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The child may experience initial pain during the maneuver with rapid relief and an expected return of normal function in 10 to 15 minutes purchase acivir pills with paypal. One frac- ture induced by violently yanking a child by their arm and causing hyperextension at the elbow is called a three-point bending fracture (compression/distraction frac- ture) buy 200mg acivir pills fast delivery. There will be soft tissue swelling on physical examination generic acivir pills 200mg with amex, and a radiograph will reveal a linear lucency in the distal humerus. The patient with these symptoms who also has failure to thrive (Case 10) or bruising may represent nonac- cidental trauma for which a subdural hematoma (Case 29) should be enter- tained. And how does the physician maneuver the child’s arm for treatment of nurse- maid’s elbow? The mother gives a history of the patient’s father swinging her by her arms earlier in the day. The doctor attempts to supinate the affected arm with the elbow in flexed position. She attempts three times but fails to hear a click and the child is still in pain and holding her arm close to her body. Reattempt reduction maneuvers until a click is heard and patient can move her arm. The father states he fell asleep on the couch and when he awoke the patient was crying and lying next to the playpen in which he had been placed earlier. Which of the following is the most appro- priate next step in the management of this child? On physical examina- tion, the left shoulder is warm and tender to palpation, and has decreased range of motion. A child with nursemaid’s elbow holds the arm close to his body with the elbow flexed and forearm pronated. Treatment consists of supinating the child’s forearm with the elbow in a flexed position while applying pressure over the radial head. Initial management includes two to four attempts about 15 minutes apart in an attempt to reduce the annular ligament. Should the expected improve- ment not be seen, radiographs of the affected extremity are indicated. A 3-month-old child would not be able to climb out of a playpen to sus- tain the injuries his father stated. The next step is to perform a detailed history and physical examination, followed by a skeletal survey (full-body radiographs) to assess for old or new injuries in the infant. If further questions remain, admission to the hospital and notification to Child Protective Services are indicated. The next step is to aspirate the joint and send labora- tory tests on the joint aspirate. Passive movement of the affected arm results in pain, and the child will resist movement of the arm. His mother says he had been playing when she noticed small red spots and a large purple area on his skin. He is playful on examination, but he has multiple petechiae and pur- puric lesions on his upper and lower extremities and on his trunk. Considerations This 3-year-old has purpuric lesions and petechiae resulting from thrombocytope- nia. A peripheral blood smear is examined to identify large normal platelets, but in diminished numbers. This child has a platelet count of 20,000/mm3 and lacks evidence of active bleeding; the next step is close observation. Causes of thrombocytopenic include decreased plate- let production, platelet sequestration, or increased platelet destruction. The syndrome may have dermatologic (petechial/purpuric rash), renal (nephritis), gastrointestinal (abdominal pain, gastrointestinal bleeding, intussusception), and joint involvement (arthritis). The evidence suggests an immunologic etiology trig- gered by a preceding viral illness with subsequent development of an autoantibody directed against the platelet surface resulting in a destructive thrombocytopenia. Young children usually pres- ent with acute onset of petechiae and purpura, and often a history of a viral illness 1 to 4 weeks previously. Bleeding from the gingivae and other mucous membranes may occur if platelet levels are severely low (typically <10,000/mm3). Examination findings most often include petechiae and purpura, especially in trauma areas. If sig- nificant lymphadenopathy or organomegaly is found, other causes for thrombocytopenia are considered. Patients with severe thrombocytopenia (<20,000/mm3), extensive mucosal bleeding, severe complications (eg, massive gastrointestinal bleeds), or without a protective environment may require medical intervention. Treatment is typically not initiated and close observation alone is a well-accepted treatment option for patients with minimal or mild symptoms. Options include intravenous immunoglobulin for 1 to 2 days, intravenous anti-D therapy, or a 2- to 3-week course of systemic corticosteroids. Splenectomy may be considered in children with serious complications not responding to other therapies. After splenectomy, pneumococcal vaccine and penicillin prophylaxis are required because of risk for sepsis. Within a month of presentation, more than half of untreated children have com- plete resolution of their thrombocytopenia and up to another 30% have resolution by 6 months. Many pharmacologic agents may cause immune-mediated thrombocytopenia, including penicillins, trimethoprim-sulfamethoxazole, digoxin, quinine, quinidine, cimetidine, benzodiazepine, and heparin. She was diagnosed with a urinary tract infection 4 days ago, which is being treated with trimethoprim-sulfamethoxazole. He is nontoxic appearing, but he has palpable petechiae on his lower extremi- ties and buttocks. His right knee is mildly edematous and he can bear weight on his right leg, but complains of pain.
