U. Osmund. Covenant College.

Chapter 5: Disorders of the liver 195 Inflammation of the portal tracts with spotty inflam- disease generic epivir-hbv 100 mg without prescription medicine bow wyoming, galactosaemia order epivir-hbv 150mg free shipping medications you cant take while breastfeeding, cystic fibrosis, Wilson’s disease mation in the parenchyma of the lobules, but there is and drugs. Pathophysiology Complications All the liver functions are impaired (bilirubin meta- Cirrhosis is the most common complication. There is bolism, bile salt synthesis, specialised protein synthesis, increased risk of hepatocellular carcinoma in patients detoxification of hormones, drugs and toxins). Femini- Investigations sation in males and amenorrhea in females are common Chronic hepatitis is diagnosed by a combination of per- in alcoholic liver disease and haemochromatosis due to sistently abnormal liver function tests and the findings alterations in the hypothalamic–pituitary–gonadal axis. Other investigations are aimed at diag- Reduced immune competence and increased suscepti- nosing the underlying cause and providing a prediction bility to infection also occur. Patients may present with complications such as bleed- ingfromoesophagealvaricesorencephalopathy. Patients Management withactivechronichepatitismaypresentwithfeaturesof r Symptomatic management includes adequate nutri- chronic liver disease before cirrhosis is established. Cirrhosis 2 Hands: Leuconychia (if hypoalbuminaemic), club- Definition bing,palmarerythema,Dupuytren’scontracture,hep- Cirrhosis is an irreversible change of the liver architec- atic flap (asterixis, sign of hepatic encephalopathy), ture,characterisedbynodulesofregeneratedlivercells tremor may occur in alcoholism and Wilson’s disease. The liver is usually enlarged, firm and irregular, but is shrunken Aetiology in late disease. The spleen may be enlarged due to Cirrhosis results from continued hepatocellular necro- portal hypertension. Fibrous scarring causes disruption of the normal architecture, although regen- eration of hepatocytes occurs between the fibrous tracts, Macroscopy their function, which depends on intact architecture, is The liver is often enlarged and nodular, with a bosselated impaired. The cut surface shows nodules of liver tissue, r Alcohol accounts for more than 80% of cirrhosis in separatedbyfineorcoarsefibrousstrands. Other rare but impor- Grading system 1 2 3 tant drug-induced causes are halothane, isoniazid and rifampicin. Hepatic time (seconds encephalopathy is thought to be due to failure of the over control) liver to metabolise toxins. Serum amino acid levels rise Child–Pugh grade A = score of 5–6; Child–Pugh grade B = score affectingthebalanceofcerebralneurotransmitters. Hep- of 7–9; Child–Pugh grade C = score of 10–15 atic dysfunction also results in renal failure (hepatorenal syndrome). Investigations Aimed at diagnosis of underlying cause and assessment of severity/degree of reversible liver injury. The severity Clinical features of liver disease may be graded A–C by means of a mod- Patients may have altered behaviour, euphoria or se- ified Child–Pugh grading system (see Table 5. On examination patients are jaundiced, there may be Management fetor hepaticus (sickly sweet odour on breath), flapping Treatment is largely supportive. Withdrawal from alco- tremor, slurred speech, difficulty in writing and copy- hol is essential in all patients. Malnutrition is common ing simple diagrams (constructional apraxia) and gen- and may require nutritional support. Prognosis Complications Cirrhosis is an irreversible, progressive condition which r Central nervous system: Cerebral oedema in 80% oftencontinuestoend-stageliverfailuredespitethewith- causing raised intracranial pressure. The higher the Child– r Cardiovascular system: Hypotension, arrhythmias Pugh grade, the worse the prognosis, particularly for due to hypokalaemia including cardiac arrest. Over50%ofcasesintheUnitedKingdom Chapter 5: Disorders of the liver 197 Investigations encephalopathy. Specific tests depend on the sus- Complications of chronic pected underlying cause, e. Othertestsincludefullbloodcount,ureaandelec- trolytes, glucose, calcium, phosphate and magnesium Portal hypertension levels. Definition Management Raised portal venous pressure is usually caused by in- Treatment is supportive as the liver failure may resolve: creased resistance to portal venous blood flow and is a r Specialisthepatologyinputisessential,ideallypatients common sequel of cirrhosis. Position- pressure is consistently above 25 cm H2O, serious com- ing at a 20˚ head up tilt can help ameliorate the ef- plications may develop. Aetiology Whilst adequate nutrition is essential the protein in- By far the most common cause in the United Kingdom take should be restricted to 0.

