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Syncope is the medical term for fainting, a sudden, usually temporary, loss of consciousness generally caused by insufficient oxygen in the brain either through cerebral hypoxia or through hypotension, but possibly for other reasons. A pre- or near-syncope is diagnosed if the individual can remember events during the loss of consciousness.
Vasovagal (situational) syncope—one of the most common types—may occur in scary, embarrassing or uneasy situations, or during blood drawing, coughing, urination or defecation. Other types include postural syncope (caused by a changing in body posture), cardiac syncope (due to heart-related conditions), and neurological syncope (due to neurological conditions). There are many other causes of syncope, including low blood-sugar levels and lung disease such as emphysema and a pulmonary embolus. The cause of the fainting can be determined by a doctor using a complete history, physical, and various diagnostic tests.
The vasovagal type can be considered in two forms:
    * Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group, and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
    * Recurrent syncope with complex associated symptoms. This is so-called Neurally Mediated Syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, light-headedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive.
Cardiac arrhythmias is the most common cause of cardiac syncope. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which requires DC cardioversion.
Aortic stenosis and mitral stenosis are the most common examples.Aortic stenosis presents with repeated episodes of syncope. Pulmonary embolism can cause obstructed blood vessels. High blood pressure in the arteries supplying the lungs (pulmonary artery hypertension) can occur during pulmonary embolism. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.

Aortic Dissection and Aneurysms

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Abdominal aortic aneurysm is a localized dilatation of the abdominal aorta exceeding the normal diameter by more than 50 percent, and is the most common form of aortic aneurysm. Approximately 90 percent of abdominal aortic aneurysms occur infrarenally,but they can also occur pararenally or suprarenally.Abdominal aortic aneurysms occur most commonly in individuals between 65 and 75 years old and are more common among men and smokers.
Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysm is usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm).If the outer diameter exceeds 5.5 cm, the aneurysm is considered to be large.
The vast majority of aneurysms are asymptomatic. However, as abdominal aortic aneurysms expand, they may become painful and lead to pulsating sensations in the abdomen or pain in the chest, lower back, or scrotum.The risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery.The complications include rupture, peripheral embolization, acute aortic occlusion, and aortocaval (between the aorta and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination, a palpable abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.
The clinical manifestation of ruptured AAA usually includes excruciating pain of the lower back, flank, abdomen and groin. The bleeding usually leads to a hypovolemic shock with hypotension, tachycardia, cyanosis, and altered mental status. The mortality of AAA rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.The bleeding can be retroperitoneal or intraperitoneal, or the rupture can create an aortocaval or aortointestinal (between the aorta and intestine) fistula.Flank ecchymosis is a sign of retroperitoneal hemorrhage, and is also called Grey Turner's sign.

Wilson's disease

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Wilson's disease  is an autosomal recessive genetic disorder in which copper accumulates in tissues; this manifests as neurological or psychiatric symptoms and liver disease. It is treated with medication that reduces copper absorption or removes the excess copper from the body, but occasionally a liver transplant is required.The condition is due to mutations in the Wilson disease protein (ATP7B) gene.If a child inherits the gene from both parents, they may develop Wilson's disease. Symptoms usually appear between the ages of 6 and 20 years, but cases in much older people have been described.
The main sites of copper accumulation are the liver and the brain, and consequently liver disease and neuropsychiatric symptoms are the main features that lead to diagnosis.
Liver disease may present as tiredness, increased bleeding tendency or confusion (due to hepatic encephalopathy) and portal hypertension. The latter, a condition in which the pressure in the portal vein is markedly increased, leads to esophageal varices that may bleed in a life-threatening fashion, splenomegaly and ascites. On examination, signs of chronic liver disease such as spider naevi may be observed. Chronic active hepatitis has caused cirrhosis of the liver in most by the time they develop symptoms. While most people with cirrhosis have an increased risk of hepatocellular carcinoma , this risk is relatively very low in Wilson's disease.
Various medical conditions have been linked with copper accumulation in Wilson's disease:
    * Eyes: Kayser–Fleischer rings (KF rings) may be visible around the iris. They are due to copper deposition in Descemet's membrane of the cornea. They do not occur in all people and may only be visible on slit lamp examination.
Kidneys: renal tubular acidosis, a disorder of bicarbonate handling by the proximal tubules leads to nephrocalcinosis
About half the people with Wilson's have neurological or psychiatric problems.neurological symptoms then follow, often in the form of parkinsonism with or without a typical hand tremor, masked facial expressions, slurred speech, ataxia or dystonia . Seizures and migraine appear to be more common in Wilson's disease.
There is no totally reliable test for Wilson's disease, but levels of ceruloplasmin and copper in the blood, as well of the amount of copper excreted in urine during a 24-hour period, are together used to form an impression of the amount of copper in the body. The gold standard or most ideal test is a liver biopsy.
Generally, penicillamine is the first treatment used. This binds copper and leads to excretion of copper in the urine.Liver transplantation is an effective cure for Wilson's disease, but is used only in particular scenarios because of the numerous risks and complications associated with the procedure. It is used mainly in people with fulminant liver failure who fail to respond to medical treatment, or in those with advanced chronic liver disease.

Late complications of fractures

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    * Delayed union
    * Nonunion
    * Malunion
    * Joint stiffness
    * Contractures
    * Myositis ossificans
    * Avascular necrosis
    * Algodystrophy (or Sudeck's atrophy)
    * Osteomyelitis
    * Growth disturbance or deformity

    * Gangrene, tetanus, septicaemia
    * Fear of mobilising
    * Osteoarthritis

Nonunion is where there are no signs of healing after >3-6 months (depending upon the site of fracture). Nonunion is one endpoint of delayed union. Malunion occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction.
Causes of delayed union include:
    * Severe soft tissue damage
    * Inadequate blood supply
    * Infection
    * Insufficient splintage
    * Excessive traction
Nonunion occurs in approximately 1% of all fractures but is more common in lower leg fractures (19% nonunion) or where there is motion at the fracture site.
Nonsurgical approaches such as early weight bearing and casting may be helpful for delayed union and nonunion.
Surgical treatments include:
    * Debridement to establish a healthy infection-free vascularity at the fracture site
    * Internal fixation to reduce and stabilise the fracture.
    * Bone grafting to stimulate new callus formation.

Avascular necrosis
Certain regions are known for their propensity to develop ischemia and necrosis after injury.
It’s Early complication because ischemia occurs during the first few hours but the clinical and radiological effects are seen until weeks or months later . Avascular necrosis causes deformation of the bone. This leads, a few years later, to secondary osteoarthritis and causes painful limitation of joint movement.

