They will want to expose them- lowed by the main text, and with Overall this is an excellent book for the selves to a large number of questions selected key references clearly stated busy clinician requiring a quick reminder and reading large volumes of text can be separately from the other main refer- about an unusual case, as well as a fantastic difficult.
The format of the answers is ences at the end. Each chapter is resource for those studying for exams or appealing to the eye, allowing the presented in a concise and legible for- undertaking higher training in paediatric reader to select areas of interest by mat. This enables the reader to dip easily anaesthesia. In their introduc- system-based approach of answering a to delve further into a subject. It thoroughly deserves information they will be given and what management issues.
Topics covered a place in any anaesthetic departmental type of questions to expect. The cases include difficult airway, difficult venous library where children require the input are longer than one would expect in the access, difficult circulations, regional of anaesthetists. This seems to Dr J A Davies have allowed the authors to approach complex pain. All the chapters are Consultant Anaesthetist more topics for discussion.
The short presented in a clear, succinct and very Nottingham University Hospitals cases and clinical science questions are readable style and are interspersed with NHS Trust more representative of the exam appropriate use of figures and tables. Regardless, they allow you book, divided equally into a wide range collection of 11 expert reviews pub- to gain some further knowledge. The of topics in a relatively predictable lished in This edition, limited; however, this is to be expected provision of care for patients following like its predecessors, is presented in within the constraints of the questions, out of hospital cardiac arrest and cardiac a sturdy, easily-portable hardback vol- and readers would have to source other output monitoring.
The lack of of subjects. It is best used to may have been an omission. With little consultants as it provides easy access to replacement therapy in the light of the exception, the reviews are well writ- information and details on a variety of more recently published studies from ten, researched and referenced. The book is relatively easy to read vary between authors; for example, the If you like reading text then allow and the questions are presented in a lengthy chapter on positioning injuries yourself enough time before your exam non-ambiguous format, an uncommon is well illustrated and extremely de- as there is a lot to get through.
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Taking all feature of any MCQ book! However, tailed, whereas the brief update on pre- things into consideration, I would rec- we did find there to be an imbalance in eclampsia is a more concise account of ommend it to candidates as a useful exam that questions on equipment proved specific areas of developing controversy. Sabharwal The book should be popular with debate. This makes for an engaging and Specialist Registrar varied read. Benington, P. Clinically it is similar to normal bupivacaine. The important difference claimed based on animal studies is lower cardiotoxicity.
What are the advantages of ropivacaine over bupivacaine? Ropivacaine, like bupivacaine, is an amide local anaesthetic. It is less lipid soluble than bupivacaine and hence its penetration in neuronal myelin sheath is limited. C fibres which are thin and unmyelinated are blocked more readily than the thick and well myelinated A fibres. Therefore, at lower concentrations the sensory blockade is more than motor.
In higher-concentration motor blockade is similar to bupivacaine. This sparing of the motor blockade at lower concentrations is the main advantage of ropivacaine over bupivacaine. The cardiotoxicity of ropivacaine is also less than that of bupivacaine. What is EMLA cream? EMLA stands for eutectic mixture of local anaesthetics. It is a mixture of 2. What do you mean by a eutectic mixture? A eutectic mixture is one in which the constituents are in such proportions that the freezing or melting point is as low as possible, with the constituents freezing or melting simultaneously.
Q3 Anticoagulants What are the anticoagulants commonly used in clinical practice? The two main types of anticoagulants used in clinical practice include heparin and vitamin K antagonists e. Can you describe the structure of heparin? Heparin is a naturally occurring negatively charged acid. It is a glycosaminoglycan formed from alternating residues of L-iduronic acid and D-glucosamine.
It has a complex sulphated polysaccharide structure. The molecular weight of unfractionated heparin UFH ranges widely from to 30, Da with an average of about 15, Da. Tell me about the mechanism of action of heparin. Heparin acts indirectly via the 2-globulin called antithrombin III.
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Antithrombin III. Although antithrombin III normally has a low level of intrinsic activity, in the presence of heparin, the reaction with thrombin increases several thousand fold. In low-doses heparin binds to antithrombin III accelerating its combination with thrombin to form an inactive complex. Activated factor Xa is inhibited by a similar mechanism. Heparin also reduces platelet aggregation at higher doses. What is low molecular weight heparin LMWH? There are various commercial preparations available e.
The anticoagulant response is more predictable. How can you reverse the action of heparin? UFH has a relatively shorter half-life and if the clinical situation permits one can wait for the effect to wear off.
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Alternatively protamine can be used. This is extracted from fish sperm and is very strongly basic. It combines with the strong acid, heparin to form stable inactive complex. How does warfarin work?
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Warfarin acts by antagonising vitamin K. This carboxylation is coupled to the conversion of vitamin K from the reduced to the oxidised form. This is impaired by warfarin. Oral anticoagulants inhibit the enzyme epoxide reductase and cofactor nicotinamide adenine dinucleotide NADH which are responsible for regeneration of the reduced form of vitamin K, thereby preventing the activation of the above factors. How long will it take for warfarin to exert its effect and how will you monitor it? Following oral administration the peak plasma concentration occurs in about 90 min but it will take about 3 days of daily dosing to achieve a steady state concentration.
The half-life of warfarin is about 36 h. Although the clinical effect is apparent in h following ingestion of warfarin, it takes 35 days to reach the desired therapeutic effect. The effect of warfarin is monitored by prothrombin time PT or the international normalised ratio INR. Tell me about drug interaction with warfarin? It is metabolised in liver and excreted in kidney, so there can be a significant degree of interaction with various drugs.
checkout.midtrans.com/puol-conocer-mujer.php Interactions increasing the effect of warfarin: Competition for protein binding sites e. Increased hepatic binding e. Inhibition of hepatic microsomal enzymes. Reduced vitamin K synthesis e.
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Synergistic anti-haemostatic actions e. Interactions decreasing the effect of warfarin: Induction of hepatic microsomal enzymes e. Increased level of clotting factors e. Binding of warfarin in gut e. Increased vitamin K intake. How can you reverse the effect of warfarin?