Schonlein¨ Purpura purchase epivir-hbv 150 mg treatment yeast diaper rash, cirrhosis purchase epivir-hbv 100 mg line treatment for uti, coeliac disease and der- r More aggressive immunosuppression may benefit matitis herpetiformis. There is a weak association with some patients, such as those with crescentic disease. Clinical features Proteinuria, renal impairment and histological evidence One third of patients present with recurrent macro- of scarring, tubular atrophy and capillary loop deposits scopic haematuria during or after upper respiratory signify a worse prognosis. Approximately a third de- tract infections, one third have persistent microscopic veloprenalimpairment,andathirdreachend-stagerenal haematuria and/or persistent mild proteinuria. M > F r Pulmonary function tests may be performed to look for increased transfer factor (evidence of alveolar Aetiology/pathophysiology haemorrhage). Crescents form as a result of ep- are used to switch off the production of antibody. The decision to treat these The usual presentation is of acute renal failure with patients if they have no evidence of pulmonary haem- oliguria, an active urine sediment with dysmorphic orrhage or other vasculitis with aggressive therapy is redblood cells, red cell casts and proteinuria. Patient survival and long-term renal function correlate well with the degree of renal impairment at presenta- Macroscopy/microscopy tion. Early diagnosis and treatment is Immunofluorescence demonstrates linear IgG and C3 the key to reducing morbidity and mortality. There is no evidence of an Patientsusuallypresentwithhaematuriaand/orprotein- immune complex process. In severe cases lial cells is believed to cause a reduction in the fixed patientsmaypresentwithnephroticsyndrome,nephritic negative charge on the glomerular capillary wall, which syndrome or a mixed picture. Features of any underlying permits protein (particularly albumin) to cross into the condition may also be present. Resultant hypoalbuminaemia causes a re- duced blood oncotic pressure and hence oedema. Underlying causes should be looked for, partic- Clinical features ularly treatable infections, malignancies and cryoglobu- Patients present with gradual development of swelling linaemia. Renal function is usually Treatment of any underlying cause may lead to partial normal in uncomplicated cases. In those without nephrotic syn- drome, conservative management is probably indicated, Macroscopy/microscopy as the prognosis is good. In those with nephrotic-range Electron microscopy reveals fusion of the foot processes proteinuria, specific treatments such as steroids and an- ofthepodocytes,thisisdiagnosticifthelightmicroscopy tiplatelet agents may be tried with very variable benefit. Cyclophosphamide, cyclosporine and other drugs have also been used to induce remission in Pathophysiology steroid-resistant cases, or to reduce the steroid dose The mechanism is unknown. Because the immune deposits are subepithe- Repeat renal biopsy may demonstrate another condition lial there is usually no marked inflammatory response. Over many years, there is increase in mesangial matrix caus- Membranous glomerulonephritis ing hyalinization of glomeruli and loss of nephrons. Definition Clinical features This is the one of the two most common causes of Patients may present with asymptomatic proteinuria, nephrotic syndrome in non-diabetic adults (together or (in most cases) nephrotic syndrome. The idiopathic form causes ∼20% usually with mild to moderate mesangial proliferation. Silver stains classically show ‘spikes’ where basement membrane has grown between subepithelial deposits. Alternatively large plasma proteins may leak through the capillary wall, accumulate in the subendothelial space and compress the capillary Prognosis lumen. Some patients develop a rapidly progressive course loss of the function of that nephron. These may develop later in the course of drome in adults and the second most common cause the illness. Incidence/prevalence Causes ∼20% of cases of nephrotic syndrome in adults Macroscopy/microscopy and children. Increase in the mesangial matrix in glomeruli in a focal segmental pattern, with collapse of the adjacent capillary loop. It is thought to be part first, the disease may be missed on renal biopsy (and of a physiological response to glomerular hyperfiltra- hence a diagnosis of minimal change disease made). Steroid resistant cases action to the drug, with lymphocytes and eosinophils may respond to ciclosporin, and steroid-dependent infiltrating the interstitium causing tissue oedema.

