Mrcs Notes

June 10, 2018 | Author: nob2011nob | Category: Transplant Rejection, Atrium (Heart), Ventricle (Heart), Heart, Foot


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Fluid resuscitation burnsIndication: >15% total body area burns in adults (>10% children)  The main aim of resuscitation is to prevent the burn deepening  Most fluid is lost 24h after injury  First 8-12h fluid shifts from intravascular to interstitial fluid compartments  Therefore circulatory volume can be compromised. However fluid resuscitation causes more fluid into the interstitial compartment especially colloid (therefore avoided in first 8-24h)  Protein loss occurs Fluid resuscitation formula Parkland formula (Crystalloid only e.g. Hartman's solution/Ringers' lactate) Total fluid requirement in 24 hours = 4 ml x (total burn surface area (%)) x (body weight (kg))  50% given in first 8 hours  50% given in next 16 hours Resuscitation endpoint:Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to achieve this) Points to note:  Starting point of resuscitation is time of injury  Deduct fluids already given After 24 hours  Colloid infusion is begun at a rate of 0.5 ml x(total burn surface area (%))x(body weight (kg))  Maintenance crystalloid (usually dextrose-saline) is continued at a rate of 1.5 ml x(burn area)x(body weight)  Colloids used include albumin and FFP  Antioxidants, such as vitamin C, can be used to minimize oxidant-mediated contributions to the inflammatory cascade in burns  High tension electrical injuries and inhalation injuries require more fluid  Monitor: packed cell volume, plasma sodium, base excess, and lactate All local anaesthetics have a chemical bond linking an amine to either an amide or an ester. Most local anaesthetics are of the amino- amide types, these have a more favorable side effect profile and are more stable in solution. Procaine and benzocaine have amino - ester groups, these are metabolised by pseudocholinesterases. Ventricular tachcardia Ventricular tachycardia (VT)is broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment. There are two main types of VT:  monomorphic VT: most commonly caused by myocardial infarction  polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval. The causes of a long QT interval are listed below Causes of a prolonged QT interval Congenital  Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)  Romano-Ward syndrome (no deafness) Drugs  amiodarone, sotalol, class 1a antiarrhythmic drugs  tricyclic antidepressants, fluoxetine  chloroquine  terfenadine*  erythromycin Other  electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia  acute myocardial infarction  myocarditis  hypothermia  subarachnoid haemorrhage Valves of the heart Mitral valve Aortic valve Pulmonary valve Tricuspid valve 2 cusps 3 cusps 3 cusps 3 cusps First heart sound Second heart sound Second heart sound First heart sound 1 anterior cusp 1 anterior cusp 2 anterior cusps 2 anterior cusps Attached to chordae tendinae No chordae No chordae Attached to chordae tendinae Acute intermittent porphyria Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect in porphobilinogen deaminase, an enzyme involved in the biosynthesis of haem. The results in the toxic accumulation of delta aminolaevulinic acid and porphobilinogen. It characteristically presents with abdominal and neuropsychiatric symptoms in 20-40 year olds. AIP is more common in females (5:1) Features  abdominal: abdominal pain, vomiting  neurological: motor neuropathy  psychiatric: e.g. depression  hypertension and tachycardia common Diagnosis  classically urine turns deep red on standing  raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)  assay of red cells for porphobilinogen deaminase  raised serum levels of delta aminolaevulinic acid and porphobilinogen Pagets disease Paget's disease is a disease of increased but uncontrolled bone turnover and is characterised by architecturally abnormal bones. It is thought to be primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity causing areas of sclerosis and deformity. Paget's disease is common (UK prevalence 5%) but symptomatic in only 1 in 20 patients Predisposing factors  increasing age  male sex  northern latitude  family history Clinical features  bone pain (e.g. pelvis, lumbar spine, femur)  classical, untreated features: bowing of tibia, bossing of skull  raised alkaline phosphatase (ALP) - calcium* and phosphate are typically normal  skull x-ray: thickened vault, osteoporosis circumscripta Indications for treatment include