By U. Vasco. Lebanon Valley College.
For example buy cheap top avana 80mg on line, when imipramine is prescribed generic top avana 80mg without prescription, the patient should understand that the objective is to relieve neuropathic pain and not depression buy generic top avana 80 mg on line, the disorder for which this drug was originally developed discount 80 mg top avana. Under the standards, accountability for pain management is shifted from individual practitioners to the institution as a whole. Compliance is mandatory: health care organizations that fail to meet the standards will lose accreditation. Loss of accreditation would mean loss of insurance reimbursement and would disqualify teaching hospitals from offering training programs. It should be noted that the standards are not a guideline on how to treat specific kinds of pain. Rather, they focus on (1) the rights of patients to receive appropriate assessment and management of pain and (2) ways for institutions to establish a formalized, systematic approach to pain management that involves interdisciplinary teams whose members have clearly identified responsibilities. Specific provisions include the following: • Institutions must recognize assessment and management of pain as a right of all patients. Many of the drugs considered here are discussed in other chapters, so discussion in this chapter is limited to ophthalmologic applications. Drugs for Glaucoma Glaucoma refers to a group of diseases characterized by a decrease in peripheral vision secondary to optic nerve damage. The most common forms of glaucoma are primary open-angle glaucoma and acute angle-closure glaucoma. Of the 120,000 Americans blinded each year by glaucoma, 90% could have saved their sight with timely treatment. Unfortunately, many afflicted persons are unaware of their condition: of the 4 million Americans with glaucoma, only 50% are diagnosed. From there it circulates around the iris into the anterior chamber and then exits the anterior chamber through the trabecular meshwork and canal of Schlemm. Pathophysiology and Treatment Overview P a t i e n t E d u c a t i o n Glaucoma • It is important to take the prescribed medications according to schedule. If days are skipped or if prescriptions are not refilled, loss of vision may occur. Allow at least 15 minutes to elapse between administration and insertion of the lenses. Management is usually initiated by specialists; however, primary care providers often play a role in ongoing monitoring and follow-up of patients taking these medications. Other options —cholinergic drugs and carbonic anhydrase inhibitors—are considered second- line choices. All of the antiglaucoma drugs are available for topical administration, which is the preferred route. Because all of these drugs are applied topically, systemic effects are relatively uncommon. Nonetheless, serious systemic reactions can occur if sufficient absorption takes place. Angle-Closure Glaucoma Angle-closure glaucoma is precipitated by displacement of the iris such that it covers the trabecular meshwork, thereby preventing exit of aqueous humor from the anterior chamber. This disorder is referred to as angle-closure or narrow-angle glaucoma because the angle between the cornea and the iris is greatly reduced (Fig. A, Note that the angle between the iris and cornea is open in open-angle glaucoma, permitting unimpeded outflow of aqueous humor through the canal of Schlemm and trabecular meshwork. B, Note that the angle between the iris and cornea is constricted in angle-closure glaucoma, thereby blocking outflow of aqueous humor through the canal of Schlemm and trabecular meshwork. Treatment consists of drug therapy (to control the acute attack) followed by corrective surgery. A combination of drugs (osmotic agents, short-acting miotics, carbonic anhydrase inhibitors, topical beta-adrenergic blocking agents) is employed to suppress symptoms. Drugs Used to Treat Glaucoma Beta-Adrenergic Blocking Agents Actions and Use in Glaucoma Five beta blockers—betaxolol, carteolol, levobunolol, metipranolol, and timolol —are approved for use in glaucoma. These agents cause minimal disturbance of vision and are considered first-line drugs for glaucoma, although prostaglandin analogs are becoming favored. Beta blockers, in combination with other drugs, are also employed for emergency management of acute angle- closure glaucoma. Local effects are generally minimal, although patients commonly complain of transient ocular stinging. Beta blockers occasionally cause conjunctivitis, blurred vision, photophobia, and dry eyes. Constriction2 of the bronchi can occur with beta -selective antagonists as well as with1 “nonselective” beta-adrenergic blockers—although the risk is greatest with the nonselective agents. This drug is preferred to other beta blockers for patients with asthma or chronic obstructive pulmonary disease. Prostaglandin Analogs Four prostaglandin analogs are approved for topical therapy of glaucoma. P ro t o t y p e D r u g s Drugs for the Eye Beta Blockers Betaxolol (beta selective)1 Timolol (blocks beta and beta receptors)1 2 Alpha-Adrenergic Agonists Brimonidine Prostaglandin Analogs Latanoprost Angiogenesis Inhibitors Ranibizumab Latanoprost is generally well tolerated, and systemic reactions are