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Hydrostatic pressure favors evaluation of the lung parenchyma (interstitial lung movement of fluid from the capillary into the intersti- disease) and possible pulmonary embolism discount epivir-hbv 150 mg mastercard treatment water on the knee. Although hypoalbu- systolic dysfunction generic epivir-hbv 150 mg on-line medications rights, pulmonary hypertension, or minemia favors movement of fluid into the tissue for valvular heart disease is suspected. Direct Injury to Lung Hydrostatic pressure is increased and fluid exits the cap- Chest trauma, pulmonary contusion Aspiration illary at an increased rate, resulting in interstitial and, in Smoke inhalation more severe cases, alveolar edema. The development of Pneumonia pleural effusions may further compromise respiratory Oxygen toxicity system function and contribute to breathing discomfort. Pulmonary embolism, reperfusion Early signs of pulmonary edema include exertional Hematogenous Injury to Lung dyspnea and orthopnea. Chest radiographs show peri- Sepsis bronchial thickening, prominent vascular markings in Pancreatitis Nonthoracic trauma the upper lung zones, and Kerley B lines. As the pul- Leukoagglutination reactions monary edema worsens, alveoli fill with fluid, and the Multiple transfusions chest radiograph shows patchy alveolar filling, typically Intravenous drug use (e. Increasing airway edema is asso- Possible Lung Injury Plus Elevated ciated with rhonchi and wheezes. Hydrostatic Pressures High-altitude pulmonary edema Neurogenic pulmonary edema Noncardiogenic Pulmonary Edema Reexpansion pulmonary edema By definition, hydrostatic pressures are normal in patients with noncardiogenic pulmonary edema. Lung water increases because of damage of the pulmonary capillary lining with leakage of proteins and other macromole- Distinguishing Cardiogenic from Noncardiogenic Pulmonary Edema cules into the tissue; fluid follows the protein as oncotic forces are shifted from the vessel to the surrounding The history is essential for assessing the likelihood of under- lung tissue. This process is associated with dysfunction of lying cardiac disease as well as for identifying one of the the surfactant lining the alveoli, increased surface forces, conditions associated with noncardiogenic pulmonary and a propensity for the alveoli to collapse at low lung edema. Physiologically, noncardiogenic pulmonary edema is notable for evidence of increased intracardiac pres- edema is characterized by intrapulmonary shunt with sures (S3 gallop, elevated jugular venous pulse, peripheral hypoxemia and decreased pulmonary compliance. In Pathologically, hyaline membranes are evident in the contrast, the physical examination in noncardiogenic pul- alveoli, and inflammation leading to pulmonary fibrosis monary edema is dominated by the findings of the precipi- may be seen. Clinically, the picture ranges from mild tating condition; pulmonary findings may be relatively nor- dyspnea to respiratory failure. The chest radiograph in cardiogenic may be relatively normal despite chest radiographs that pulmonary edema typically shows an enlarged cardiac sil- show diffuse alveolar infiltrates. Finally, lung is likely to result from direct, indirect, or pulmonary the hypoxemia of cardiogenic pulmonary edema is largely vascular causes (Table 2-2). Direct injuries are mediated attributable to ventilation-perfusion mismatch and responds via the airways (e. Indirect injury is the consequence of hypoxemia in noncardiogenic pulmonary edema is primar- mediators that reach the lung via the blood stream. The ily attributable to intrapulmonary shunting and typically third category includes conditions that may be the con- persists despite high concentrations of inhaled O. These stimuli may affect or bothersome, it is also one of the most common receptors in the upper airway (especially the pharynx and symptoms for which patients seek medical attention. The afferent limb includes receptors within sophageal reflux is caused only partly by irritation of the sensory distribution of the trigeminal, glossopharyn- upper airway receptors or by aspiration of gastric con- geal, superior laryngeal, and vagus nerves. The efferent tents; a vagally mediated reflex mechanism secondary to limb includes the recurrent laryngeal nerve and the acid in the distal esophagus may also contribute. The cough starts with a deep inspiration Any disorder resulting in inflammation, constriction, followed by glottic closure, relaxation of the diaphragm, infiltration, or compression of the airways may be associ- and muscle contraction against a closed glottis. Inflammation commonly results from resulting markedly positive intrathoracic pressure causes airway infections, ranging from viral or bacterial bron- narrowing of the trachea. In viral bronchitis, airway inflam- large pressure differential between the airways and the mation sometimes persists long after resolution of the atmosphere coupled with tracheal narrowing produces typical acute symptoms, thereby producing a prolonged rapid flow rates through the trachea. Pertussis infection is also a that develop aid in the elimination of mucus and foreign possible cause of persistent cough in adults; however, materials. At its onset, were there associated symptoms sug- asthma, some patients present with cough in the absence gestive of a respiratory infection? Is it associated with symptoms suggestive of post- the airway wall, such as bronchogenic carcinoma or a nasal drip (nasal discharge, frequent throat clear- carcinoid tumor, is commonly associated with cough. Compression of airways results from extrinsic toms does not exclude either of these diagnoses.