As a result of transmitter-receptor binding discount 200mg acivir pills with mastercard, a series of events is initiated in the postsynaptic cell discount acivir pills line, leading to a change in its behavior discount acivir pills 200 mg line. The precise nature of the change depends on the identity of the neurotransmitter and the type of cell involved. If the postsynaptic cell is another neuron, it may increase or decrease its firing rate; if the cell is part of a muscle, it may contract or relax; and if the cell is glandular, it may increase or decrease secretion. There are two basic steps in the process by which neurons elicit responses from other cells: (1) axonal conduction and (2) synaptic transmission. This is to our advantage because drugs that alter synaptic transmission can produce effects that are much more selective than those produced by drugs that alter axonal conduction. Axonal Conduction Drugs that act by altering axonal conduction are not very selective. Recall that the process of conducting an impulse along an axon is essentially the same in all neurons. As a consequence, a drug that alters axonal conduction will affect conduction in all nerves to which it has access. Because these agents produce nonselective inhibition of axonal conduction, they suppress transmission in any nerve they reach. Hence, although local anesthetics are certainly valuable, their indications are limited. Synaptic Transmission In contrast to drugs that alter axonal conduction, drugs that alter synaptic transmission can produce effects that are highly selective. In addition, for most transmitters, the body employs more than one type of receptor. Hence, by using a drug that selectively influences a specific type of neurotransmitter or receptor, we can alter one neuronally regulated process while leaving most others unchanged. Because of their relative selectivity, drugs that alter synaptic transmission have many uses. Receptors The ability of a neuron to influence the behavior of another cell depends, ultimately, on the ability of that neuron to alter receptor activity on the target cell. As discussed, neurons alter receptor activity by releasing transmitter molecules, which diffuse across the synaptic gap and bind to receptors on the postsynaptic cell. If the target cell lacked receptors for the transmitter that a neuron released, that neuron would be unable to affect the target cell. The effects of neuropharmacologic drugs, like those of neurons, depend on altering receptor activity. That is, no matter what its precise mechanism of action, a neuropharmacologic drug ultimately works by influencing receptor activity on target cells. In fact, this concept is so critical to our understanding of neuropharmacologic agents that I will repeat it: the effect of a drug on a neuronally regulated process is dependent on the ability of that drug to directly or indirectly influence receptor activity on target cells. Steps in Synaptic Transmission To understand how drugs alter receptor activity, we must first understand the steps by which synaptic transmission takes place because it is by modifying these steps that neuropharmacologic drugs influence receptor function. Step 3, Release of transmitter: in response to an action potential, vesicles fuse with the terminal membrane and discharge their contents into the synaptic gap. Step 4, Action at receptor: transmitter binds (reversibly) to its receptor on the postsynaptic cell, causing a response in that cell. Step 5, Termination of transmission: transmitter dissociates from its receptor and is then removed from the synaptic gap by (a) reuptake into the nerve terminal, (b) enzymatic degradation, or (c) diffusion away from the gap. Step 1: Transmitter Synthesis For synaptic transmission to take place, molecules of transmitter must be present in the nerve terminal. In the figure, the letters Q, R, and S represent the precursor molecules from which the transmitter (T) is made. Step 2: Transmitter Storage After transmitter is synthesized, it must be stored until the time of its release. Transmitter storage takes place within vesicles—tiny packets present in the axon terminal. Step 3: Transmitter Release Release of transmitter is triggered by the arrival of an action potential at the axon terminal. The action potential initiates a process in which vesicles undergo fusion with the terminal membrane, causing release of their contents into the synaptic gap. Each action potential causes only a small fraction of all vesicles present in the axon terminal to discharge their contents. Step 4: Receptor Binding After release, transmitter molecules diffuse across the synaptic gap and then undergo reversible binding to receptors on the