rare. The most significant side effect is a harmless heightened brown pigmentation of the iris, which is most noticeable in patients whose irides are green-brown, yellow- brown, or blue/gray-brown. Heightened pigmentation stops progressing when latanoprost is discontinued but does not usually regress. Topical latanoprost may also increase pigmentation of the eyelid and may increase the length, thickness, and pigmentation of the eyelashes. Other side effects include blurred vision, burning, stinging, conjunctival hyperemia, and punctate keratopathy. Other Prostaglandin Analogs In addition to latanoprost, three other topical prostaglandins are approved for topical therapy of glaucoma. In clinical trials, these agents were at least as effective as timolol, a representative beta blocker. Interestingly, one drug— travoprost—was more effective in blacks than in nonblacks. Like latanoprost, these prostaglandins can cause a gradual increase in brown pigmentation of the iris, which may be irreversible. In addition, these drugs can increase pigmentation of the eyelid and growth of the eyelashes. In fact, bimatoprost, marketed as Latisse, is used for the specific purpose of increasing eyelash length, darkness, and thickness. With prostaglandins used to treat glaucoma, the most common adverse effect is ocular hyperemia (engorgement of ocular blood vessels). Less commonly, these drugs cause blurred vision, eye discomfort, ocular pruritus, conjunctivitis, dry eye, light intolerance, and tearing. The other agent—brimonidine—has emerged as a first-line drug for long-term therapy. This possibility arises from the ability of alpha agonists to protect2 neurons from injury caused by ischemia. The most common adverse effects are dry mouth, ocular hyperemia, local burning and stinging, headache, blurred vision, foreign body sensation, and ocular itching. In contrast to apraclonidine (see later), brimonidine can cross the blood-brain barrier and hence can cause drowsiness, fatigue, and hypotension. Accordingly, at least 15 minutes should elapse between drug administration and lens installation. Side effects include headache, dry mouth, dry nose, altered taste, conjunctivitis, lid reactions, pruritus, tearing, and blurred vision. Apraclonidine does not cross the blood-brain barrier and thus does not promote hypotension. Benefits and adverse effects are about equal to those seen when the two drugs are applied separately. Formulations and dosages for the alpha agonist and the alpha agonist/beta blocker combination are shown1 2 in Table 84. Effects on the Eye By stimulating cholinergic receptors in the eye, pilocarpine produces two direct effects: (1) miosis (constriction of the pupil secondary to contraction of the iris sphincter) and (2) contraction of the ciliary muscle (an action that focuses the lens for near vision). In angle-closure glaucoma, contraction of the iris sphincter pulls the iris away from the pores of the trabecular meshwork, thereby removing the impediment to aqueous humor outflow. Therapeutic Uses Although used widely in the past, pilocarpine is now considered a second-line drug for open-angle glaucoma. Pilocarpine can also be used for emergency treatment of acute angle-closure glaucoma. Contraction of the ciliary muscle focuses the lens for near vision; corrective lenses can provide partial compensation for this problem. Occasionally, sustained contraction of the ciliary muscle causes retinal detachment. Constriction of the pupil, caused by contraction of the iris sphincter, may decrease visual acuity. Stimulation of muscarinic receptors throughout the body can produce a variety of responses, including bradycardia, bronchospasm, hypotension, urinary urgency, diarrhea, hypersalivation, and sweating. Pilocarpine solutions have a relatively short duration of action and must be administered more frequently than the gel. The basic pharmacology of echothiophate and other cholinesterase inhibitors is discussed in Chapter 12. Effects on the Eye Cholinesterase inhibitors inhibit breakdown of acetylcholine by cholinesterase and thereby promote accumulation of acetylcholine at muscarinic receptors. However, because of concerns about adverse effects, the drug is not a first-choice agent. Rather, it is reserved for patients who have responded poorly to preferred medications (e. However, of much greater concern is the association between long-acting cholinesterase inhibitors and development of cataracts. Absorption of echothiophate into the systemic circulation can produce typical parasympathomimetic responses, including bradycardia, bronchospasm, sweating, salivation, urinary urgency, and diarrhea. Preparations, Dosage, and Administration Echothiophate iodide [Phospholine Iodide] is supplied as a powder for reconstitution to solution. Carbonic Anhydrase Inhibitors: Topical Dorzolamide Dorzolamide [Trusopt] was the first carbonic anhydrase inhibitor available for topical administration. The most common side effects are ocular stinging and bitter taste immediately after dosing. Between 10% and 15% of patients experience allergic reactions, primarily conjunctivitis and lid reactions. In contrast to systemic carbonic anhydrase inhibitors, dorzolamide does not produce acidosis or electrolyte imbalance. Dorzolamide is also available in a fixed-dose combination with timolol, marketed as Cosopt. Formulations and dosages for these products as well as other carbonic anhydrase inhibitors shown in Table 84.