Hypokalemic Periodic Paralysis

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Hypokalemic periodic paralysis is a rare channelopathy characterized by muscle weakness or paralysis with a matching fall in potassium levels in the blood. In individuals with this mutation, attacks often begin in adolescence and are triggered by strenuous exercise followed by rest, high carbohydrate meals, meals with high sodium content, sudden changes in temperature, and even excitement, noise or flashing lights. Weakness may be mild and limited to certain muscle groups, or more severe full body paralysis. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.
Mutations in CACNA1S, SCN4A and KCNE3 genes cause hypokalemic periodic paralysis.Respectively, these genes code for a voltage-gated calcium channel Cav1.1 found in the transverse tubules of skeletal muscle cells, a voltage-gated sodium channel Nav1.4 found at the neuromuscular junction, and a voltage-gated potassium channel.
The CMAP (Compound Muscle Amplitude Potential) test, also called the exercise EMG or X-EMG, is diagnostic in 70-80% of cases when done correctly. Besides the patient history or a report of serum potassium low normal or low during an attack, the CMAP is the current standard for medical testing. Genetic diagnosis is often unreliable as only a few of the more common gene locations are tested. Standard EMG testing cannot diagnose a patient unless they are in a full blown attack at the time of testing. Provoking an attack with exercise and diet then trying oral potassium can be diagnostic.
Treatment of hypokalemic periodic paralysis focuses on preventing further attacks and relieving acute symptoms. Avoiding carbohydrate-rich meals and strenuous exercise, and taking Acetazolamide or another carbonic anhydrase inhibitor, may help prevent attacks of weakness. Paralysis attacks can be managed by drinking effervescent potassium bicarbonate dissolved in water, or potassium gluconate oral solution. Treatment with potassium chloride or use of intravenious sterroids can cause intensification of symptoms.

In intensive care medicine, extracorporeal membrane oxygenation (ECMO) is an extracorporeal technique of providing both cardiac and respiratory support oxygen to patients whose heart and lungs are so severely damaged that they can no longer serve their function.
An ECMO machine is similar to a heart-lung machine. To initiate ECMO, cannulae are placed in large blood vessels to provide access to the patient's blood. Anticoagulant drugs, usually heparin, are given to prevent blood clotting. The ECMO machine continuously pumps blood from the patient through a membrane oxygenator that imitates the gas exchange process of the lungs, i.e. it removes carbon dioxide and adds oxygen. Oxygenated blood is then returned to the patient. Management of the ECMO circuit is done by a team of ECMO specialists that includes intensive care unit (ICU) physicians, physician assistants, perfusionists, Registered Nurses, respiratory therapists, and Medical Laboratory Technologists that have received training in this specialty.
There are several forms of ECMO, the two most common of which are veno-arterial (VA) and veno-venous (VV). In both modalities, blood drained from the venous system is oxygenated outside of the body. In VA ECMO, this blood is returned to the arterial system and in VV ECMO the blood is returned to the venous system. In VV ECMO, no cardiac support is provided.
VV ECMO can provide sufficient oxygenation for several weeks, allowing diseased lungs to heal while the potential additional injury of aggressive mechanical ventilation is avoided. It may therefore be life-saving for some patients.
Fatal sepsis may occur when the large catheters inserted in the neck provide fertile field for infection.Additional risks include bleeding. In adults, ECMO survival rates are around 60%. ECMO has yet to have proven survival benefit in adults with acute respiratory distress syndrome (ARDS).

Elevated Liver Function Tests

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Abnormal LFTs are frequently detected in asymptomatic patients (1-4%).
They do not always reflect liver diseases.
They may be a marker of worse health outcomes.

Isolated elevation of transaminases:
Medications  (NSAIDs, Anitbiotics, statins,
   antiepileptics  and herbal preparations)
Alcohol (AST/ALT >2:1,  twofold elevation
   of GGT)
Hereditary hemochromatosis (Caucasian, iron,
   TIBC, ferritin +/- liver biospy)
Viral hepatitis:  HBV ( HBsAg, anti HBsAg, anti HBc)  and HCV ( ELISA, RIBA, PCR )
Hepatic steatosis and NASH ( AST/ALT<1, ultrasound, CT or MRI) 
Muscular disorders (AST/ALT>3 if immediately after injury, CK, LDH, aldoalse)
Thyroid diseases (TSH)
Celiac disease (ALT>AST, reversible with gluten free diet)
Adrenal insufficency ( reversible within week of treatment)
Anorexia nervosa
Wilson ‘s disease (age 5-25, serum ceruloplasmin, 24hr urine  for copper, liver biopsy)
Autoimmune hepatitis ( SPEP, ANA , SMA, LKMA, liver biopsy)
Alpha 1 antitrypsin (associated emphysema, protein electrophoresis)
Isolated Hyperbilirubinemia
Hemolysis (smear, retic count, haptoglobin) can be inherited or acquired. Rarely exceeds 5mg/dl
Impaired uptake or conjugation, drugs, Crigller Najjar and Gilbert’s syndrome.

Dubin Johnson with altered excretion
Rotor syndrome with defective storage.

Isolated elevation of alkaline phosphatase
Alkaline phosphatase is derived from liver, bones, intestins and placenta.
Levels vary with age, more elevated in children.
To determine the source we check GGT or 5’ nucleotidase.
Initial evaluation includes U/S and AMA followed by ERCP v/s liver biopsy.

Isolated elevation of GGT
Very sensisitive for hepatobiliary disease but not specific.
Can reflect pancreatic disease, MI, renal failure, diabetes, COPD, alcoholism.

Total parenteral nutrition in Children

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Parenteral nutrition (PN) is feeding a person intravenously, bypassing the usual process of eating and digestion. The person receives nutritional formulas that contain nutrients such as salts, glucose, amino acids, lipids and added vitamins.Total Parenteral nutrition (TPN) is provided when the gastrointestinal tract is nonfunctional because of an interruption in its continuity or because its absorptive capacity is impaired.TPN may be the only feasible option for nutrition patients who do not have a functioning GI tract or who have disorders requiring complete bowel rest, such as the following: Some stages of Crohn's disease or ulcerative colitis, bowel obstruction, short gut syndrome, high-output fistula, certain pediatric GI disorders, e.g., congenital GI anomalies, prolonged diarrhoea regardless of its cause, or short bowel syndrome due to surgery.
TPN is an artifical method of feeding, fully passing the GI tract. As advanced is science is, this unnatural way of feeding the body is far from perfect and comes with several significant complications.Complications are either related to catheter insertion, or metabolic, including refeeding syndrome.
Catheter complications include pneumothorax, accidental arterial puncture, and catheter-related sepsis. The complication rate at the time of insertion should be less than 5%. Catheter-related infections may be minimised by appropriate choice of catheter and insertion technique.Metabolic complications include the refeeding syndrome characterised by hypokalemia, hypophosphatemia and hypomagnesemia.
Fatty liver is usually a more long term complication of TPN, though over a long enough course it is fairly common. The pathogenesis is still unknown.