bone pain, skull or long bone deformity, fracture, periarticular Paget's  bisphosphonate (either oral risedronate or IV zoledronate)  calcitonin is less commonly used now Complications  deafness (cranial nerve entrapment)  bone sarcoma (1% if affected for > 10 years)  fractures  skull thickening  high-output cardiac failure naesthetic agents The table below summarises some of the more commonly used IV induction agents Agent Specific features Propofol  Rapid onset of anaesthesia  Pain on IV injection  Rapidly metabolised with little accumulation of metabolites  Proven anti emetic properties  Moderate myocardial depression  Widely used especially for maintaining sedation on ITU, total IV anaesthesia and for daycase surgery Sodium thiopentone  Extremely rapid onset of action making it the agent of choice for rapid sequence of induction  Marked myocardial depression may occur  Metabolites build up quickly  Unsuitable for maintenance infusion  Little analgesic effects Ketamine  May be used for induction of anaesthesia  Has moderate to strong analgesic properties  Produces little myocardial depression making it a suitable agent for anaesthesia in those who are haemodynamically unstable  May induce state of dissociative anaesthesia resulting in nightmares Etomidate  Has favorable cardiac safety profile with very little haemodynamic instability  No analgesic properties  Unsuitable for maintaining sedation as prolonged (and even brief) use may result in adrenal suppression  Post operative vomiting is common ower limb- Muscular compartments Anterior compartment Muscle Nerve Action Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe Peroneal compartment Muscle Nerve Action Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint Superficial posterior compartment <muscle< b=""></muscle<> Nerve Action Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee Soleus Tibial nerve Plantar flexor Deep posterior compartment Muscle Nerve Action Flexor digitorum longus Tibial Flexes the lateral four toes Flexor hallucis longus Tibial Flexes the great toe Tibialis posterior Tibial Plantar flexor, inverts the foot Lumbar spinal stenosis Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk prolapse or other similar degenerative changes. Patients may present with a combination of back pain, neuropathic pain and symptoms mimicking claudication. One of the main features that may help to differentiate it from true claudication in the history is the positional element to the pain. Sitting is better than standing and patients may find it easier to walk uphill rather than downhill. The neurogenic claudication type history makes lumbar spinal stenosis a likely underlying diagnosis, the absence of such symptoms makes it far less likely. Pathology Degenerative disease is the commonest underlying cause. Degeneration is believed to begin in the intervertebral disk where biochemical changes such as cell death and loss of proteoglycan and water content lead to progressive disk bulging and collapse. This process leads to an increased stress transfer to the posterior facet joints, which accelerates cartilaginous degeneration, hypertrophy, and osteophyte formation; this is associated with thickening and distortion of the ligamentum flavum. The combination of the ventral disk bulging, osteophyte formation at the dorsal facet, and ligamentum flavum hyptertrophy combine to circumferentially narrow the spinal canal and the space available for the neural elements. The compression of the nerve roots of the cauda equina leads to the characteristic clinical signs and symptoms of lumbar spinal stenosis. Diagnosis MRI scanning is the best modality for demonstrating the canal narrowing. Historically a bicycle test was used as true vascular claudicants could not complete the test. Treatment Laminectomy Cardiac physiology  The heart has four chambers ejecting blood into both low pressure and high pressure systems.  The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on the left.  At rest diastole comprises 2/3 of the cardiac cycle.  The product of the frequency of heart rate and stroke volume combine to give the cardiac output which is typically 5-6L per minute. Detailed descriptions of the various waveforms are often not a feature of MRCS A (although they are on the syllabus). However, they are a very popular topic for surgical physiology vivas in the oral examination. Electrical properties  Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is capable of contraction.  