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By V. Barrack. Central Methodist College. 2019.

The organelles usually present in animal cells are mitochondria trusted 10mg rosuvastatin, ribo­ some rosuvastatin 10mg with amex, peroxisome buy rosuvastatin american express, lysosomes discount rosuvastatin master card, centrioles, endoplasmic reticulum and Golgi apparatus. Cytoplasm also contains filamentous cytoskeletal structures such as microfila­ ments, intermediate filaments and microtubules. Cell Membrane Structure of Cell Membrane Cell membrane is the protective sheath of the cell. It the cell membrane is basically a double layer of lipid mole­ exchanges materials between the cytoplasm and the cules having thickness of 7–10 nm, into which are inserted 14 Section 1: General Physiology Fig. The major lipids in the cell membrane are phospholipids, glycolipids and cholesterol. The phospholipids are phosphatidylcholine, sphingo­ Though, many models for cell membrane have been myelin, phosphatidylserine and phosphatidyl ethano­ described in the past, the widely accepted one is Fluid- lamine. Special features of this model are: Lipids are amphipathic (“amphi” means both) mole­ 1. Cell membrane consists of a double­layer of phospho­ cules as their head or polar region is hydrophilic lipid that contains protein molecules. The model is called fluid mosaic model as the mem­ the globular or the head end contains phosphate or brane lipids are present in the fluid form that allows hydroxyl moieties that are positively charged and solu­ the flexibility of the membrane without disturbing the ble in water. The membrane proteins are loosely attached and float in is such that the hydrophobic tail ends are directed the fluid phospholipid bilayer. Rapid and random redistri­ toward the center and the hydrophilic head is located bution of integral proteins occurs in the membrane. Also, phospholipids undergo rapid redistribution in the to periphery of the membrane (as depicted in Figure plane of the membrane. This type of diffusion within the plane of the mem­ the aqueous phase from both inside and outside the brane is called translational diffusion. A similar bilayer arrangement is found in bile salts rapidly for phospholipids, which can move several where they form spherical micelles. The fluidity of the membrane is mainly dependent on regions of the membrane, and serves to reinforce the the lipid composition of the membrane. Effect of temperature: In a lipid bilayer, the hydropho­ bic chains of fatty acids are highly aligned or arranged Application Box 4. When tempe­ Determinant of the fluidity of membrane: the fluidity of a membrane rature increases, the hydrophobic side chains undergo a depends on the composition of lipids and the degree of unsaturation. Higher cholesterol content reduces order or melting occurs is called transition temperature the fluidity of the membrane. Chapter 4: Cellular Organization and Intercellular Connections 15 of the membrane (intracellular fluid). Serve as channel proteins: Channels or pores are inte­ gral proteins through which water­soluble substances like glucose and electrolytes can diffuse across the cell membrane. Act as carriers: Carrier proteins transport substances through cell membrane by facilitated diffusion; for exam­ ple transport of glucose through glucose transporter. Serve as receptor and enzyme proteins: Integral pro­ (outer membrane and inner membrane) proteins. A membrane teins that are present toward the outer half of the channel is formed by a transmembrane protein. Antigenic functions: Complex membrane proteins within the specific layer (but not from one layer to another). Functions of the Lipid Bilayer Peripheral Proteins the main function of the lipid bilayer of a cell membrane Some protein molecules are inserted lightly in the outer is to create a permeability barrier between the interstitial or inner border of the membrane or are just bound to the fluid and the cytoplasm. Such proteins are called peri­ depends on whether it is lipid­soluble or water­soluble. Lipid soluble substances like oxygen and alcohol can pass They are of two types: Intrinsic and extrinsic proteins. Intrinsic proteins: They are present on the inner sur­ easily through the cell membrane, whereas water soluble face of the membrane. They usually serve as enzymes or substances like urea and glucose cannot pass easily. Thus, anchor proteins for cytoskeleton and other microfilaments lipid