Arteriovenous Malformations (AVMs)

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Arteriovenous malformation or AVM is an abnormal connection between veins and arteries, usually congenital. This pathology is widely known because of its occurrence in the central nervous system, but can appear in any location.An AVM lacks the dampening effect of capillaries on the blood flow; it also causes the surrounding area to be deprived of the functions of the capillaries - removal of CO2 and delivery of nutrients to the cells. The resulting tangle of blood vessels, often called a nidus has no capillaries and abnormally direct connections between high-pressure arteries and low-pressure veins. It can be extremely fragile and prone to bleeding.
Symptoms of AVM vary according to the location of the malformation. Roughly 88%of people affected with AVM are asymptomatic; often the malformation is discovered as part of an autopsy or during treatment of an unrelated disorder ; in rare cases its expansion or a micro-bleed from an AVM in the brain can cause epilepsy, deficit or pain.
The most general symptoms of a cerebral AVM include headache and epilepsy, with more specific symptoms occurring that normally depend on the location of the malformation and the individual. Such possible symptoms include:[2]
    * Difficulties with movement or coordination, including muscle weakness and even paralysis;
    * vertigo (dizziness);
    * Difficulties of speech (dysarthria) and communication, such as aphasia;
    * Difficulties with everyday activities, such as apraxia;
    * Abnormal sensations (numbness, tingling, or spontaneous pain);
    * Memory and thought-related problems, such as confusion, dementia or hallucinations.

AVMs may occur in isolation or as a part of another disease (e.g. Von Hippel-Lindau disease or hereditary hemorrhagic telangiectasia).Treatment can be symptomatic, or it can involve surgery or radiation therapy.Ebolization, that is, cutting off the blood supply to the AVM with coils or particles or glue introduced by a radiographically guided catheter, can be used in addition to either, but is rarely successful in isolation except for in smaller AVMs.

Lupus Nephritis

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Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system.Sufferers of lupus nephritis may or may not have symptoms of kidney disease, but it can manifest itself through weight gain, high blood pressure, darker foamy urine or swelling around the eyes, legs, ankles or fingers.
Histologically a wire-loop lesion will be present. The wire loop lesion is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop.
Furthermore, patients may suffer from other symptoms of lupus unrelated to kidney function. Such symptoms can include arthritis, fevers, gastro-intestinal disturbances, headaches, fatigue, and fluid in the joints.
The diagnosis of lupus nephritis depends on blood tests, urinalysis, X-rays, ultrasound scans of the kidneys, and a kidney biopsy.
The World Health Organization has divided lupus nephritis into five classes based on the biopsy.
    * Class I is minimal mesangial glomerulonephritis which is histologically normal on light microscopy but with mesangial deposits on electron microscopy.
    * Class II is based on a finding of mesangial proliferative lupus nephritis. This form typically responds completely to treatment with corticosteroids.
    * Class III is focal proliferative nephritis and often successfully responds to treatment with high doses of corticosteroids.
    * Class IV is diffuse proliferative nephritis. This form is mainly treated with corticosteroids and immunosuppressant drugs.
    * Class V is membranous nephritis and is characterized by extreme edema and protein loss.
The medical therapy for lupus nephritis depends on the severity of the disease. For mild disease, corticosteroids are, in general, prescribed. More severe disease requires treatment with immunosuppressant agents. The two most commonly-used agents are mycophenolate mofetil and intravenous cyclophosphamide.

Mechanical ventilation

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Mechanical ventilation is a method to mechanically assist or replace spontaneous breathing.
Mechanical ventilation is indicated when the patient's spontaneous ventilation is inadequate to maintain life. It is also indicated as prophylaxis for imminent collapse of other physiologic functions, or ineffective gas exchange in the lungs.
Common medical indications for use include:

    * Acute lung injury (including ARDS, trauma)
    * Apnea with respiratory arrest, including cases from intoxication
    * Chronic obstructive pulmonary disease (COPD)
    * Acute respiratory acidosis with partial pressure of carbon dioxide (pCO2) > 50 mmHg and pH < 7.25, which may be due to paralysis of the diaphragm due to Guillain-Barré syndrome, Myasthenia Gravis, spinal cord injury, or the effect of anaesthetic and muscle relaxant drugs
    * Increased work of breathing as evidenced by significant tachypnea, retractions, and other physical signs of respiratory distress
    * Hypoxemia with arterial partial pressure of oxygen (PaO2) with supplemental fraction of inspired oxygen (FiO2) < 55 mm Hg
    * Hypotension including sepsis, shock, congestive heart failure
    * Neurological diseases such as Muscular Dystrophy and Amyotrophic Lateral Sclerosis

Modes of ventilation
Assist Control (AC). In this mode the ventilator provides a mechanical breath with either a pre-set tidal volume or peak pressure every time the patient initiates a breath.When a preset peak pressure is used this is also sometimes termed Intermittent Positive Pressure Ventilation or IPPV.
Synchronized Intermittent Mandatory Ventilation (SIMV). In this mode the ventilator provides a pre-set mechanical breath (pressure or volume limited) every specified number of seconds
Controlled Mechanical Ventilation (CMV). In this mode the ventilator provides a mechanical breath on a preset timing.
Pressure Support Ventilation (PSV). When a patient attempts to breathe spontaneously through an endotracheal tube, the narrowed diameter of the airway results in higher resistance to airflow, and thus a higher work of breathing.
Continuous Positive Airway Pressure (CPAP). A continuous level of elevated pressure is provided through the patient circuit to maintain adequate oxygenation, decrease the work of breathing, and decrease the work of the heart
Positive end-expiratory pressure (PEEP) is functionally the same as CPAP, but refers to the use of an elevated pressure during the expiratory phase of the ventilatory cycle.

Neonatal seizures

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The neonatal period is limited to the first 28 days of life in a term infant. For premature infants, this term usually is applied until gestational age 44 weeks.The most prominent feature of neurological dysfunction in the neonatal period are seizures. Determining the underlying etiology for neonatal seizures is critical. Most neonatal seizures occur over only a few days, and fewer than half of affected infants develop seizures later in life. Seizures occur when a large group of neurons undergo excessive, synchronized depolarization. Depolarization can result from excessive excitatory amino acid release (eg, glutamate) or deficient inhibitory neurotransmitter (eg, gamma amino butyric acid [GABA]).
The differential diagnosis for neonatal seizures is voluminous. Important causes include the following:

    * Seizures resulting from hypoxic-ischemic encephalopathy may be seen in both term and premature infants. They frequently present within the first 72 hours of life. Seizures may include subtle, clonic, or generalized seizures.
    * Intracranial hemorrhage occurs more frequently in premature than in term infants. Distinguishing infants with pure hypoxic-ischemic encephalopathy from those with intracranial hemorrhage often is difficult.
Metabolic disturbances include hypoglycemia, hypocalcemia, and hypomagnesemia. Less frequent metabolic disorders, such as inborn errors of metabolism, are seen more commonly in infants who are older than 72 hours. Typically, they may be seen after the infant starts feeding.
Intracranial infections (which should be ruled out vigorously) that are important causes of neonatal seizures include meningitis, encephalitis (including herpes encephalitis), toxoplasmosis, and cytomegalovirus (CMV) infections. The common bacterial pathogens include Escherichia coli and Streptococcus pneumoniae.
While most cerebral malformations present with seizures at a later age, major malformation syndromes are important to consider. Lissencephaly, pachygyria, polymicrogyria, and linear sebaceous nevus syndrome can present with seizures in the neonatal period.