postsynaptic cell. This binding initiates a cascade of events that result in altered behavior of the postsynaptic cell. Step 5: Termination of Transmission Transmission is terminated by dissociation of transmitter from its receptors, followed by removal of free transmitter from the synaptic gap. Transmitter can be removed from the synaptic gap by three processes: (1) reuptake, (2) enzymatic degradation, and (3) diffusion. In those synapses where transmission is terminated by reuptake, axon terminals contain “pumps” that transport transmitter molecules back into the neuron from which they were released (Step 5a in Fig. After reuptake, molecules of transmitter may be degraded, or they may be packaged in vesicles for reuse. In synapses where transmitter is cleared by enzymatic degradation (Step 5b), the synapse contains large quantities of transmitter-inactivating enzymes. Although simple diffusion away from the synaptic gap (Step 5c) is a potential means of terminating transmitter action, this process is very slow and generally of little significance. Effects of Drugs on the Steps of Synaptic Transmission As emphatically noted, all neuropharmacologic agents (except local anesthetics) produce their effects by directly or indirectly altering receptor activity. We also noted that the way in which drugs alter receptor activity is by interfering with synaptic transmission. Because synaptic transmission has multiple steps, the process offers a number of potential targets for drugs. In this section, we examine the specific ways in which drugs can alter the steps of synaptic transmission. Before discussing specific mechanisms by which drugs can alter receptor activity, we need to understand what drugs are capable of doing to receptors in general terms. From the broadest perspective, when a drug influences receptor function, that drug can do just one of two things: it can enhance receptor activation, or it can reduce receptor activation.
It can be classified in a variety of ways discount acivir pills 200mg without a prescription, but one useful schema divides the causes int o hypovolemic shock buy 200 mg acivir pills, cardiogenic shock cheap acivir pills 200mg mastercard, or dist ribut ive shock, usually caused by sepsis. It results from either hemorrhage or profound vomiting or diarrhea, resulting in loss of 20% to 40% of blood volume. Cardiogenic shock results from a primary cardiac insult, such as a myocardial infarct ion, arrhythmias, or end-st age heart failure such that the heart no longer pumps effectively. Both hypovolemic and cardiogenic shocks cau se a mar ked fall in car diac out put an d may app ear clin ically similar wit h tachycardia, hypotension, and cold clammy extremities. It is essential to differ- ent iat e bet ween t he t wo, however, because t he t reat ment s are markedly differ- ent. Pat ient s wit h hypovolemic shock should have flat neck veins and clear lung fields; t h ose wit h cardiogenic shock are more likely to have markedly elevated jugular veno us pressure and pulmonary edema. Tr eat ment of h ypovolemic sh ock is aggressive volume resuscit at ion, eit her wit h cryst alloid solut ion or wit h blood products as necessary. Treatment of cardiogenic shock focuses on maintaining blood pressure with dopamine or norepinephrine infusions, relief of pulmonary edema wit h diuret ics, and reducing cardiac aft erload, for example, wit h an int ra- aort ic balloon pump. Distributive shock, in cont r ast, is ch ar act er ized by an increase in cardiac output but an inability to maintain systemic vascular resistance, that is, there is inappro- priate vasodilation. Clin ically, it appears differ ent t h an the ot h er for ms of sh ock in that, despite the hypotension, the extremities are warm and well perfused, at least init ially. If sept ic shock cont inues, cardiac output falls as a consequence of myocar- dial depression, multiorgan dysfunction ensues, and intense vasoconstriction occu r s in an att empt t o maint ain blood pressure, t he so-called “c o l d p h a s e. Although distributive shock may occur in neurogenic shock as a consequence of spinal cord injury or adrenal crisis, t he most common cause is septic shock, with the most common infectious etiologies of sepsis being urinary tract infections and pneu- monia. T h e in it ial t reat ment is isot on ic fluid r esu scit at ion t o maint ain adequat e int ravascular volume. O t her cornerst ones of t herapy include broad-spect rum ant i- biotics targeted to the underlying infection or likely source of underlying infection and removal of t he infect ion source. Pat ient s often require vasopressor support (norepinephrine is the agent of choice) and mechanical ventilation to optimize tis- sue oxygenat ion. Int ravenous hydrocort isone may be administ ered t o pat ient s wit h hypotension that is refractory to fluid resuscitation and vasopressors. Early diagnosis and prompt treatment are imperative because untreated shock progresses to an irreversible point that is refractory to volume expansion and other medical therapies. H is abdomen is tender, particularly in the right lower quadrant, and acute appendicitis is diagnosed. T reat ment