric region are thickened by the apposition of new bone. A solid layer of new bone along the inner aspect of the cortex of the femoral shaft causes narrowing of the medullary canal. Gene therapy requires removing a defective cell, fixing the gene, and replanting the new cell into the bone marrow. This procedure may help manage and control symptoms and, in some cases, may even provide a cure. If an Rh-negative mother delivers or aborts an Rh-positive infant, she is given a vaccine of Rh immunoglobulin within 24 hours to prevent the production of antibodies against the Rh factor. Blood testing to determine whether Rh incompatibility exists is now an essential part of prenatal care. An Rh-positive infant born to an Rh-negative mother receives a blood transfusion within 24 hours after birth. It must be emphasized, however, that the radiographic findings of atrophic gastritis are often seen in older persons with no evidence of pernicious anemia. The treatment of megaloblastic anemia consists of correcting the deficiency of vitamin B12 or folic acid. Vitamin B12 deficiency requires an injection because taking vitamin B12 orally does not reverse the process. The most common cause of vitamin B12 deficiency is pernicious anemia, in which there is inadequate intrinsic factor secretion related to atrophy of the gastric mucosa. Intrinsic factor acts as a carrier in the small bowel absorption of vitamin B12, which is essential for erythrocyte development. A deficiency of folic acid (and vitamin B12) may also be related to intestinal malabsorption. This in turn may be related to intestinal parasites or bacterial overproduction, especially in patients with stasis of bowel contents, such as in blind loop syndrome and multiple jejunal diverticula. Other causes of megaloblastic anemia include a poor diet, such as strict vegetarianism, in which there are no sources of vitamin B12, and long-term alcoholism, in which no folic acid is available. Gastric atrophy is seen radiographically as a tubular stomach with a bald appearance that reflects Aplastic Anemia A generalized failure of the bone marrow to function (aplastic anemia) results in decreased levels of erythrocytes, leukocytes, and platelets. In addition to anemia, the patient cannot fight infection (a white blood cell function) and has a bleeding tendency (platelet depletion). Causes of aplastic anemia include exposure to chemical agents or drugs, infections, and invasion of the bone marrow by cancer. Patient prognosis depends on the severity and duration of the bone marrow aplasia. Regular blood transfusions are generally necessary for survival and to reduce symptoms. Because the patient has a suppressed immune response, preventive antibiotics are sometimes prescribed. Situations exposing the patient to an infection or a viral illness should be avoided. Some clinicians recommend medications to stimulate the bone marrow to produce more blood cells. Bone marrow transplantation is a new technique for treating patients with aplastic anemia. A patient with chronic atrophic gastritis, which is signified by the tubular stomach with a striking decrease in the usually prominent rugal folds. Tumors may arise from cells that are normally found in the bone marrow (leukemia, lymphoma, and myeloma), or the marrow may be invaded by extensive metastases to bone (from carcinomas of the breast, prostate, lung, and thyroid). Skeletal images may demonstrate lytic or blastic lesions, depending on the progression of metastases. A radionuclide bone scan detects bone marrow abnormalities and skeletal metastases. A packed red blood cell transfusion is used to treat the anemia and help stabilize the patient. Severe hypoventilation caused by profound obesity causes engorgement of pulmonary vessels. Although cardiomegaly is uncommon in polycythemia, in this case it reflects pronounced elevation of the diaphragm as a result of a huge abdominal girth and some underlying cardiac decompensation. Primary Polycythemia (Polycythemia Vera) Polycythemia vera is a hematologic disorder characterized by hyperplasia of the bone marrow (neoplastic) that results in increased production of erythrocytes, granulocytes, and platelets. The disease is slowly progressive and produces symptoms associated with increased blood volume and viscosity. Cerebrovascular and peripheral vascular insufficiencies are common, and many patients give a history of some thrombotic or hemorrhagic event during the course of their disease. There is an increased incidence of peptic ulcer disease, and the excessive cellular proliferation often results in increased levels of uric acid with secondary gout and the formation of urate stones. The spleen is often massively enlarged and may be seen as a left upper quadrant mass. Intravascular thrombosis may cause pulmonary infarctions that appear as focal areas of consolidation or as bands of fibrosis. Treatment of Polycythemias Treatment for both primary and secondary polycythemias starts with bloodletting to remove excessive cellular elements. This maneuver improves circulation by lowering blood viscosity and is continued until the hemoglobin and hematocrit levels become normal. Chemotherapy helps lower the platelet count and suppresses production of blood elements by the marrow.

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