Shock is a A physiological state characterized by a significant, systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery and insufficient removal of cellular metabolic products, resulting in tissue injury.

Hypovolemic Shock
Decreased preload->small ventricular end-diastolic volumes -> inadequate cardiac generation of pressure and flow
 -- bleeding: trauma, GI bleeding, ruptured aneurysms,    hemorrhagic pancreatitis
 -- protracted vomiting or diarrhea
 -- adrenal insufficiency; diabetes insipidus
 -- dehydration
 -- third spacing: intestinal obstruction, pancreatitis, cirrhosis

Septic/Inflammatory Shock
Mechanism: release of inflammatory mediators leading to
Disruption of the microvascular endothelium
Cutaneous arteriolar dilation and sequestration of blood in cutaneous venules and small veins
Anaphylaxis, drug, toxin reactions
Trauma: crush injuries, major fractures, major burns.
infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis, meningitis, cholangitis, pyelonephritis, necrotic tissue, pancreatitis, wet gangrene, toxic shock syndrome, etc.

Cardiogenic Shock
Mechanism: Intrinsic abnormality of heart -> inability to deliver blood into the vasculature with adequate power
Cardiomyopathies: myocardial ischemia, myocardial infarction, cardiomyopathy, myocardiditis, myocardial contusion
Mechanical: cardiac valvular insufficiency, papillary muscle rupture, septal defects, aortic stenosis
Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrial fibrillation, atrial flutter, ventricular fibrillation)
Obstructive disorders: PE, tension peneumothorax, pericardial tamponade, constrictive pericaditis, severe pulmonary hypertension
Characterized by high preload (CVP) with low CO
Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP, oliguria
Monitor/findings: CXR pulm venous congestion, elevated CVP, Low CO.

Chronic Kidney Disease_Case Studies

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Chronic kidney disease is a progressive loss in renal function over a period of months or years. The symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia or pericarditis.
The most common causes of CKD are diabetes mellitus, hypertension, and glomerulonephritis.Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.
Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a falling glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products.Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis shows that the kidney is allowing the loss of protein or red blood cells into the urine.To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renal biopsy are employed to find out if there is a reversible cause for the kidney malfunction.Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated terms end-stage renal disease (ESRD).
There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly with treatments aimed to slow the damage. In more advanced stages, treatments may be required for anemia and bone disease. Severe CKD requires one of the forms of renal replacement therapy; this may be a form of dialysis, but ideally constitutes a kidney transplant.

Neonatal Meningitis

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Neonates are at greater risk of sepsis and meningitis than other age groups because of deficiencies in humoral and cellular immunity and in phagocytic function.Despite development of effective vaccines, tools for rapid identification of pathogens, and potent antimicrobial drugs, neonatal meningitis continues to contribute substantially to neurological disability worldwide. The persistence of neonatal meningitis results from increasing numbers of infants surviving premature delivery and from limited access to medical resources in developing countries.Regardless of the specific pathogen involved, neonatal meningitis is most often caused by vertical transmission during labor and delivery. It occurs most frequently in the days following birth and is more common in premature infants than term infants.
Risk factors for the development of meningitis include low birth weight (<2500 g), preterm birth (<37 weeks' gestation), premature rupture of membranes, traumatic delivery, fetal hypoxia, and maternal peripartum infection (including chorioamnionitis).
Early onset bacterial meningitis,
    * Symptoms appearing in the first 48 hours of life are referable primarily to systemic illness rather than meningitis. These include temperature instability, episodes of apnea or bradycardia, hypotension, feeding difficulty, hepatic dysfunction, and irritability alternating with lethargy.
Late onset bacterial meningitis,
    * Late-onset bacterial meningitis (symptom onset beyond 48 hours of life) is more likely to be associated with neurologic symptoms.Between 25% and 50% of neonates will exhibit the following neurological signs: seizures; bulging anterior fontanel; extensor posturing/ opisthotonus; focal cerebral signs including gaze deviation and hemiparesis; cranial nerve palsies. Nuchal rigidity per se is the least common neurologic sign in neonatal bacterial meningitis.

Infantile Diarrhoea

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Diarrhoea is a condition in which loose, watery stools are passed with greater frequency than normal.Diarrhoea occurs when the bowel or large intestine becomes irritated. This can be caused by many things, including infection, chemical toxins, inflammation, or stress and anxiety. The bowel responds to this irritation in three ways.
Diarrhoea in infants can cause:
    * belly cramping or pain, which may disrupt sleep.
    * vomiting.
    * loss of appetite.
    * frequent, watery stools. In more serious situations, stools may contain pus or blood.
    * fussiness.
    * sluggishness and less activity than usual.
    * less interest in feeding.
It is important to be able to tell the difference between diarrhoea and the normal, loose, watery stools of infants in the first 6 to 8 weeks of life. Breast-fed infants normally have stools that look like watery, yellow cottage cheese, although a greenish colour can be noted on occasions. Their stools also are frequent, often occurring during or after each feeding. Breast milk stools usually are sweet-smelling as compared to the stools of formula-fed infants.
Most infants, even those fed formula, have frequent, watery stools until they are 6 to 8 weeks old. After that, the stools become firmer and less frequent. In fact, infants that are only fed breast milk beyond the first 2 months of life may have a stool only every 7 to 10 days. As long as the stool is soft, this is normal. Babies' stools are firmer once they start on solid food.
Most diarrhoea in infants is caused by stomach viruses, This condition is viral gastroenteritis. Although diarrhoea is common, there are side effects that can become serious if left untreated.Diarrhoea results in more fluid than normal going into the stools. This can leave a baby's body without enough fluid to meet its needs, a condition called dehydration. Infants are small and do not have a lot of fluid in their bodies.
Diarrhoea, especially in toddlers, can last a long time. If it is accompanied by persistent loss of appetite, it can lead to nutritional problems, although this is unusual.

Cardiac Arrhythmias

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SA Node and AV node cells are slow conductors activated by calcium, thus blocked by calcium channel blockers such as verapamil.Atrium, Bundle of His, and ventricle cells are fast conducting and activated by sodium, thus blocked by sodium channel blockers (class 1 anti-arrhythmics) such as quinidine, lidocaine and propafenone.
Four Mechanisms of Arrhythmia
Reentry (most common)
Triggered activity

Reentry Requires
2 distinct pathways that come together at beginning and end to form a loop. 
A unidirectional block in one of those pathways. 
Slow conduction in the unblocked pathway.  

Reentry Mechanism
An arrhythmia is triggered by a premature beat
The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway
The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement.  This creates the re-entry circuit

Heart cells other than those of the SA node depolarize faster than SA node cells, and take control as the cardiac pacemaker. 
Parasystole is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells. 