is undertaken to prevent upper tract infection, preterm delivery, and possible fet al loss. T h e patient in this scen ar io h as sym p t om s of an u p p er u r in ar y t r act in fec- tion, for example, pyelonephritis, and is moderately ill with nausea. She will need a 14-day course of treatment and may not be able to take oral antibiotics init ially, so hospit alizat ion and t reat ment wit h int ravenous ant ibiot ics likely will be necessary. Single-dose and 3-day regimens are useful only for acute uncomplicated cystitis in women. T h e patient is h yp o t en sive wit h sign s of left an d r igh t h ear t failu r e, that is, probably cardiogenic shock. Septic shock and adrenal crisis both are forms of distributive shock that would produce warm extremities. When septic shock is refractory to volume resuscitation with at least 30 cc isot on ic flu id p er kilogr am id eal body weigh t adm in ist r at ion, t h en ad di- tion of intravenous norepinephrine is the next step. Corticosteroids can be administ ered empirically if hypot ension is refract ory t o vasopressors. Int ra- ven o u s m o r p h in e m igh t lo wer h is b lo o d p r essu r e fu r t h er. F F P is u sed wh en the patient shows evidence of coagulopathy such as disseminated intravascu- lar coagulat ion. It re q u ire s early and aggressive intervention to prevent clinical deterioration. On physical examination, he is febrile to 103°F, tachycardic with heart rate 122 bpm, blood pressure 118/65 mm Hg, and respira- tory rate 22 bpm. He has no oral lesions, his chest is clear to auscultation, his heart rate is tachycardic but regular with a soft systolic murmur at the left sternal border, and his abdominal examination is benign. The perirectal area is normal, and digital re ct al e xamin ation is d e fe rre d, b ut h is stool is n e g ative for occult b lood. He h as a tunneled vascular catheter at the right internal jugular vein without erythema overlying the subcutaneous tract and no purulent discharge at the catheter exit site. Of note, he reports an onset of shaking chills 30 minutes after the catheter was flushed. He has no respiratory or abdominal symp- 3 toms, a clear chest x-ray, and an absolute neutrophil count of 286/ mm. H e h as a cent ral venous catheter, with a history suggest ive of possible cat heter infect ion. Most likely diagnosis: Neutropenic fever and possible infected vascular cat h et er. Next therapeutic step:A ft e r d r a w i n g b l o o d c u l t u r e s, the p a t i e n t s h o u l d u n d e r go broad-spectrum intravenous antibiotic administration, including coverage for gr am-p osit ive or gan isms su ch as Staphylococcus spp. Co n s i d e r a t i o n s This patient is being treated for a hematologic malignancy with combination che- motherapy, which has a common side effect of leukopenia and, especially, neutro- penia. Generally, the nadir of the white cell count occurs 7 to 14 days after the ch em ot h er apy. This pat ient h as neutropenia, defined as an absolute neutrophil count 3 less than 500 cells/ mm. Infection in this immunosuppressed con- dition is life threatening, and immediate antibiotic coverage is paramount. Neutro- penic patients are at risk for a variety of bacterial, fungal, or viral infections, but the most common sources of infection are gram-positive bacteria from the skin or oral cavit y or gram-n egat ive bact er ia from the bowel. Becau se of the absen ce of wh it e blood cells, the patient may not manifest the cardinal signs of infection: inflam- mation or high fever. Rapid institution of empiric antibiotic therapy is critical while attempts to find a source of infection are in progress. Approximat ely 5% t o 10% of cancer pat ient s will die of neut ropenia-associat ed infect ion.
It is often dificult to distinguish between the signs and symptoms caused by phys iologic adaptations to pregnancy and those oftrue cardiac disease 200mg acivir pills mastercard. S1 becomes louder by the end of the first trimester generic acivir pills 200 mg with visa, and 90% of pregnant women will develop an Sy Systolic ejection murmurs along the left sternal border develop in more than 90% of pregnant women purchase acivir pills paypal, and is thought to be caused by increased blood fow across the pulmonic and aortic valves. Respiratory System Because of increased hyperemia and estrogen levels, the nasopharyngeal mucosa becomes edematous and irritated. Nasal stufiness, epistaxis, and nasal polyps occur fequently during pregnancy, and resolve spontaneously postpartum. Due primarily to change in the size and shape of the chest cavity, the following alterations in lung capacities are seen: 1. Functional residual capacity-decreased 20% During pregnancy, increased levels ofprogesterone cause a state of relative hyper ventilation, resulting in a chronic respiratory alkalosis. This relatively low Pco in2 the pregnant mother is beneficial in clearing C0 from the fetal circulation. Since at mid-pregnancy the plasma volume increases more than that of red blood cell mass, there appears a transient physiologic anemia of pregnancy. A gradual decline in platelets has been observed throughout pregnancy, 3 but 98% of