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Rapid and early correction of acidosis with sodium bicarbonate may worsen hypokalemia and cause paradoxical cellular acidosis 150mg epivir-hbv amex denivit intensive treatment. Bicarbonate typically is not replaced as acidosis will improve with the above treatments alone epivir-hbv 100mg mastercard symptoms xanax. Treatment of Concurrent Infection In the presence of infection, the administration of proper antibiotics is guided by the results of culture and sensitivity studies. Starting empiric antibiotics on suspicion of infection until culture results are available may be advisable ( see the septic guideline). We are encourage to use this scale • High dose scale: patient with infection or those who receiving high dose corticosteroids. Ideally patient can be discharge home by day 4 or 5 after resuming current medication or insulin adjustment therapy. In patient Vital sign every hour in the first 24 hours then every 2 hours according to patient condition Fluid balance: input and output. Make sure your patient is understanding and give instruction if newly insulin injection. The clinical presentation and management is similar in nonpregnant women except blood sugar level < 200mg /dl. Maternal hyperglycemia should be avoided during labor to reduce the risk of fetal acidosis and neonatal hypoglycemia. The risk of adverse neonatal metabolic outcomes (hypoglycemia, hyperbilirubinemia, hypocalcemia, erythremia) is related to both antepartum and intrapartum maternal hyperglycemia and appears to increase with the degree of maternal hyperglycemia. Intrapartum management of diet, glucose, and insulin and management of insulin before cesarean delivery are discussed in detail separately. Alter mental status: Present Diagnostic work up: Blood sugar, electrolyte, Creatinine, Anion gap, osmolarity, Urine analysis to detect Ketonuria Management: Immediate within the first 24hours 1. Fluid resuscitation at least 4-6 L in the first 6 hours unless cardiac disease or pulmonary congestion 3. Should think of myocardial Patient and family Education infarction, infection, … 3. Normal laboratory values vary; check local labmEq/l, and moderate ketonuria or ketonemia. Normal laboratory values vary; check local lab normal ranges for all electrolytes. Obtain electrocardiogram, chest X-ray, and specimens for bacterial cultures, as needed. Copyright ©2006 American Diabetes Association From Diabetes Care Vol 29, Issue 12, 2006. Normal laboratory values vary; check local labmEq/l, and minimal ketonuria and ketonemia. Normal laboratory values vary; check local labmEq/l, and minimal ketonuria and ketonemia. Normal laboratory values vary; check local lab normal ranges for all electrolytes. Obtain electrocardiogram, chest X-ray, and specimens for bacterial cultures, as needed. Copyright © 2006 American Diabetes Association From Diabetes Care Vol 29, Issue 12, 2006. Etat de choc = mise en jeu des mécanismes compensateurs, qui évoluent au cours du temps. Choc décompensé • Hypoperfusion • Hypoxie tissulaire • Métabolisme anaérobie - production des lactates • Acidose lactique • Libération dans le sang des substances vasocardio-actives aggravant encore la défaillance circulatoire avec répercussion sur tous les organes • Défaillance progressive et successive des divers organes : défaillance multiviscérale. Signes de gravité : → Hypoperfusion tissulaire: organes vitaux et nobles Poumon : polypnée, bradypnée (gravité extrême), cyanose, sueurs. Cerveau : agitation, confusion, obnubilation, torpeur, somnolence, convulsions, perte de connaissance, coma.