However discount 80 mg top avana amex, optimal glucose control can only be achieved if the patient is actively involved in his or her own therapy best top avana 80 mg. Complications of Insulin Treatment Hypoglycemia Hypoglycemia (blood glucose below 70 mg/dL) occurs when insulin levels exceed insulin needs generic top avana 80mg with amex. Imbalance between insulin levels and insulin needs can also result from reduced intake of food quality 80mg top avana, vomiting and diarrhea (which reduce absorption of nutrients), excessive consumption of alcohol (which promotes hypoglycemia), unusually intense exercise (which promotes cellular glucose uptake and metabolism), and childbirth (which reduces insulin requirements). P a t i e n t E d u c a t i o n Hypoglycemia Patients with diabetes and their families should be familiar with the signs and symptoms of hypoglycemia. Establishing whether patients are experiencing hypoglycemia and whether they recognize hypoglycemic symptoms is recommended as a critical component of an encounter with a patient with diabetes. When glucose levels fall rapidly, activation of the sympathetic nervous system occurs, resulting in tachycardia, palpitations, sweating, and nervousness. Rapid treatment of hypoglycemia is mandatory: if hypoglycemia is allowed to persist, irreversible brain damage or even death may result. In conscious patients, glucose levels can be restored with a fast-acting oral sugar (e. However, if the swallowing reflex or the gag reflex is suppressed, nothing should be administered by mouth. Some prescribers recommend that patients keep glucagon on hand, too —particularly people on insulin therapy. In some patients, hypoglycemia occurs without producing the symptoms noted previously. As a result, the patient remains unaware of hypoglycemia until blood sugar has become dangerously low. Hypoglycemia unawareness is a particular problem among patients practicing tight glucose control. This is because as patients experience more frequent hypoglycemia, they start to have diminished symptoms over time. The risk for dangerous hypoglycemia can be minimized by frequently monitoring blood glucose. Additionally, current recommendations state that treatment goals should be temporarily loosened (such as for several weeks) for people experiencing hypoglycemia unawareness so that they can regain hypoglycemia awareness. The most definitive diagnosis is made by measuring plasma glucose levels: in hypoglycemic coma, glucose levels are very low. Hence, in addition to lowering blood levels of glucose, insulin can lower blood levels of potassium. However, if insulin dosage is excessive, clinically significant hypokalemia can result. Effects on the heart are of greatest concern: hypokalemia can reduce contractility and can cause potentially fatal dysrhythmias. Lipohypertrophy (accumulation of subcutaneous fat) can occur when insulin is injected too frequently at the same site. These reactions develop rapidly and are characterized by the widespread appearance of red and intensely itchy welts. If severe allergy develops in a patient who nonetheless must continue insulin use, a desensitization procedure can be performed. This process entails giving small initial doses of human insulin, followed by a series of progressively larger doses. Drug Interactions Hypoglycemic Agents Drugs that lower blood glucose levels can intensify hypoglycemia induced by insulin. Among these drugs are sulfonylureas, glinides, and alcohol (used acutely or long term in excessive doses). When these drugs are combined with insulin, special care must be taken to ensure as best as possible that blood glucose does not fall too low. When these agents are combined with insulin, insulin dosage may need to be increased. Beta-Adrenergic Blocking Agents Beta blockers can delay awareness of and response to hypoglycemia by masking signs that are associated with stimulation of the sympathetic nervous system (e. Noninsulin Medications for the Treatment of Diabetes The noninsulin medications for the treatment of diabetes fall into two major groups: oral drugs and noninsulin injectable drugs. Liraglutide (liraglutide, [Victoza] exenatide extended- Albiglutide release, and [Tanzeum] albiglutide) Amylin Mimetics Pramlintide [Symlin] Delays gastric emptying and suppresses glucagon secretion, Hypoglycemia decreasing the postprandial rise in glucose Nausea Injection-site reactions * Commonly known as glibenclamide outside the United States. In the past, the oral agents were used only after a program of diet modification and exercise had failed to yield sufficient glycemic control. Today, one oral agent—metformin—is usually started immediately after type 2 diabetes has been diagnosed. Some of them—notably the sulfonylureas, and glinides (collectively referred to as “insulin secretagogues”) —actively drive blood glucose down by increasing insulin release from beta cells of the pancreas. This distinction is not just academic: if taken when blood glucose is normal or low, agents that drive glucose down can cause hypoglycemia. Hypoglycemia is not a large risk with the drugs that simply impair the