In the normal situation the cardiac impulse is generated in the sino atrial node in the right atrium and conveyed to the ventricles via the atrioventricular node.  The sino atrial node is also capable of spontaneous discharge and in the absence of background vagal tone will typically discharge around 100x per minute. Hence the higher resting heart rate found in cardiac transplant cases. In the SA and AV nodes the resting membrane potential is lower than in surrounding cardiac cells and will slowly depolarise from -70mV to around -50mV at which point an action potential is generated.  Differences in the depolarisation slopes between SA and AV nodes help to explain why the SA node will depolarise first. The cells have a refractory period during which they cannot be re- stimulated and this period allows for adequate ventricular filling. In pathological tachycardic states this time period is overridden and inadequate ventricular filling may then occur, cardiac output falls and syncope may ensue. Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA node and increases the rate of pacemaker potential depolarisation. Cardiac cycle Image sourced from Wikipedia  Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic pressure is high.  Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic volume 130-160ml.  Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial pressure (x-descent).  Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular pressure drops the aortic pressure remains constant owing to peripheral vascular resistance and elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke volume is 70ml (i.e. Volume ejected).  Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave associated with closure of the aortic valve increases aortic pressure. The pressure dip before this rise can be seen on arterial waveforms and is called the incisura. During systole the atrial pressure increases such that it is now above zero (v- wave). Eventually atrial pressure exceed ventricular pressure and AV valves open - atria empty passively into ventricles and atrial pressure falls (y -descent ) The negative atrial pressures are of clinical importance as they can allow air embolization to occur if the neck veins are exposed to air. This patient positioning is important in head and neck surgery to avoid this occurrence if veins are inadvertently cut, or during CVP line insertion. Mechanical properties  Preload = end diastolic volume  Afterload = aortic pressure It is important to understand the principles of Laplace's law in surgery.  It states that for hollow organs with a circular cross section, the total circumferential wall tension depends upon the circumference of the wall, multiplied by the thickness of the wall and on the wall tension.  The total luminal pressure depends upon the cross sectional area of the lumen and the transmural pressure. Transmural pressure is the internal pressure minus external pressure and at equilibrium the total pressure must counterbalance each other.  In terms of cardiac physiology the law explains that the rise in ventricular pressure that occurs during the ejection phase is due to physical change in heart size. It also explains why a dilated diseased heart will have impaired systolic function. Starlings law  Increase in end diastolic volume will produce larger stroke volume.  This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke volume will fall once more. It is important for the regulation of cardiac output in cardiac transplant patients who need to increase their cardiac output. Baroreceptor reflexes  Baroreceptors located in aortic arch and carotid sinus.  Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal nerve.  They are stimulated by arterial stretch.  Even at normal blood pressures they are tonically active.  Increase in baroreceptor discharge causes: *Increased parasympathetic discharge to the SA node. *Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in stroke volume. *Decreased sympathetic discharge to venous system causing increased compliance. *Decreased peripheral arterial vascular resistance Atrial stretch receptors  Located in atria at junction between pulmonary veins and vena cava.  Stimulated by atrial stretch and are thus low pressure sensors.  Increased blood volume will cause increased parasympathetic activity.  Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors: the Bainbridge reflex.  Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal blood flow-decreases GFR-decreases urinary sodium excretion-renin secretion by juxtaglomerular apparatus-Increase in angiotensin II.  