Triggered activity
 is like a domino effect where the arrhythmia is due to the preceding beat. 
 Delayed after-depolarizations arise during the resting phase of the last beat and may be the cause of digitalis-induced arrhythmias. 
 Early after-depolarizations arise during the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced)

Cholangiocarcinoma is a cancer of the bile ducts which drain bile from the liver into the small intestine. Other biliary tract cancers include pancreatic cancer, gall bladder cancer, and cancer of the ampulla of Vater. Cholangiocarcinoma is a relatively rare adenocarcinoma but rates of cholangiocarcinoma have been rising worldwide over the past several decades.
The most common physical indications of cholangiocarcinoma are abnormal liver function tests, jaundice (yellowing of the eyes and skin), which occurs only, when bile ducts are blocked by the tumor, abdominal pain (30%–50%), generalized itching (66%), weight loss (30%–50%), fever (up to 20%), or changes in stool or urine color.To some extent, the symptoms depend upon the location of the tumor: Patients with cholangiocarcinoma in the extrahepatic bile ducts (outside the liver) are more likely to have jaundice, while those with tumors of the bile ducts within the liver often have pain without jaundice.
The disease is diagnosed through a combination of blood tests, imaging, endoscopy, and sometimes surgical exploration. Cholangiocarcinoma is often in an advanced stage by the time symptoms develop, which may limit treatment options. Known risk factors for cholangiocarcinoma include primary sclerosing cholangitis (an inflammatory disease of the bile ducts), congenital liver malformations, infection with the parasitic liver flukes Opisthorchis viverrini or Clonorchis sinensis, and exposure to Thorotrast (thorium dioxide), a chemical formerly used in medical imaging. However, most patients with cholangiocarcinoma have no specific risk factors.
Cholangiocarcinoma is considered to be an incurable and rapidly lethal disease unless all of its tumors can be fully resected (cut out surgically). There is no potentially curative treatment except surgery, but unfortunately most patients have advanced and inoperable disease at the time of diagnosis. Patients with cholangiocarcinoma are generally managed, though never cured, with chemotherapy or radiation therapy as well as palliative care measures, and these are also used as adjuvant therapies post-surgically in cases where resection has been successful. Some areas of ongoing medical research in cholangiocarcinoma include the use of newer targeted therapies (such as erlotinib) or photodynamic therapy for treatment, and the concentration of byproducts of cancer stromal cell formation in the blood for diagnosis.

Disseminated intravascular coagulation (DIC) or consumptive coagulopathy, is a pathological activation of coagulation that happens in response to a variety of diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body.As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin,the gastrointestinal tract, the respiratory tract and surgical wounds.The small clots also disrupt normal blood flow to organs , which may malfunction as a result.

DIC can occur in the following conditions:
    Cancers of lung, pancreas, prostate and stomach, as well as acute myeloid leukemia (particularly APML)
    Obstetric: abruptio placentae, pre-eclampsia, amniotic fluid embolism
    Massive tissue injury: Trauma, burns, extensive surgery
    Infections: Gram-negative sepsis, Neisseria meningitidis, Streptococcus pneumoniae, malaria, histoplasmosis, aspergillosis, Rocky mountain spotted fever
    Miscellaneous: Liver disease, snake bite, giant hemangioma, shock, heat stroke, vasculitis, aortic aneurysm, Serotonin syndrome    
Viral: Arenaviruses causing Argentine hemorrhagic fever or Bolivian Hemorrhagic Fever
Diagnosis is usually suggested by following conditions:
Severe cases with hemorrhage: The PT and APTT are usually very prolonged and the fibrinogen level markedly reduced. High levels of fibrin degradation products, including D-dimer, are found owing to the intense fibrinolytic activity stimulated by the presence of fibrin in the circulation. There is severe thrombocytopenia. The blood film may show fragmented red blood cells.
The only effective treatment is the reversal of the underlying cause. Anticoagulants are given exceedingly rarely when thrombus formation is likely to lead to imminent death. Platelets may be transfused if counts are less than 5,000-10,000/mm3 and massive hemorrhage is occurring, and fresh frozen plasma may be administered in an attempt to replenish coagulation factors and anti-thrombotic factors, although these are only temporizing measures and may result in the increased development of thrombosis.

Compartment Syndromes

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An elevation of the interstitial pressure in a closed osteofascial compartment that results in micrvascular compromise.If left untreated will cause tissue damage.Compartments with relatively noncompliant fascial or osseous structures most commonly are involved ,especially the anterior compartment  of the leg and the volar compartment of the forearm.Compartment syndromes can be classified as :
Acute compartment syndrome (ACS)    or
Chronic compartment syndrome (CCS) depending on the cause of increased intra-compartmental pressure and the duration of symptoms
Acute compartment syndrome can develop anywhere a skeletal muscle is surrounded by a substantial fascia.
ACS  may occur in foot, leg, thigh, buttocks, lumbar paraspinous muscles, hand, forearm, arm and shoulder. 

Etiology of Acute compartment syndrome
Hemorrhage (e.g. due to vascular injury )
Coagulopathy (e.g. hemophilia ,  ASA overdose , thrombolytics , heparin infusion , sickle cell disease or trait )
Muscle edema (e.g. severe exercise , crush injury [trauma,alcohol,or drug-induced]  ,trauma with or without fracture  )
 Surgically related  (e.g. knee arthroscopy , tibial osteotomy without drainage , after epidural anesthesia )
Massive crystalloid infusion
Ruptured Backer’s cyst
Muscle hypertrophy ( androgens )
Intracompartmental fluid infusion (interosseosus infusion )
Capillary leak syndrome
Intra-arterial injections of sclerosing agents
Post –ischemic reperfusion

Benign prostatic obstruction (BPO) is a common cause of urinary symptoms in men older than 40-years of age.
Management Options for patients with BPO
Medical Therapies
5 α reductase inhibitors:
Finasteride (Proscar)
Alpha- blockers:Trazosin (Itrin),Doxazosin (Cardura),Alfuzosin (Xatral).,Tamsulosin (Flomax, Omnic)

Surgical Therapy of BPO
Open prostatectomy
Transurethral prostatectomy
TURP (Resection)
TUVP (Vaporization)
TUVRP (Vaporization-Resection)
Transurethral resection of the Prostate (TURP) using a standard wire loop and electrosurgical unit is still regarded as the “Gold Standard” in the treatment of men with BPO
Transurethral vaporization of the prostate (TUVP)
Rolling cylinder (The Vaportrode) provides enhanced contact with prostatic tissue using augmented electrocutting energy.Electrovaporization current maintained efficacy of TURP with minimal bleeding and electrolyte disturbances.
Disadvantages: Slow and Lack of prostatic tissue for histopathological examination.