postprandial rise in blood glucose. Typically, metformin is started immediately after the diagnosis of type 2 diabetes. Mechanism of Action Metformin lowers blood glucose and improves glucose tolerance in three ways. And third, it sensitizes insulin receptors in target tissues (fat and skeletal muscle) and thereby increases glucose uptake in response to whatever insulin may be available. In contrast to the sulfonylureas (see later), metformin does not stimulate insulin release from the pancreas. As a result, metformin does not actively drive blood glucose levels down and hence poses little if any added risk for hypoglycemia when used alone. Pharmacokinetics After oral dosing, metformin is slowly absorbed from the small intestine. Hence, in the event of renal impairment, metformin can accumulate to toxic levels. In the past, treatment was reserved for patients who had not responded adequately to a program of diet modification and exercise. Today, however, treatment is usually begun as soon as type 2 diabetes is diagnosed. When metformin is used as a component of combination therapy, the combination lowers blood sugar more effectively than either drug alone—which is to be expected because other available agents act through different mechanisms. In contrast, drugs that actively lower blood glucose, such as the sulfonylureas, can drop a normal or slightly low blood glucose into clinically significant hypoglycemia. Participants were randomly assigned to one of three protocols: (1) intensive lifestyle changes with the aim of reducing body weight by 7% through moderate exercise (e. However, benefits were limited primarily to younger patients and to those who were most overweight; the drug was relatively ineffective in older patients and those less overweight. It must be stressed, however, that metformin is not a substitute for diet and exercise. For decades, insulin was considered the preferred, if not the only, antidiabetic drug for managing diabetes during pregnancy, whether the mother had type 1 or type 2 diabetes. Recent clinical studies have compared metformin with insulin in pregnant women with type 2 diabetes. Multiple outcomes were assessed, including glycemic control in the mother, and blood glucose and Apgar scores in the neonate. Outcomes with metformin were essentially the same as those with insulin, the traditional agent for managing gestational diabetes— suggesting that metformin may become an acceptable alternative for many women. Symptoms include irregular periods, anovulation, infertility, acne, and hirsutism. Metformin treatment increases insulin sensitivity and decreases insulin levels, which, through an indirect mechanism, lowers androgen levels. The net result is improved glucose tolerance, improved ovulation, and increased pregnancy rates. Side Effects The most common side effects are decreased appetite, nausea, and diarrhea. Metformin decreases absorption of vitamin B12 and folic acid and can thereby cause deficiencies of both. Deficiency of B12, in turn, can contribute to peripheral neuropathy, a common long-term consequence of diabetes. However, there is no proof (yet) that metformin actually makes diabetic neuropathy worse. Likewise, there is no current recommendation about prescribing vitamin B12 for patients who are taking the drug. As a result, metformin is considered a “weight-neutral” antidiabetic drug, in contrast to several other antidiabetic drugs that tend to increase weight (“weight-positive” drugs). Appetite suppression and weight loss in response to metformin can occur both in the presence and absence of nausea, indicating that reduced food intake because of metformin-induced nausea is not the only reason for weight loss in those patients who lose weight. B l a c k B o x Wa r n i n g : M e t f o r m i n Severe metabolic acidosis can occur with accumulation of metformin. Metformin and other biguanides inhibit mitochondrial oxidation of lactic acid and can thereby cause lactic acidosis. Fortunately, lactic acidosis is rare (about 3 cases/100,000 patient-years) when metformin is used at recommended doses in patients with good renal function. However, in patients with renal insufficiency, metformin can rapidly accumulate to toxic levels. In addition, metformin must be avoided in patients who are prone to increased lactic acid production. Among these are patients with liver disease, severe infection, or a history of lactic acidosis; patients who consume alcohol to excess; and patients with shock and other conditions that can result in hypoxemia. All patients taking metformin should be informed about early signs of lactic acidosis—hyperventilation, myalgia, malaise, and unusual somnolence—and instructed to report these to the prescriber. If lactic acidosis is diagnosed, hemodialysis can correct the condition and remove accumulated metformin. Like metformin, alcohol can inhibit breakdown of lactic acid, and can thereby intensify lactic acidosis caused by metformin. To minimize risk, patients should avoid consuming alcohol in excess, whether acutely or long term. Cimetidine [Tagamet], a histamine-2 (H ) blocker used to reduce gastric acidity,2 can increase the risk for lactic acidosis. Accordingly, if an H blocker is2 indicated, another member of the family should be used because cimetidine is the only H blocker that poses this risk. Intravenous radiocontrast media that contain iodine pose a risk for acute renal failure, which could exacerbate metformin-induced lactic acidosis. To reduce risk, patients should discontinue metformin 1 to 2 days before elective radiography. Metformin can then be resumed 48 hours after the procedure, provided laboratory tests show that renal function is normal. In addition, the drug is available in several fixed-dose combinations with other drugs for type 2 diabetes mellitus (see later).