pregnant women will have platelet counts of > 116,000/mm • Values below this should be evaluated for causes of thrombocytopenia. Glomerular fltration rate rises as early as 5 to 7 weeks and reaches a level 50% greater than in the nonpregnant female. The altered mechanism of handling glucose in the proximal tubules during pregnancy remains to be completely understood. While the nonpregnant female excretes < 100 mg/d, in pregnancy this can reach 1 to 10 g of glucose per day. Respirator Diseases in Pregnancy Asthma exacerbations are typically slightly decreased in pregnant women with mild disease, while those with severe disease may have worse deterioration. Because of the uterine pressure on the diaphragm, there is decreased pulmonary reserve. Treatment of the asthmatic pregnant patient is identical to that of the nonpreg nant patient, beginning with 1-agonist respiratory therapy and steroids, and pro gressing to magnesium sulfate. Epinephrine is relatively contraindicated in pregnancy due to its possible vasoconstrictive efects on the uterine arteries. Influenza mortality is increased in the pregnant woman due to respiratory changes as well as the relatively immunocompromised state. Thus, obstetrical patients are one of the key groups that should receive annual infuenza immuni zation. Those women who have suspected or confirmed infuenza should promptly receive anti infuenza therapy. These agents are best begun within 2 days of the beginning of infection, and are taken for 5 days. The pregnant patient may have flminant and severe disease, and prompt admission and respiratory support should be enacted if the patient dete riorates. In a large series ofpatients with H1N1 infuenza in pregnant and postpartum women in Califoria, 10% of those with infections were hospitalized, which is 4 times higher than the general population. Airway Difculties Several anatomic changes occur throughout pregnancy such as weight gain, includ ing increase in breast size, respiratory tract mucosal edema, and capillary engorge ment ofnasal and oropharyngeal mucosaand laryngeal tissues. Decreased fnctional residual volume ofup to 50% with concomitant increase in oxygen needs can lead to rapid development of hypoxemia in the hypoventilating patient. Also, because of the risk of bronchospasm or further distortion of the airway anatomy, there may be only one good attempt to place the endotracheal tube. Ca rdiac Disease in Pregnancy Hypertensive diseases in pregnancy are common, afecting approximately 8% of obstetrical patients. These can be gestational hypertension which is isolated elevated blood pressure, preeclampsia (hypertension with proteinuria), or superimposed pre eclampsia on chronic hypertension. Preeclampsia alters the hemodynamic param eters by increasing systemic vascular resistance and decreasing intravascular volume. Thus, preeclamptic women are more sensitive to volume changes, either blood loss which can lead to hypotension, or fluid overload leading to pulmonary edema. Peripartum cardiomyopathy is a 4-chamber dilated cardiomyopathy of unknown etiology afecting women in pregnancy or postpartum. Afected patients present with congestive heart failure, and noted on chest radiograph to have a markedly enlarged cardiac silhouette. The cardiac output is below 45% and other causes of ventricu lar dysfunction are ruled out. Many cases are discovered late after onset of severe symptoms, and thus, a high index of suspicion is needed. The mainstays of treatment are digoxin, loop diuretics, afterload reduction with hydralazine and nitrates, and [-blocker use. Unless a patient is decompensating, expectant management of the preterm patient (less than 37 weeks) is advisable. The prognosis depends on recovery of left ventricular fnction, which occurs in about 50% of patients. As many as 80% of women who become pregnant again may develop congestive heart failure with future pregnancies. Liver Disease in Pregnancy Acute fatty liver of pregnancy is an extremely dangerous condition characterized by microvesicular steatosis of the liver, thought to be due to mitochondrial dysfunc tion of fatty acid oxidation, which leads to fat accumulation in hepatocytes. Liver insuficiency results, and if it is not diagnosed and promptly treated with delivery, then maternal and neonatal morbidity or mortality results. Patients present with nonspecific symptoms such as mal aise, nausea and vomiting, and possibly right upper quadrant pain. The laboratory analysis is important and usually shows elevated liver function tests and decreased glucose levels. The most common cause of sepsis is pyelonephritis, typically due to Escherichia coli, particularly caused by to 0127 subtype; however, a large number of gram-negative rods are possible etiologies. The most common cause of sepsis in the postpartum patient is post cesarean endometritis. Early diagnosis, aggressive antibiotic therapy, supportive therapy, and removal of the source of the sepsis are important. The decision ofdelivery is difficult due to the fact that the gestation may be premature; nevertheless, the pregnancy may alter the cardiovascular hemodynamics such as decreasing the venous return.