bilayer makes the membrane semipermeable. Membrane Proteins Extrinsic proteins: They are present on the outer sur­ face of the membrane. They serve as cell adhesion mole- the protein content of biological membrane depends cules for anchoring cells with basal lamina and with neigh­ on the function of the membrane. They can be removed without disrupting the Schwann cell, the cell membrane is concerned with insu­ membrane. Therefore, protein constitutes less than 25 percent Membrane Carbohydrates of the membrane. In membrane of mitochondria, which is the external surface of the cell membrane is loosely involved in cell metabolism, 75 percent of the membrane covered by a carbohydrate layer known as the cell coat or is protein. Thus, the outer surface of the lipid bilayer is Some membrane proteins that span the entire thickness covered by a layer of glycoproteins and glycolipids. Band-3 proteins: Band­3 protein is a dimeric protein with molecular weight 93,000 that traverses membrane about 12 times. It acts as “pore” or transport protein that exchanges bicarbonate ions in the capillaries of lungs. Note the presence of cial proteins that are linked to the cytoskeleton and are special proteins such as ankyrin, spectrin and adducin that provide essential for stabilization of membrane and biconcave plasticity (deformability) to the membrane, in addition to the pres- shape of the cell. Spectrin: Spectrin is a fibrous protein that contains an α-chain with molecular weight of 240,000 and a β-chain with molecular weight of 220,000. Some of the transmembrane glycoproteins like selec­ attached to cytoskeletal protein that maintains membrane tins recognize and bind with specific oligosaccharides integrity and cell shape. Ankyrin has molecular weight occurs between neutrophils and endothelial cells at of 200,000. Stronger adhesion between and other with N­terminal region of band­3 protein that cells is formed by integral membrane proteins such as extends into cytoskeleton (Application Box 4. Diseases due to membrane protein defects: Disorders of red cells such as hereditary spherocytosis and elliptocytosis occur due to Functions of Cell Membrane defects in the membrane proteins (for details, refer “Red Blood Cell”). Cell membrane maintains a constant and distinctive Cell Organelles intracellular environment, which is essential for func­ tioning of the organelles. For example, the intracellu­ the usually occurring organelles in animal cells are mito­ lar fluid has lower concentration of sodium and chlo­ chondria, endoplasmic reticulum, Golgi apparatus, ribo­ ride, low pH, but higher concentration of potassium, some, peroxisome, lysosome and centriole. Cell membrane maintains cell volume by actively of its organelles such as mitochondria, ribosome and lyso­ transferring ions across it, especially by pumping some during maturation. In neurons and muscle cells, it maintains a potential Mitochondria difference between intracellular and extracellular sur­ Mitochondria are the “power house” of the cell. Cell membrane helps in recognizing foreign cells or vary in different tissues of the body. Mitochondrial Membranes Electron microscopy shows that each mitochondrion has Integral Proteins two layers of membranes: the outer and inner membranes. Two special types of integral proteins are found in red cell Outer Mitochondrial Membrane: This forms a continuous membrane (Fig. The carbohy­ that permit substances with molecular weight of less than drate component is oligosaccharide and the polypeptide 10,000 to diffuse freely across the outer membrane. Enzymes in inter-membrane space membrane is folded into multiple incomplete septa like 1. Citrate synthase Number of cristae: Number of cristae is more in resting state of 3. Ornithine transcarbamylase the region enclosed by the inner membrane is called matrix. Mitochondrial diseases: the disease that affects mitochondrial energy transduction is called Luft’s disease. Therefore, it is Mitochondria are also damaged by free radicals and affected in age- abundant in cells of endocrine glands and cells secreting related degenerations. It also plays some role in the conjugation of carbohy­ rylated here, and then pass to the trans­face, where drates with proteins to form glycoproteins, a function they are packaged into the secretory vesicles (Fig. It is the site for the incorporation of carbohydrates into the newly synthesized proteins to form glycopro­ Smooth Endoplasmic Reticulum teins.