A: As follows: Causes: • Sudden withdrawal of steroid (common cause purchase top avana 80mg, if patient is on steroid for long time) order 80mg top avana overnight delivery. Initially hydrocortisone 20 mg 8 hourly cheap top avana 80mg with mastercard, reducing to 20 to 30 mg in divided doses for few days (then original replacement therapy should be given) discount 80 mg top avana visa. Remember the following: • In severe hyponatraemia (,125 mmol/L), hypertonic saline is unnecessary. No extra treatment is usually necessary, but occasionally requires specifc therapy. Site Primary involvement of adrenal Cause in pituitary or prolonged use of steroid gland 2. If Marfan’s syndrome is suspected, then see the following points: • Measure the height of the patient (from crown to heel). If Klinefelter’s syndrome is suspected, then see the following points: • Gynaecomastia. A: It is a chromosomal abnormality in which there is an extra X-chromosome associated with hypogonadism (due to small testis). It is characterized by: • Tall stature (eunuchoid body proportion: Arm span is greater than height and leg is more long, lower extremity is greater than upper extremity). A: Due to increased oestradiol levels and increased oestradiol testosterone ratio. Physical examination: • Height and weight chart (if height is below third percentile, it is considered as short stature). A: After exclusion of systemic disease, following investigations should be done: 1. Chronic systemic disease: • Cardiac—congenital cyanotic heart disease (Fallot’s tetralogy). Skeletal dysplasia: • If there is short limb and normal trunk, may be due to achondroplasia. A: It is defned as short stature in which height of a person is much below than the normal, according to the chronological age. Usual cases are: • Diabetic foot (page 80) • Leg ulcer (page 74) • Diabetic amyotrophy (page 85) • Lipodystrophy of thigh (page 87) • Necrobiosis lipoidica diabeticorum (page 88) • Diabetic neuropathy (page 580) • Diabetic retinopathy (page 864). Examine the neck and axilla for acanthosis nigricans (associated with insulin resistance). Look for dehydration (in diabetic ketoacidosis) and sweating (in hypoglycaemia) or oedema (diabetic nephropathy). Look for any obvious muscle wasting (in thigh called diabetic amyotrophy) or joint deformity (Charcot’s joint) and Dupuytren’s contracture or trigger fnger. Also in lower limbs, look for calluses, nail change, ankle refex and foot deformities such as hammer or claw toes. Feel the peripheral pulses (reduced or absent in atherosclerosis), look for fxed heart rate or loss of sinus dysrhythmia (autonomic neuropathy) and auscultate carotid arteries (for bruit in atherosclerosis). Inspection: • Necrobiosis lipoidica diabeticorum (central yellow scar with surrounding red margin, found over the shins, due to atrophy of subcutaneous collagen). Palpation: • Temperature (may be cold and blue due to peripheral vascular disease and associated skin atrophy or absent pulses). Perform neurological examination of lower limbs to see peripheral neuropathy (see in chapter ‘Neurology’ page 648). Remember the following points: • Random means without regard to time since the last meal. The patient is advised for weight reduction of about 5 to 10% of their body weight, regular exercise and follow-up. A: It means blood glucose is usually normal, but may be high under certain stressful conditions (such as pregnancy, infection, obesity, stress or drugs like steroid, thiazide diuretics). This leads to irregular and unpredictable hyperglycaemia, frequently with ketosis and some- times serious hypoglycaemia. It may be caused by gastrointestinal absorption problems including delayed stomach emptying (gastroparesis), drug interactions, problems with insulin absorption or hormonal malfunction. Other features are hyperinsulinaemia, microalbuminuria, elevated fibrinogen and plasminogen activator inhibitor 1, plasma uric acid and increased sympathetic activity. Microvascular: - Neuropathy: Peripheral neuropathy (sensory, motor or mixed), mononeuritis multiplex, mononeuropathy, autonomic neuropathy. History Excess insulin, but no or insuffcient food Too little or no insulin but there may be intake, heavy exercise concurrent infection or digestive disturbance 2. Slow onset, patient has ill health for Patient is in good health prior to this several days 3. Symptoms Weakness, tremor, sweating, palpitation, Excessive thirst, polyuria, dehydration, hunger, occasional vomiting from depot vomiting, air hunger, abdominal pain insulin 4. Blood • Glucose Hypoglycaemia Hyperglycaemia • Bicarbonate Normal Reduced • pH Normal Low (metabolic acidosis) • Acetone Normal High 7. A: It is defned as any degree of glucose intolerance with the onset or frst recognition