Increased atrial stretch will also result in increased release of atrial natriuretic peptide. Organ Transplant A number of different organ and tissue transplants are now available. In many cases an allograft is performed, where an organ is transplanted from one individual to another. Allografts will elicit an immune response and this is one of the main reasons for organ rejection. Graft rejection occurs because allografts have allelic differences at genes that code immunohistocompatability complex genes. The main antigens that give rise to rejection are:  ABO blood group  Human leucocyte antigens (HLA)  Minor histocompatability antigens ABO Matching ABO incompatibility will result in early organ rejection (hyperacute) because of pre existing antibodies to other groups. Group O donors can give organs to any type of ABO recipient whereas group AB donor can only donate to AB recipient. HLA System The four most important HLA alleles are:  HLA A  HLA B  HLA C  HLA DR An ideal organ match would be one in which all 8 alleles are matched (remember 2 from each parent, four each = 8 alleles). Modern immunosuppressive regimes help to manage the potential rejection due to HLA mismatching. However, the greater the number of mismatches the worse the long term outcome will be. T lymphocytes will recognise antigens bound to HLA molecules and then will then become activated. Clonal expansion then occurs with a response directed against that antigen. Types of organ rejection  Hyperacute. This occurs immediately through presence of pre formed antigens (such as ABO incompatibility).  Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates and vascular lesions.  Chronic. Occurs after the first 6 months. Vascular changes predominate. Hyperacute Renal transplants at greatest risk and liver transplants at least risk. Although ABO incompatibility and HLA Class I incompatible transplants will all fare worse in long term. Acute All organs may undergo acute rejection. Mononuclear cell infiltrates predominate. All types of transplanted organ are susceptible and it may occur in up to 50% cases. Chronic Again all transplants with HLA mismatch may suffer this fate. Previous acute rejections and other immunosensitising events all increase the risk. Vascular changes are most prominent with myointimal proliferation leading to organ ischaemia. Organ specific changes are also seen such as loss of acinar cells in pancreas transplants and rapidly progressive coronary artery disease in cardiac transplants. Surgical overview-Renal transplantation A brief overview of the steps involved in renal transplantation is given. Patients with end stage renal failure who are dialysis dependent or likely to become so in the immediate future are considered for transplant. Exclusion criteria include; active malignancy, old age (due to limited organ availability). Patients are medically optimised. Donor kidneys, these may be taken from live related donors and close family, members may have less HLA mismatch than members of the general population. Laparoscopic donor nephrectomy further minimises the operative morbidity for the donor. Other organs are typically taken from brain dead or dying patients who have a cardiac arrest and in whom resuscitation is futile. The key event is to minimise the warm ischaemic time in the donor phase. The kidney once removed is usually prepared on the bench in theatre by the transplant surgeron immediately prior to implantation and factors such as accessory renal arteries and vessel length are assessed and managed. For first time recipients the operation is performed under general anaesthesia. A Rutherford-Morrison incision is made on the preferred side. This provides excellent extraperitoneal access to the iliac vessels. The external iliac artery and vein are dissected out and following systemic heparinisation are cross clamped. The vein and artery are anastamosed to the iliacs and the clamps removed. The ureter is then implanted into the bladder and a stent is usually placed to maintain patency. The wounds are then closed and the patient recovered from surgery. In the immediate phase a common problem encountered in cadaveric kidneys is acute tubular necrosis and this tends to resolve. Graft survival times from cadaveric donors are typically of the order of 9 years and monozygotic twin transplant (live donor) may survive as long as 25 years. Voice production There are 2 main nerves involved: Superior laryngeal nerve (SLN)  Innervates the cricothyroid muscle