Ocular Trauma

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A blowout fracture is a fracture of the walls or floor of the orbit. Intraorbital material may be pushed out into one of the paranasal sinuses. This is most commonly caused by blunt trauma of the head, generally personal altercations.
Orbital floor fractures can increase volume of the orbit with resultant hypoglobus and enophthalmos.The inferior rectus muscle or orbital tissue can become entrapped within the fracture, resulting in tethering and restriction of gaze and diplopia.
Significant orbital emphysema from a communication with the maxillary sinus can occur. Orbital hemorrhage is possible with risk of a compressive optic neuropathy.
The globe can be ruptured or suffer less severe forms of trauma, resulting in hyphema, retinal edema, and profound visual loss.
Periorbital ecchymosis and edema accompanied by pain are obvious external signs and symptoms, respectively. Enophthalmos is possible but initially can be obscured by surrounding tissue swelling. This swelling can restrict ocular motility, giving the impression of soft tissue or inferior rectus entrapment. Retrobulbar or peribulbar hemorrhage may be heralded by proptosis. A bony step-off of the orbital rim and point tenderness are possible during palpation.
Examination of the globe is essential, albeit difficult because of soft tissue edema. Desmarres retractors may be helpful to spread edematous eyelids.
Pupillary dysfunction coupled with decreased visual acuity should alert one to the possibility of a traumatic or compressive optic neuropathy.Ocular misalignment, hypotropia or hypertropia, and limitation of elevation ipsilateral to the fracture are possible. Forced duction testing can differentiate entrapment versus neuromyogenic etiologies of muscle underaction.The supratarsal crease may deepen, along with narrowing of the palpebral fissure stemming from enophthalmos or fibrous tissue contraction. Although the palpebral fissure may in fact narrow, the geometric shape is preserved, since dehiscence or disruption of the canthal tendons is uncommon.

Marfan syndrome

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Marfan syndrome is a genetic disorder of the connective tissue. It is carried by a gene called FBN1, which encodes a connective protein called fibrillin-1.This syndrome has a range of expressions, from mild to severe. The most serious complications are defects of the heart valves and aorta. It may also affect the lungs, eyes, the dural sac surrounding the spinal cord, skeleton and the hard palate.
Although there are no unique signs or symptoms of Marfan syndrome, the constellation of long limbs, the dislocated lenses, and the aortic root dilation are sufficient to make the diagnosis with confidence. There are more than 30 other clinical features that are variably associated with the syndrome, most involving the skeleton, skin, and joints.
Many individuals with Marfan syndrome grow to above average height. Some have long slender limbs with long fingers and toes (arachnodactyly). This condition of elongated limbs is known as dolichostenomelia. Abnormal curvature of the spine (scoliosis) is common, as is abnormal indentation (pectus excavatum) or protrusion (pectus carinatum) of the sternum. Other signs include abnormal joint flexibility, a high palate, malocclusions, flat feet, hammer toes, stooped shoulders, unexplained stretch marks on the skin.
Marfan syndrome can also seriously affect the eyes and vision. Nearsightedness and astigmatism are common, but farsightedness can also result. Subluxation (dislocation) of the crystalline lens in one or both eyes (ectopia lentis) also occurs.
Marfan syndrome is a risk factor for spontaneous pneumothorax.
Mitral valve prolapse, aortic regurgitation are commonly associated with Marfan's syndrome

Severe acute respiratory syndrome

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Severe acute respiratory syndrome is a respiratory disease in humans which is caused by the SARS coronavirus.Coronaviruses are positive-strand, enveloped RNA viruses that are important pathogens of mammals and birds. This group of viruses cause enteric or respiratory tract infections in a variety of animals including humans, livestock and pets.Initial symptoms are flu-like and may include: fever, myalgia, lethargy, gastrointestinal symptoms, cough, sore throat and other non-specific symptoms. The only symptom that is common to all patients appears to be a fever above 38 °C (100.4 °F). Shortness of breath may occur later.
SARS may be suspected in a patient who has:
   1. Any of the symptoms, including a fever of 38 °C (100.4 °F) or higher, and
   2. Either a history of:
         1. Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days OR
         2. Travel to any of the regions identified by the WHO as areas with recent local transmission of SARS
A probable case of SARS has the above findings plus positive chest X-ray findings of atypical pneumonia or respiratory distress syndrome.White blood cell and platelet counts are often high.
Three possible diagnostic tests have emerged, each with drawbacks. The first, an ELISA (enzyme-linked immunosorbent assay) test detects antibodies to SARS reliably but only 21 days after the onset of symptoms. The second, an immunofluorescence assay, can detect antibodies 10 days after the onset of the disease but is a labour and time intensive test, requiring an immunofluorescence microscope and an experienced operator. The last test is a polymerase chain reaction (PCR) test that can detect genetic material of the SARS virus in specimens ranging from blood, sputum, tissue samples and stools. The PCR tests so far have proven to be very specific but not very sensitive.M

Imaging Evaluation of Thyroid Nodules

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Malignant Thyroid Nodules
No clear evidence that treatment of thyroid cancers of < 1 cm alters life expectancy
Most thyroid cancers: papillary or follicular histology with excellent prognosis
Risk of malignancy greater for patients < 20 years and > 60 years of age
Higher risk with previous radiation exposure
Cancer risk of 10 - 13%  whether thyroid contains solitary or multiple nodules

US Features of Malignant Thyroid Nodules
Taller than wide
Marked hypoechogenicity (less than adjacent strap muscles)
Coarse internal calcifications
Irregular margins
Internal blood flow
Solid composition


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In the United States, microalbuminuria is found in 43%, and macroalbuminuria, in 8% of those with a history of diabetes.
Annual incidence rates of microalbuminuria of 1% to 2% are reported consistently for both type 1 and type 2 diabetes
Moreover, diabetes accounts for 45% of prevalent kidney failure, up from 18% in 1980.

Diabetic Kidney Disease (CKD)
Although kidney biopsy is required to diagnose diabetic glomerulopathy definitively, in most cases, careful screening of diabetic patients can identify people with DKD
DKD is based in part on the finding of elevated urinary albumin excretion, which is divided arbitrarily into:  microalbuminuria, a modest elevation of albumin thought to be associated with stable kidney function, but a greater risk of macroalbuminuria and kidney failure
 macroalbuminuria, a higher elevation of albumin associated with progressive decline in glomerular filtration rate (GFR), an increase in systemic blood pressure, and a high risk of kidney failure.

An elevated ACR should be confirmed in the absence of urinary tract infection with 2 additional first-void specimens collected during the next 3 to 6 months.
Microalbuminuria is defined as an ACR between 30-300 mg/g.
Macroalbuminuria is defined as an ACR > 300 mg/g.
2 of 3 samples should fall within the microalbuminuric or macroalbuminuric range to confirm classification.

In most patients with diabetes, CKD should be attributable to diabetes if:
Macroalbuminuria is present;  or
Microalbuminuria is present
In the presence of diabetic retinopathy
In type 1 diabetes of at least 10 years' duration.