during pregnancy. More than 50% women ulti- mately develop diabetes in the next 20 years and this is linked with obesity. As a result, foetal islet cells secrete excess insulin, which may cause neonatal hypoglycaemia). It is due to persistent maternal hyperglycaemia leading to foetal hyperglycaemia and prolonged foetal hyperin- sulinism. Insulin defciency is partial, some en- dogenous insulin is present, which is suffcient to inhibit hepatic ketogenesis, but insuffcient to control hyperglycaemia. Glucose infusion should be adjusted to maintain between 250 to 300 mg/dL in order to reduce the risk of cerebral oedema. Once asked to examine the abdomen in relation to nephrology, very likely fndings are: • Unilateral renal mass (which may be due to renal cell carcinoma or hydronephrosis). Once a renal mass or suspicion of any renal disease is present, examiner may ask ‘What relevants do you like to see? After fnishing the physical examination, examiner may ask, ‘Do you like to perform any bedside investigation? My diagnosis is Renal mass (mention right or left), which may be due to (causes of unilateral renal mass): • Renal cell carcinoma (in elderly) or Wilms tumour (in children). My diagnosis is Bilateral renal mass, which may be due to (causes of bilateral renal mass): • Polycystic kidney disease. It is rare and associated with hepatic fbrosis, usually fatal in the frst year due to hepatic or renal failure. Other features: polycythaemia (due to increased erythropoietin secretion), renal stone in 10% cases (associated with uric acid, which is radiolucent), renal neoplasm rarely. A: As follows: • Cystic liver in 30% (common in infantile type), hepatic dysfunction is rare. A: It is rare, inherited as autosomal recessive and is associated with cyst in other organs and hepatic fbrosis. It is fatal in the frst year of life, death is due to renal failure or hepatic failure. A: Renal cell carcinoma (or hypernephroma) is an adenocarcinoma arising from proximal tubular epithelial cells. Haemorrhage and necrosis give the cut surface a characteristic mixed golden yellow and red appearance. In von Hippel–Lindau syndrome, inherited as autosomal dominant, there may be bilateral renal cyst, renal adenoma and renal cell carcinoma. The patient may be asymptomatic in 50% cases, detected incidentally on routine investigation. Other features: • In 20% cases, pyrexia of unknown origin may be the only manifestation. Carcinoma of left kidney may spread along the left renal vein, which may obstruct the left testicular vein leading to left sided varicocele. Blood borne metastasis to any distant organ may occur (commonly lung, bone and brain). Q:If the patient has fever with unilateral renal mass, what other diagnosis is possible? A: Due to bony metastasis or secretion of parathormone like substance by the tumour. Surgery: • Radical nephrectomy including removal of peri-renal fascial envelope and ipsilateral para-aortic lymph nodes should be done, if possible (it should be done even if metastasis is present, as it reduces the systemic features and regresses metastasis). Prognosis: 5 year survival rate is 60 to 70%, if tumour is confned to the renal parenchyma, 15 to 35%, if there is lymph node involvement and 5%, if there is distant metastasis. Treatment: • In early stage (stage 1 and 2): Nephrectomy followed by chemotherapy (vincristine, dactinomycin, doxorubicin). Presentation of a Case: • There is a mass in right (or left) iliac fossa, 5 3 5 cm, non-tender, round in shape, surface is regular, with clear margin. Donor renal vessels are anastomosed with recipient’s exter- nal or internal iliac artery and vein. Q:Is there any bad effect of repeated blood transfusion before kidney transplantation? But pre-treatment with multiple transfusions from donor tends to increase graft survival (in contrast to bone marrow transplantation). Absolute: • Active malignancy: A period of at least 2 years of complete remission is recommended for most tumours. Relative: • Age: While practice varies, transplants are not routinely done to children (,1 year) or older people (. A: combination of: prednisolone plus cyclosporine or tacrolimus plus azathioprine or mycophenolate mofetil or sirolimus or everolimus. Acute tubular necrosis: It is the commonest cause of cadaveric graft dysfunction (40 to 50%), associated with worse long term outcome and increases risk of graft rejection. Technical failures: Occlusion or stenosis of arterial anastomosis, occlusion of venous anastomosis and urinary leaks. Post-transplantation lymphoproliferative disorder: Epstein Barr virus associated malignancies (such as lymphoma) are common in patients who receive biological agents and in children. A: As follows: Survival in transplant from living donor: • 1 year survival 85 to 90%. Survival in transplant from cadaver donor: • 96% patient survival and 93% graft survival at 1 year. Presentation of a Case: • The patient is grossly oedematous, face is puffy with baggy eyelids, pitting oedema is present. A: I want to examine the abdomen to see ascites, also chest to see any pleural effusion (which may be bilateral). Red cells and red cell casts are absent (also urine sugar to exclude diabetic nephropathy). Other investigations: according to history and suspicion of cause • Blood sugar (to exclude diabetic nephropathy).