Since the cricothyroid muscle is involved in adjusting the tension of the vocal fold for high notes during singing, SLN paresis and paralysis result in: a. Abnormalities in pitch b. Inability to sing with smooth change to each higher note (glissando or pitch glide) Recurrent laryngeal nerve (RLN)/Inferior laryngeal nerve  Innervates intrinsic larynx muscles a. Opening vocal folds (as in breathing, coughing) b. Closing vocal folds for vocal fold vibration during voice use c. Closing vocal folds during swallowing Hormonal regulation of calcium Hormone Actions Parathyroid hormone (PTH)  Increase calcium levels and decrease phosphate levels  Increases bone resorption  Immediate action on osteoblasts to increase ca 2+ in extracellular fluid  Osteoblasts produce a protein signaling molecule that activate osteoclasts which cause bone resorption  Increases renal tubular reabsorption of calcium  Increases synthesis of 1,25(OH)2D (active form of vitamin D) in the kidney which increases bowel absorption of Ca 2+  Decreases renal phosphate reabsorption 1,25-dihydroxycholecalciferol (the active form of vitamin D)  Increases plasma calcium and plasma phosphate  Increases renal tubular reabsorption and gut absorption of calcium  Increases osteoclastic activity  Increases renal phosphate reabsorption Calcitonin  Secreted by C cells of thyroid  Inhibits intestinal calcium absorption  Inhibits osteoclast activity  Inhibits renal tubular absorption of calcium Both growth hormone and thyroxine also play a small role in calcium metabolism. Dorsal column lesion  Loss vibration and proprioception  Tabes dorsalis, SACD Spinothalamic tract lesion  Loss of pain, sensation and temperature Central cord lesion  Flaccid paralysis of the upper limbs Osteomyelitis  Normally progressive  Staph aureus in IVDU, normally cervical region affected  Fungal infections in immunocompromised  Thoracic region affected in TB Infarction spinal cord  Dorsal column signs (loss of proprioception and fine discrimination Cord compression  UMN signs  Malignancy  Haematoma  Fracture Brown-sequard syndrome  Hemisection of the spinal cord  Ipsilateral paralysis  Ipsilateral loss of proprioception and fine discrimination  Contralateral loss of pain and temperature Coagulation cascade Two pathways lead to fibrin formation Intrinsic pathway (components already present in the blood)  Minor role in clotting  Subendothelial damage e.g. collagen  Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and Factor 12  Prekallikrein is converted to kallikrein and Factor 12 becomes activated  Factor 12 activates Factor 11  Factor 11 activates Factor 9, which with its co-factor Factor 8a form the tenase complex which activates Factor 10 Extrinsic pathway (needs tissue factor released by damaged tissue)  Tissue damage  Factor 7 binds to Tissue factor  This complex activates Factor 9  Activated Factor 9 works with Factor 8 to activate Factor 10 Common pathway  Activated Factor 10 causes the conversion of prothrombin to thrombin  Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to form links between fibrin molecules Fibrinolysis Plasminogen is converted to plasmin to facilitate clot resorption Image sourced from Wikipedia Intrinsic pathway Increased APTT Factors 8,9,11,12 Extrinsic pathway Increased PT Factor 7 Common pathway Increased APTT & PT Factors 2,5,10 Vitamin K dependent Factors 2,7,9,10 Upper limb fractures Colles' fracture  Fall onto extended outstretched hands  Described as a dinner fork type deformity  Classical Colles' fractures have the following 3 features: Features of the injury 1. Transverse fracture of the radius 2. 1 inch proximal to the radio-carpal joint 3. Dorsal displacement and angulation Smith's fracture (reverse Colles' fracture)  Volar angulation of distal radius fragment (Garden spade deformity)  Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed Bennett's fracture  Intra-articular fracture of the first carpometacarpal joint  Impact on flexed metacarpal, caused by fist fights  X-ray: triangular fragment at ulnar base of metacarpal Monteggia's fracture  Dislocation of the proximal radioulnar joint in association with an ulna fracture  Fall on outstretched hand with forced pronation  Needs prompt diagnosis to avoid disability Galeazzi fracture  Radial shaft fracture with associated dislocation of the distal radioulnar joint  Occur after a fall on the hand with a rotational force superimposed on it.  On examination, there is bruising, swelling and tenderness over the lower end of the forearm.  