Legg–Calvé–Perthes syndrome

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Legg–Calvé–Perthes syndrome is a degenerative disease of the hip joint, where growth/loss of bone mass leads to some degree of collapse of the hip joint and to deformity of the ball of the femur and the surface of the hip socket. The disease is characterized by idiopathic avascular osteonecrosis of the capital femoral epiphysis of the femoral head leading to an interruption of the blood supply of the head of the femur close to the hip joint. The disease is typically found in young children, and it can lead to osteoarthritis in adults.
Although no-one has identified the cause of Perthes disease it is known that there is a reduction in blood flow to the joint. It is thought that the artery of the ligamentum teres femoris closes too early, not allowing time for the medial circumflex femoral artery to take over.
Common symptoms include hip, knee, or groin pain, exacerbated by hip/leg movement. The pain feels like a tooth ache, possibly severe. There is a reduced range of motion at the hip joint and a painful or antalgic gait. There may be atrophy of thigh muscles from disuse and an inequality of leg length. In some cases, some activity can cause severe irritation or inflammation of the damaged area including standing, walking, running, kneeling, or stooping repeatedly for an extended period of time.
X-Rays of the hip confirm the diagnosis. X-rays usually demonstrates a flattened and later fragmented head of femur. A bone scan or MRI may be useful in making the diagnosis in those cases where x-rays are inconclusive. Neither bone scan or MRI offer any additional useful information beyond that of x-rays in an established case.
The goal of treatment is to avoid severe degenerative arthritis. Orthopedic assessment is crucial. Younger children have a better prognosis than older children.


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Osteoarthritis (OA) also known as degenerative arthritis or degenerative joint disease, is a group of mechanical abnormalities involving degradation of joints,including articular cartilage and subchondral bone.Symptoms may include joint pain, tenderness, stiffness, locking, and sometimes an effusion. A variety of causes—hereditary, developmental, metabolic, and mechanical—may initiate processes leading to loss of cartilage. When bone surfaces become less well protected by cartilage, bone may be exposed and damaged.
The main symptom is pain,causing loss of ability and often stiffness."Pain" is generally described as a sharp ache, or a burning sensation in the associate muscles and tendons. OA can cause crepitus when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. OA is the most common cause of joint effusion, sometimes called water on the knee in lay terms, an accumulation of excess fluid in or around the knee joint.
OA commonly affects the hands, feet, spine, and the large weight bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel worse, the more they are used throughout the day, thus distinguishing it from rheumatoid arthritis.
In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen. Some people notice these physical changes before they experience any pain.

Cerebral Anatomy and Physiology

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Divided into four principle parts:
    Brain stem
Brain is protected by cranial bones, cranial meninges, and CSF.
Brain stem consists of the medulla oblongata, pons, and midbrain. Lower end is a continuation of the spinal cord.
Diencephalon consists primarily of the thalamus and hypothalamus.
Cerebrum spreads over the diencephalon and occupies most of the cranium.
Inferior to the cerebrum and posterior to the brain stem is the cerebellum.
Cranial meninges surround the brain and are continuous with the spinal meninges.

Tough fibrous structure containing an inner (meningeal) layer and outer (periosteal) layer
Most of the dura’s venous sinuses lie between the dural layers
Dural layers are generally fused, except where they separate to provide space for the venous sinuses and where the inner layer forms septa between the brain portions
Outer layer firmly attached to inner surface of cranial bones; inner layer continuous with spinal dura

Delicate avascular membrane covers the subarachnoid space
Between the arachnoid and dura mater lies the subdural space
Arachnoid granulations project into the superior sagittal sinus
Subarachnoid space between the arachnoid and the pia is relatively narrow over the surface of the cerebral hemisphere and is much wider at areas at the base of the brain

Thin connective tissue membrane that covers the brain surface and extends into sulci and fissures and around blood vessels throughout the brain
Invaginations of the pia form choroid plexuses of the ventricles
Clinical considerations:
Various types of lesions, malformations, or pathology may present in one or more intracranial compartments

Tuberculous pericarditis

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Incidence low secondary to low incidence of TB in general
Occurs in 1-2% of patients with pulmonary TB
One Spanish study found 4.4% of pulmonary TB patient s had pericarditis
Keep in mind that Spanish (and South African) figures on incidence far exceed that in the USA
A Mayo clinic study found 2% cases of pericarditis in pulmonary TB patients as apposed to a similar study at Mayo fifty years ago
However, parts of the USA have high immigrant populations where TB pericarditis rates are much higher, as established at Baylor in 1990.
TB pericarditis is usually associated with TB somewhere else in body
Usually represent reactivation disease thus a primary infective location usually not found
4 Stages
Do not necessarily occur in order or individually
Inflammatory process thought secondary to hypersensitivity reaction to tuberculoprotein
Serosangiouness fluid with leukocytes and high protein and tubercle bacilli found in low concentration
Pressures consistent with cardiac tamponade are found

Pericarditis caused by tuberculosis is difficult to diagnose, because definitive diagnosis requires culturing Mycobacterium tuberculosis from aspirated pericardial fluid or pericardial biopsy, which requires high technical skill and is often not diagnostic (the yield from culture is low even with optimum specimens). The Tygerberg scoring system helps the clinician to decide whether pericarditis is due to tuberculosis or whether it is due to another cause

Urinary Incontinence

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Urinary incontinence is any involuntary leakage of urine.Continence and micturition involve a balance between urethral closure and detrusor muscle activity. Urethral pressure normally exceeds bladder pressure, resulting in urine remaining in the bladder. The proximal urethra and bladder are both within the pelvis. Intraabdominal pressure increases (from coughing and sneezing) are transmitted to both urethra and bladder equally, leaving the pressure differential unchanged, resulting in continence. Normal voiding is the result of changes in both of these pressure factors: urethral pressure falls and bladder pressure rises.
    * Stress incontinence, also known as effort incontinence, is due essentially to insufficient strength of the pelvic floor muscles.

    * Urge incontinence is involuntary loss of urine occurring for no apparent reason while suddenly feeling the need or urge to urinate.

    * Overflow incontinence: Sometimes people find that they cannot stop their bladders from constantly dribbling, or continuing to dribble for some time after they have passed urine. It is as if their bladders were like a constantly overflowing pan, hence the general name overflow incontinence.

    * Polyuria - uncontrolled diabetes mellitus,central diabetes insipidus and nephrogenic diabetes insipidus.
    * Caffeine stimulates the bladder.
    * Enlarged prostate is the most common cause of incontinence in men after the age of 40; sometimes prostate cancer may also be associated with urinary incontinence. Moreover drugs or radiation used to treat prostate cancer can also cause incontinence.
    * Brain disorders like multiple sclerosis, Parkinson's disease, strokes and spinal cord injury can all interfere with nerve function of the bladder.