Fascial disr upt ion top avana 80mg visa, separ at ion of the fascia but n ot the p er it on eu m cheap 80mg top avana with visa, occu rs in about 1% of all abdominal surgeries top avana 80 mg mastercard, and about 0 discount top avana 80mg line. It is more common with vertical incisions, obesity, intra-abdominal distension, diabe- tes, exposure to radiation, corticosteroid use, infection, coughing, and malnutrition. This condition often presents as profuse drainage from the incision 5 to 14 days aft er surgery. Evi s cerat i o n is d efin ed as pr ot r u sion of bowel or oment u m t h r ou gh the in cision, wh ich connot es complet e separat ion of all layers of the wound. This condit ion car- ries a significant mortality due to sepsis, and is considered a surgical emergency. When encountered, a sterile sponge wet with saline should be placed over the bowel, and the patient taken to the operating room. An ad dit ion al d ose is given for pr olon ged op en abd om in al cases ( > 4 h ou r s) or if the est imat ed blood loss exceeds 1500 mL. For penicillin allergic individuals, a combination of clindamycin and gent amicin is a reasonable choice. Antibiotics should be given for clean-contaminated surgeries such as hysterectomies (because of entry into the vagin al ar ea) ; h o wever, an t ib io t ic p r o p h ylaxis is n o t given fo r clean u n co m p licat ed cases (n o ent r y int o vagin al or ut er u s) su ch as lapar oscopic ooph or ect omy. H air on the skin should not be rout inely removed, and if required, t hen elect ric clippers rat her than razors should be used immediately before the incision. The surgeon is concerned that it may represent lymph at ic drainage versus a fist ula from the urinary t ract. Which of the following studies of the fluid would most likely help to differ- ent iat e bet ween t hese t wo ent it ies? D iabet es is associat ed wit h an in cr eased r isk for fascial separ at ion becau se it is more difficult for wounds t o h eal in pat ient s wit h this disease. T h e int eg- rity of blood vessels is disrupted in a wound; this, along with the fact that diabetics typically have poor blood circulation, makes it more difficult to ade- quately perfuse the wounded area (blood contains the necessary clotting fac- tors and immunoglobulins required to heal a wound and prevent infection). A vert ical incision as opposed t o a t ransverse incision is associat ed wit h a great er risk of fascial disruption. Addison disease is a state of hypocortisolism, whereas Cushing disease is a state of hypercortisolism. Since increased cortisol levels are associated wit h immunosuppression, wound dehiscence would be more likely t o occur in Cush ing disease, not Addison disease. Fascial breakdown (disruption) is not usually due to suture breakage or knot slippage, but rather due to the suture tearing through the fascia. It is more common with vertical incisions, obesity, intra-abdominal distension, diabetes, exposure to radiation, corticosteroid use, infection, coughing, and malnutrition. Fascial disrupt ion and eviscerat ion t ypically occur bet ween 5 and 14 days postoperatively. Fluid may appear to be serous and can be clinically indistinguishable between urine and peritoneal fluid. A broad-spectrum antimicrobial agent is recommended, wit h wet -to-dry dressing changes. The wound can be allowed t o close secondarily or be approximat ed after several days. O bserva- tion in the face of infection would not be the best management and may lead to septicemia. Ointments and oral antibiotic therapy are not sufficient treat- ment options until the drainage is removed. Because the ut er us and vagina are not ent ered, and t h ere is no over t infec- tion, no prophylactic antibiotics are required. If the patient were penicillin allergic, t hen clindamycin and gent amicin should be given. A u rin e cu lt u re p e rfo rm e d 1 m o n t h p re vio u sly wa s n e g a t ive. Her blood pressure is 130/80 mm Hg, her heart rate is 80 b e ats p er minute, and her temp erature is 99°F (37. T h ere is no urge component, and no delay from the Valsalva maneuver to the loss of urine. Physical examination finding: H ypermobile urethra, cystocele, loss of urethro- vesical an gle, o r p o sit ive co u gh st r ess t est. Best initial treatment: Lifestyle modifications, Kegel exercises, and bladder training. Know that the cystometric examination can be used to distinguish between the two etiologies. Co n s i d e r a t i o n s This patient’s history is very typical for genuine stress incontinence. There is no urge component or a delay from cough, as t hese findings would be consist ent wit h urge incont inence. There is no evidence of diabetes or a neuropathy, making overflow incontinence unlikely. In patients with urge incontinence, or mixed symptoms (loss of urine with Valsalva and urge to void), cystometric examination can be helpful to differentiate bet ween gen u in e st r ess an d u r ge in con t in en ce. An accu r at e d iagn osis is imp or t ant, sin ce the therapies for these two conditions are very different, and surgical therapy may actu- ally worsen urge incont inence. With genuine stress urinary incontinence, initial treatment usually entails pel- vic flo or st r en gt h en in g exer cises, called Kegel