X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to dislocation of the inferior radio-ulnar joint. Barton's fracture  Distal radius fracture (Colles'/Smith's) with associated radiocarpal dislocation  Fall onto extended and pronated wrist Scaphoid fractures  Scaphoid fractures are the commonest carpal fractures.  Surface of scaphoid is covered by articular cartilage with small area available for blood vessels (fracture risks blood supply)  Forms floor of anatomical snuffbox  Risk of fracture associated with fall onto outstretched hand (tubercle, waist, or proximal 1/3)  The main physical signs are swelling and tenderness in the anatomical snuff box, and pain on wrist movements and on longitudinal compression of the thumb.  Ulnar deviation AP needed for visualization of scaphoid  Immobilization of scaphoid fractures difficult Radial head fracture  Fracture of the radial head is common in young adults.  It is usually caused by a fall on the outstretched hand.  On examination, there is marked local tenderness over the head of the radius, impaired movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination). Benign liver lesions Benign liver lesions Haemangioma  Most common benign tumours of mesenchymal origin  Incidence in autopsy series is 8%  Cavernous haemangiomas may be enormous  Clinically they are reddish purple hypervascular lesions  Lesions are normally separated from normal liver by ring of fibrous tissue  On ultrasound they are typically hyperechoic Liver cell adenoma  90% develop in women in their third to fifth decade  Linked to use of oral contraceptive pill  Lesions are usually solitary  They are usually sharply demarcated from normal liver although they usually lack a fibrous capsule  On ultrasound the appearances are of mixed echoity and heterogeneous texture. On CT most lesions are hypodense when imaged prior to administration of IV contrast agents  In patients with haemorrhage or symptoms removal of the adenoma may be required Mesenchymal hamartomas Congential and benign, usually present in infants. May compress normal liver Liver abscess  Biliary sepsis is a major predisposing factor  Structures drained by the portal venous system form the second largest source  Common symptoms include fever, right upper quadrant pain. Jaundice may be seen in 50%  Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in chronic abscesses Amoebic abscess  Liver abscess is the most common extra intestinal manifestation of amoebiasis  Between 75 and 90% lesions occur in the right lobe  Presenting complaints typically include fever and right upper quadrant pain  Ultrasonography will usually show a fluid filled structure with poorly defined boundaries  Aspiration yield sterile odourless fluid which has an anchovy paste consistency  Treatment is with metronidazole Hyatid cysts  Seen in cases of Echinococcus infection  Typically an intense fibrotic reaction occurs around sites of infection  The cyst has no epithelial lining  Cysts are commonly unilocular and may grow to 20cm in size. The cyst wall is thick and has an external laminated hilar membrane and an internal enucleated germinal layer  Typically presents with malaise and right upper quadrant pain. Secondary bacterial infection occurs in 10%.  Liver function tests are usually abnormal and eosinophilia is present in 33% cases  Ultrasound may show septa and hyatid sand or daughter cysts.  Percutaneous aspiration is contra indicated  Treatment is by sterilisation of the cyst with mebendazole and may be followed by surgical resection. Hypertonic swabs are packed around the cysts during surgery Polycystic liver disease  Usually occurs in association with polycystic kidney disease  Autosomal dominant disorder  Symptoms may occur as a result of capsular stretch Cystadenoma  Rare lesions with malignant potential  Usually solitary multiloculated lesions  Liver function tests usually normal  Ultrasonography typically shows a large anechoic, fluid filled area with irregular margins. Internal echos may result from septa  Surgical resection is indicated in all cases Muscle relaxants Suxamethonium  Depolarising neuromuscular blocker  Inhibits action of acetylcholine at the neuromuscular junction  Degraded by plasma cholinesterase and acetylcholinesterase  Fastest onset and shortest duration of action of all muscle relaxants  Produces generalised muscular contraction prior to paralysis  Adverse effects include hyperkalaemia, malignant hyperthermia and lack of acetylcholinesterase Atracurium  Non depolarising neuromuscular blocking