Airway Management in the Trauma Patient

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Airway and Ventilation Methods
Orotracheal Intubation- preferred in almost all situations
   present or impending respiratory failure
   unable to protect own airway (<8)
   secures airway
   route for a few medications
   optimizes ventilation and oxygenation

Nasotracheal Intubation-  rarely if ever used in the initial management of the injured patient.
Many drawbacks
Goal of safe endotracheal intubation with cervical spine precautions can be better accomplished with orotracheal intubation

Surgical Cricothyrotomy
  absolute need for a definitive airway AND
   unable to perform ETT due for structural or anatomic reasons, AND
   risk of not intubating is > surgical airway risk
  absolute need for a definitive airway AND
   unable to clear an upper airway obstruction, AND
   multiple unsuccessful attempts at ETT, AND
   other methods of ventilation do not allow for effective ventilation and respiration

Surgical Cricothyrotomy
Contraindications (relative)
Age < 8 years (some say 10)
evidence of fx larynx or cricoid cartilage
evidence of tracheal transection

Needle Cricothyrotomy & Transtracheal Jet Ventilation
Same as surgical cricothyrotomy along with
Contraindication for surgical cricothyrotomy
caution with tracheal transection

Diabetic Retinopathy

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Diabetic retinopathy is retinopathy caused by complications of diabetes mellitus, which can eventually lead to blindness. It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more.
Diabetic retinopathy often has no early warning signs. Even macular edema, which may cause vision loss more rapidly, may not have any warning signs for some time.As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (ocular hemorrhage) and blur vision. The first time this happens, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots, floating in a person's visual field, though the spots often go away after a few hours.
On funduscopic exam, a doctor will see cotton wool spots, flame hemorrhages and dot-blot hemorrhages.
As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage when blood vessels proliferate.The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma.

Lupus Erythematosus

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Lupus erythematosus is a category for a collection of diseases with similar underlying problems with immunity (autoimmune disease).Lupus erythematosus may manifest as a systemic disease or in purely cutaneous forms.Four main types of lupus exist — systemic lupus erythematosus, discoid lupus erythematosus, drug-induced lupus erythematosus, and neonatal lupus erythematosus. Of these, systemic lupus erythematosus is the most common and serious form of lupus.Symptoms of these diseases can affect many different body systems, including joints, skin, kidneys, blood cells, heart, and lungs.
Photosensitivity's relationship to and influence on the systemic manifestations of lupus remain to be defined. Mechanisms for photosensitivity might include: modulation of autoantibody location, cytotoxic effects, apoptosis induction with autoantigens in apoptotic blebs, upregulation of adhesion molecules and cytokines, induction of nitric oxide synthase expression and ultraviolet-generated antigenic DNA. Tumor necrosis factor alpha also seems to play a role in the development of photosensitivity.

Fragile X syndrome

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Fragile X syndrome is a genetic syndrome which results in a spectrum of characteristic physical and intellectual limitations and emotional and behavioral features which range from severe to mild in manifestation.The syndrome is associated with the expansion of a single trinucleotide gene sequence (CGG) on the X chromosome, and results in a failure to express the protein coded by the FMR1 gene, which is required for normal neural development. Fragile X is the most common known single gene cause of autism and the most common inherited cause of intellectual disability.
Aside from intellectual disability, prominent characteristics of the syndrome include an elongated face, large or protruding ears, flat feet, larger testes (macroorchidism), and low muscle tone. Speech may include cluttered speech or nervous speech.Behavioral characteristics may include stereotypic movements (e.g., hand-flapping) and atypical social development, particularly shyness, limited eye contact, memory problems, and difficulty with face encoding.
Fragile X syndrome was originally diagnosed by culturing cells in a folate deficient medium and then assessing the cultures for X-chromosome breakage by cytogenetic analysis of the long arm of the X chromosome. This technique proved unreliable for both diagnosis and carrier testing.
The fragile X abnormality is now directly determined by analysis of the number of CGG repeats and their methylation status using restriction endonuclease digestion and Southern blot analysis.
Fragile X syndrome is an X-linked dominant condition with variable expressivity and possibly reduced penetrance.Because males normally have only one copy of the X chromosome, those males with significant trinucleotide expansion at the FMR1 locus are symptomatic. Females have two X chromosomes and thus have an increased probability of having a working FMR1 allele. Females carrying one X chromosome with an expanded FMR1 gene can have some signs and symptoms of the disorder or be normal.

Local Complications of Fractures

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Visceral injury:
Fractures around the trunk are often complicated by visceral injury. E.g. Rib fractures are associated with life threatening pneumothorax or with spleen, liver injuries. E.g. Pelvic injuries are associated with bladder or urethral rupture and cause sever hematoma in the retroperitoneum .Surgery of visceral injuries should take precedence over the treatment of fracture.
Vascular Injuries:
Most associated with injuries around knee, elbow, humerus and femoral shaft.
Commonly associated with high-energy open fractures.
They are rare but well-recognized.
Cause : From initial trauma or from bone fragment
Mechanism of injuries:
** The artery may be cut or torn.
** Compressed by the fragment of bone.
** normal appearance with intimal detachment that lead to thrombus formation.
** segment of artery may be in spasm.
Classical presentation of ischemia 5 Ps: Pain , Pallor, Pulseless , Paralysis , and Paraesthesia
X-ray: suggest high-risk fracture. Angiogram should be performed to confirm diagnosis.

This is an emergency because the effect of ischemia especially on the muscle is irrevesible after 6 hours.
1. Temporary vascular shunt to perfuse distal limb.
2. Skeletal stabilization – temporary external fixation often used.
3. Definitive vascular repair.
4. Staged definitive skeletal internal fixation if required.
Nerve injury:
- It’s more common than arterial injuries. - The most commonly injured nerve is the radial nerve in its groove or in the lower third of the upper arm especially in oblique fracture of the humerus. - Common with humerus, elbow and knee fractures - Most nerve injuries are due to tension neuropraxia.
Compartment syndrome:
**Most commonly in forearm and calfs. **Muscles are arranged in different compartments and surrounded by one fascia , this arrangement called osteofascial compartment. **Compartment syndrome occurs when muscle swells within osteofacial compartment and occluds its blood supply >infarction and late ischemic contracture. **Trauma is the most common cause. reasons that lead to increase the pressure inside: 1. Bleeding 2. Edema 3. Infection

Colorectal Polyps

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A lesion which projects into the lumen of the bowel.
Size of a few mm to several cm in diameter.
Single or multiple. In polyposis syndrome hundreds may be found
Larger polyps are found in the rectum
5% may contain invasive carcinoma at discovery
The type of cell that forms the polyp varies and is important in determining its potential for developing into a cancer
Most polyps are asymptomatic until they grow to 2cm in diameter
They can lead to bleeding, frank blood or microscopic bleeding (presenting with anaemia)
Polyps rarely present with a change in bowel habit – but large polyps in the rectum can present with tenesmus.
A large amount of mucus can also be passed.
Rarely a polyp will prolapse through the anus or act as an apex for an intussception.

Classification of polyps
Metaplastic (90%)
Adenomatous (~10%)
    Familial adenomatous polyposis (FAP)
    Gardeners syndrome
    Peutz-Jeghers Syndrome
    Cowden Syndrome
Protrusions of mesenchymal tissue
Inflammatory polyps
    Pseudopolyps in Ulcerative colitis   

Dyspnea and Acute Respiratory Failure

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Respiratory failure is a condition in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 mm Hg. Furthermore, respiratory failure may be acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.
Hypoxemic respiratory failure (type I) is characterized by a PaO2 of less than 60 mm Hg with a normal or low PaCO2. This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units.
Hypercapnic respiratory failure (type II) is characterized by a PaCO2 of more than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders.

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