exer cises. If t h ese are u n su ccessfu l, then options for treatment include pessaries or surgical management. Surgical manage- ment focuses on restoring urethral support through various methods (suburethral slings, ret ropubic colposuspension). Retropubic colposuspension (Burch procedure) involves suspending the vaginal wall adjacent t o t he proximal uret h ra and bladder neck t o a ligament (Cooper ’s ligament ) next to the pubic bone. Today, the midurethral sling procedures are the most popular methods to address this issue. If a patient is a poor surgical candidate and does not desire pessary manage- ment, then urethral bulking agents that aim to approximate urethral mucosa may be used. This is often associated wit h diabetes mellitus, spinal cord injuries, or lower motor neuropathies. Pessaries support the pelvic st ruct ures, and some compr ess the u r et h r a. T h ey are u sefu l for women wh o do not want or cannot h ave surgery t o correct t h eir incont inence. The bladder and proximal uret hra are normally int ra- abdominal in posit ion, t hat is, above t he pelvic diaph ragm. In this sit uat ion, a Va ls a lva m a n eu ver t r a n s m it s p r es su r e t o b o t h the b la d d er a n d p r o xim a l u r et h r a so t hat cont inence is maint ained. In the normal anatomic situat ion, t he uret hral pressure exceeds the bladder pressure, and also the pelvic diaphragm supports the bladder and urethra. Me c h a n is m s o f In c o n t in e n c e Genuine Stress Incontinence: Following trauma and/ or other causes of weakness of the pelvic diaphragm (such as childbearing), the proximal urethra may fall below the pelvic diaphragm. W hen the bladder pres- sure equals or exceeds t he maximal uret h ral pressure, urinary flow occurs. Because this is a mechanical problem, the patient feels no urge to void, and the loss of urine occurs simultaneously with coughing. Urethropexy replaces the proximal urethra and urethrovesical junction back to its intra-abdominal position (Figure 35– 1). More recently, narrow strips P A P Pe lvic diaphragm B P Cystourethrocele (proxima l ure thra below intra- a bdomina l cavity) C Figure 35–1. No rm a lly, a Va lsa lva m a n e u ve r ca u se s the in cre a se d in t ra -a b d o m in a l p re ssu re (P) t o b e t ran sm it - ted equally to the bladder and urethra (A). Wit h g e n u in e st re ss u rin ary in co n t in e n ce, the p roxim al urethra has fallen outside the abdominal cavity (B) so that the in t ra -a b d o m in a l p re ssu re n o lo n g e r is transferred to the proximal urethra, leading to incontinence. Notethatthehookedapplicatorinstrument is u se d to p ass t hroug h the ob turator foramen, and then tension is ad juste d. These procedures act as a hammock to support the urethra, and also act to compress the urethra somewhat. These include various tension-free vaginal or obturator tape pro- cedu r es, an d ou t com es are favor able as comp ar ed t o u r et h r op exy ( Figu r e 35– 2). Because of the minimally invasive nature of these procedures and shorter operating times, they have gained popularity. Urge Incontinence: With uninhibited spasms of the detrusor muscle, the blad- der pressure overcomes the urethral pressure. Dysuria and/ or the urge to void are prominent symptoms, reflect ing the bladder spasms. Somet imes, coughing or sneezing can provoke a bladder spasm, so t hat a delay of several seconds is not ed before urine loss. Overflow Incontinence: W ith an over distended bladder, coughing will increase the bladder pressure and eventually lead to dribbling or small loss of urine. Wo r k - Up The history, physical examination, urinalysis, and post void residual are part of the init ial evaluat ion of urinary incont inence. Lifest yle modificat ions include weight loss, diet ary ch anges (less caffein e/ alcoh ol), avoidin g con st ipat ion, an d smoking cessat ion. Note: A combined stress and mixed incontinence is probably the most common type of incontinence encountered; these patients will have symptoms of both stress and urge. Which of the following is the best method to diagnose the etiology of urinary incontinence? Neurological profile of the sacral nerves Match the following sin gle b est t h er ap y ( A-G ) that will m ost likely h elp in the clin i- cal situat ion described (35. P l a c e m e n t o f a n a r t i f i c i a l u r e t h r a l s p h i n c t e r G. She feels as t h ou gh sh e n eeds t o void, but can n ot make it t o the rest room in t ime. She notes uri- nary loss six to seven times a day concurrently with coughing or sneezing. Post operat ively, the pat ient is not ed t o be voiding but “feels like the bladder is still full. Place a Foley catheter and discharge the patient with catheter if second voiding trial fails. This patient likely has a vesicovaginal (between bladder and vagina) fis- tula from the surgery. If the leakage is slow, sometimes a t ampon is placed into the vagin a an d r em oved aft er 3 0 t o 6 0 m in u t es. C o n st an t wet n ess aft er a p elvic operation suggests a fistula, such as vesicovaginal fistula, which is best treated with surgical repair, since it is an anatomic problem. The operation would include excision of the fis- tulous tract which usually may be infected or weakened, and then closure of the opening.