drug  Duration of action usually 30-45 minutes  Generalised histamine release on administration may produce facial flushing, tachycardia and hypotension  Not excreted by liver or kidney, broken down in tissues by hydrolysis  Reversed by neostigmine Vecuronium  Non depolarising neuromuscular blocking drug  Duration of action approximately 30 - 40 minutes  Degraded by liver and kidney and effects prolonged in organ dysfunction  Effects may be reversed by neostigmine Pancuronium  Non depolarising neuromuscular blocker  Onset of action approximately 2-3 minutes  Duration of action up to 2 hours  Effects may be partially reversed with drugs such as neostigmine Image sourced from Wikipedia Renal stones Type of stones Features Percentage of all calculi Calcium oxalate Hypercalciuria is a major risk factor (various causes) Hyperoxaluria may also increase risk Hypocitraturia increases risk because citrate forms complexes with calcium making it more soluble Stones are radio-opaque (though less than calcium phosphate stones) Hyperuricosuria may cause uric acid stones to which calcium oxalate binds 85% Cystine Inherited recessive disorder of transmembrane cystine transport leading to decreased absorption of cystine from intestine and renal tubule Multiple stones may form Relatively radiodense because they contain sulphur 1% Uric acid Uric acid is a product of purine metabolism May precipitate when urinary pH low May be caused by diseases with extensive tissue breakdown e.g. malignancy More common in children with inborn errors of metabolism 5-10% Radiolucent Calcium phosphate May occur in renal tubular acidosis, high urinary pH increases supersaturation of urine with calcium and phosphate Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2 and 4 do not) Radio-opaque stones (composition similar to bone) 10% Struvite Stones formed from magnesium, ammonium and phosphate Occur as a result of urease producing bacteria (and are thus associated with chronic infections) Under the alkaline conditions produced, the crystals can precipitate Slightly radio-opaque 2-20% Laxatives Bulk forming laxatives Bran Psyllium Methylcellulose Osmotic laxatives Magnesium sulphate Magnesium citrate Sodium phosphate Sodium sulphate Potassium sodium tatrate Polyethylene glycol Stimulant laxatives Docusates Bisacodyl Sodium picosulphate Senna Ricinoleic acid Diseases affecting the vertebral column Ankylosing spondylitis  Chronic inflammatory disorder affecting the axial skeleton  Sacro-ilitis is a usually visible in plain films  Up to 20% of those who are HLA B27 positive will develop the condition  Affected articulations develop bony or fibrous changes  Typical spinal features include loss of the lumbar lordosis and progressive kyphosis of the cervico-thoracic spine Scheuermann's disease  Epiphysitis of the vertebral joints is the main pathological process  Predominantly affects adolescents  Symptoms include back pain and stiffness  X-ray changes include epiphyseal plate disturbance and anterior wedging  Clinical features include progressive kyphosis (at least 3 vertebrae must be involved)  Minor cases may be managed with physiotherapy and analgesia, more severe cases may require bracing or surgical stabilisation Scoliosis  Consists of curvature of the spine in the coronal plane  Divisible into structural and non structural, the latter being commonest in adolescent females who develop minor postural changes only. Postural scoliosis will typically disappear on manoeuvres such as bending forwards  Structural scoliosis affects > 1 vertebral body and is divisible into idiopathic, congential and neuromuscular in origin. It is not correctable by alterations in posture  Within structural scoliosis, idiopathic is the most common type  Severe, or progressive structural disease is often managed surgically with bilateral rod stabilisation of the spine Spina bifida  Non fusion of the vertebral arches during embryonic development  Three categories; myelomeningocele, spina bifida occulta and meningocele  Myelomeningocele is the most severe type with associated neurological defects that may persist in spite of anatomical closure of the defect  Up to 10% of the population may have spina bifida occulta, in this condition the skin and tissues (but not not bones) may develop over the distal cord. The site may be identifiable by a birth mark or hair patch  The incidence of the condition is reduced by use of folic acid supplements during pregnancy Spondylolysis  Congenital or acquired deficiency of the pars interarticularis of the neural arch of a particular vertebral body, usually affects L4/ L5  May be asymptomatic and affects up to 5% of the population  Spondylolysis is the commonest cause of spondylolisthesis in children  Asymptomatic cases do not require treatment Spondylolisthesis  This occurs when one vertebra is displaced relative to its immediate inferior vertebral body  May occur as a result of stress fracture or spondylolysis  Traumatic cases may show the classic "Scotty Dog" appearance on plain films  Treatment depends upon the extent of deformity and associated neurological symptoms, minor cases may be actively monitored. Individuals with radicular symptoms or signs will usually require spinal decompression and stabilisation Branches of the trigeminal nerve Ophthalmic nerve Sensory only Maxillary nerve Sensory only Mandibular nerve Sensory and motor Sensory Ophthalmic Exits skull via the superior orbital fissure Sensation of: scalp and forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose (including the tip of the nose, except alae nasi), the nasal mucosa, the frontal sinuses, and parts of the meninges (the dura and blood vessels). Maxillary nerve Exit skull via the foramen rotundum Sensation: lower eyelid and cheek, the nares and upper lip, the upper teeth and gums, the nasal mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses, and parts of the meninges. Mandibular nerve Exit skull via the foramen ovale Sensation: lower lip, the lower teeth and gums, the chin and jaw (except the angle of the jaw), parts of the external ear, and parts of the meninges. Motor Distributed via the mandibular nerve. The following muscles of mastication are innervated:  Masseter  Temporalis  Medial pterygoid  Lateral pterygoid Other muscles innervated include:  Tensor veli palatini  Mylohyoid  Anterior belly of digastric  Tensor tympani  Neo-intimal hyperplasia in distal arterial anastamoses may be reduced by use of a Miller Cuff when PTFE is the bypass conduit. PTFE may induce neo-intimal hyperplasia with subsequent occlusion of the distal anastomosis. In more proximal arterial bypass surgery the process of neo-intimal hyperplasia is not sufficient to cause anastomotic occlusion. However, distal bypasses are at greater risk and if vein cannot be used as a conduit then the distal end of the PTFE should anastomosed to a vein cuff to minimise the risk of neo- intimal hyperplasia. 'Machine' - Causes of Increased Serum K + M - Medications - ACE inhibitors, NSAIDS A - Acidosis - Metabolic and respiratory C - Cellular destruction - Burns, traumatic injury H - Hypoaldosteronism, haemolysis I - Intake - Excessive N - Nephrons, renal failure E - Excretion - Impaired Familial periodic paralysis has subtypes associated with hyper and hypokalaemia. Lower limb- Muscular compartments Anterior compartment Muscle Nerve Action Tibialis anterior Deep peroneal nerve Dorsiflexes ankle joint, inverts foot Extensor digitorum longus Deep peroneal nerve Extends lateral four toes, dorsiflexes ankle joint Peroneus tertius Deep peroneal nerve Dorsiflexes ankle, everts foot Extensor hallucis longus Deep peroneal nerve Dorsiflexes ankle joint, extends big toe Peroneal compartment Muscle Nerve Action Peroneus longus Superficial peroneal nerve Everts foot, assists in plantar flexion Peroneus brevis Superficial peroneal nerve Plantar flexes the ankle joint Superficial posterior compartment <muscle< b=""></muscle<> Nerve Action Gastrocnemius Tibial nerve Plantar flexes the foot, may also flex the knee Soleus Tibial nerve Plantar flexor Deep posterior compartment Muscle Nerve Action Flexor digitorum longus Tibial Flexes the lateral four toes Flexor hallucis longus Tibial Flexes the great toe Tibialis posterior Tibial Plantar flexor, inverts the foot Type of Murmur Conditions Ejection systolic Aortic stenosis Pulmonary stenosis, HOCM ASD, Fallot's Pan-systolic Mitral regurgitation Tricuspid regurgitation VSD Late systolic Mitral valve prolapse Coarctation of aorta Early diastolic Aortic regurgitation Graham-Steel murmur (pulmonary regurgitation) Mid diastolic Mitral stenosis Austin-Flint murmur (severe aortic regurgitation) Causes of decreased compliance:  pulmonary oedema  pulmonary fibrosis  pneumonectomy  kyphosis Causes of increased compliance  age  emphysema - this is due to loss alveolar walls and associated elastic tissue A unilateral dilated pupil is a classic sign of transtentorial herniation. The subclavian artery passes anterior to the middle scalene.
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