Dr R Van der Berg 76 Turlington Terrace London the Consultant Breast Surgeon King George’s Hospital London Re: Cornelia Tristan-Davies order rosuvastatin with a visa, 45 Bleinham Square order rosuvastatin cheap, London Dear Doctor I would be grateful if you could see this 56-year-old lady who came to us with a lump in her left breast order 5 mg rosuvastatin free shipping. Best wishes Yours sincerely Dr K Sanderson (locum) Take a standard focused surgical history (presenting complaint buy 10 mg rosuvastatin otc, history presenting complaint, past medical history, drug history and allergies, social history, family history, systemic enquiry), but in particular enquire about the following: Age Lump site, single or multiple Lump onset, growth rate, variations with menstrual cycle Presence or absence of pain – Cyclical Change in breast size or shape Skin and nipple changes Discharge – Serous, serosanguinous, green, bloody, milk Temperature/fevers Weight loss Bone or abdominal pain Arm swelling (lymphoedema) Previous radiation or surgery – E. After you have taken the history, you will be asked to present it to one of the examiners as though he or she were the consultant. He or she will then ask you for your differential diagnosis, what signs you would look for on examination and what investigations you would request. Drs A Goldberg, S Patel, and P Carter 21 the Avenue London the Consultant Surgeon St John’s Hospital London Re: Olivier de Bourbon, 143 Daffodil Close, Surrey Dear Doctor This professional 41-year-old gentleman is describing some changes in bowel habit, diarrhoea, and an episode of bleeding. Focussed inspection – Abdomen moving freely with respiration, distension, scars, fistulae, pulsatility, lift head off bed (accentuates abdominal herniae), stomas, tubes (suprapubic catheter, nephrostomy), drains. You must look at the patient’s face at all times as you superficially palpate the quadrants and central area for tenderness and obvious masses. Gently pinch skin over it Lift head off the bed (tense the rectus sheath) to determine mobility/fixity of mass Cough impulse Reducibility/compressibility Fluctuance Pulsatility and expansility Does it move with respiration? Extension distance beneath the costal margin (cm/finger breadths) Percuss upper liver border of the liver (to assess whether it is pushed down by lung hyperexpansion) Consistency – Soft, firm, hard, craggy (cirrhosis, tumour) Liver edge – Smooth, nodular (cirrhosis, tumour) Liver tenderness (hepatitis) Liver pulsatility Presence or absence of a Reidel’s lobe What might be causing it? Spleen is usually dull to percussion but the left kidney may be resonant due to overlying bowel. Hands – Leukonychia (hypoalbuminaemia), clubbing, palmar erythema, Dupuytren’s contracture, bruising (coagulopathy), liver flap (encephalopathy), pruritus/scratch marks (accumulation of bile salts in the skin). Face – Jaundice (hyperbilirubinaemia), scratch marks, spider naevi (portal hypertension), foetor hepaticus. Chest – Gynaecomastia (oestrogen metabolism dysfunction), loss of body hair, spider naevi (portal hypertension), bruising, pectoral muscle wasting. Abdomen – Signs of portal hypertension (hepatosplenomegaly, ascites, caput medusae), testicular atrophy. The opening Introduce yourself to the patient (permission) Ask for a nurse chaperone Obtain consent Ensure adequate privacy, patient comfort and exposure (lie flat with one pillow) Ask whether any pain is present Wash hands Inspection From foot of bed and patient’s right-hand side. Illuminate stomal tract – Shine a light down into the stoma to check the mucosa is healthy. Auscultation Bowel sounds the closure Inspection of perineum for scars and presence of anal opening Complete examination of abdomen Assess stoma position during sitting, lying and standing Thank the patient Wash hands Summarise and offer differential diagnosis (Figures 9. However, be prepared to be flexible depending on the patient’s mobility) Ask whether any pain is present Wash hands. Each time you ask the patient to cough, there should be a precise purpose (examiners will be watching how many times you make the patient cough and at which stage). Inspection Lumps in the groin – Define its characteristics Scars (especially overlying any lumps) Cough 1 – Look away and cough (inspect superficial ring of affected side for a cough impulse) Cough 2 – Look away and cough (inspect superficial ring of contralateral side) Palpation Stand to patient’s side with one hand on their back and the other hand on the lump itself. Reducibility – Ask the patient ‘to push it back in if possible’ (direct course: direct hernia, oblique course: indirect hernia). Cough 4 – Place one finger on pubic tubercle and ask the patient to cough again (note the relation of lump to the pubic tubercle as it protrudes). Auscultation Bowel sounds – Viability of bowel the closure Examination of contralateral groin Examination of genitalia – Coincidental hydrocoele, varicocele Examination of regional lymph nodes Full history Examination of the abdomen Digital rectal examination Assess fitness for surgery Thank the patient Wash hands Summarise and offer differential diagnosis So you have found a lump in the groin – what do you think it is? However, be prepared to be flexible depending on the patient’s mobility) Ask the patient whether they have any pain Wash hands Inspection Lumps in the groin – Look away and cough Scars (including posterior aspect of scrotum) Palpation Any pain? Set the agenda Begin with open-ended questions to ascertain the patient’s perspective. Look at the patient as a whole (well/unwell; pain/pain free; shortness of breath, cyanosis and obesity). Scars (vein harvest, reconstruction procedures, grafts/flaps for soft tissue cover of ulcers and areas of tissue loss). Muscles – Wasting (often due to disuse atrophy), loss of prominence of extensor tendons on the dorsum of foot (oedema). Palpation (ask the patient whether they are in pain before you begin) Upper limbs Temperature of the upper limbs (with the back of the hand) Assess for the capillary refill time Palpate the radial pulses for rate and rhythm. Moreover, assess for radial, radio-radial delay, collapsing pulse Palpate the brachial pulse Assess the patient’s blood pressure in both upper limbs Palpate the axillary artery in axilla Palpate the subclavian artery (subclavian aneurysm, post-stenotic dilatation) Palpate the carotid pulses for rate, rhythm and character Palpate the superficial temporal artery Palpate for a cervical rib Figure 10. Palpate for a popliteal pulse – Flex the knee and wrap both hands around knee with fingertips into the popliteal fossa and compress artery against tibia posteriorly. Note the popliteal pulse is often difficult to assess as the popliteal artery lies deep within the popliteal fossa. Palpate the dorsalis pedis pulse – Palpate between the head of the first and second metatarsals. Auscultation Upper limb Listen for bruits in the supraclavicular fossa, infraclavicular space (subclavian) and over the carotid artery. Locate the dorsalis pedis and posterior tibial pulses with the handheld Doppler and inflate the cuff until the Doppler sound disappears. You may now release the pressure on the ulnar artery (the hand should re-perfuse). The leg angle from the examination couch when the leg turns white is Buerger’s angle (<20° = severe ischaemia). Assist the patient in allowing them to drop their leg over the side of the couch and inspect for reactive hyperaemia. Assess for varicose veins (abnormal prominent superficial, tortuous and dilated veins), note their distribution (long or short saphenous veins or both) and location (the medial gaiter area). Assess for saphena varix (varicosity in the saphenous vein at its confluence with the femoral vein) (Figure 10. Inspect the lower limbs for ‘chronic venous hypertension’: Ulceration Haemosiderin deposition Thrombophlebitis Venous eczema and stars Lipodermatosclerosis (‘inverted champagne bottle leg’) Pitting oedema Healed ulceration (atrophie blanche) (Figure 10. Tap proximally and palpate distally (retrograde transmission) to detect venous valvular incompetence/reflux. Tap distally and palpate proximally (orthograde transmission) to assess venous continuity, venous patency and to detect thrombosis/venous occlusion. Place the patient in a supine position then elevate the lower limb to empty the veins. If the incompetence is above the tourniquet site, the veins will be controlled and will not fill. This should be repeated with the tourniquet positioned at a lower level on the thigh. Perthes’ Test Place the tourniquet on the patient’s thigh and then ask the patient to stand on their toes. If the veins enlarge or the patient experiences pain, the deep veins are likely to be involved. Perform a full abdominal examination (abdominal, pelvic exam, digital rectal examination and examine the external genitalia) to exclude secondary causes of varicose veins. You will need to ascertain the underlying aetiology of the ulcer (arterial, venous, neuropathic or mixed). Specific Inspect between the toes, tips of toes, pressure points, heel, sole, malleoli, under the fifth metatarsal head, ball of foot. Informed consent is the process by which a patient is provided with sufficient information to make an informed, reasoned decision regarding the proposed treatment. In surgical practice, respect for autonomy translates into the clinical duty to obtained informed consent before the commencement of treatment. It must be Informed Voluntary (non-coerced) Patient should be competent Competence to take the decision requires the ability To understand the information given To retain and believe it To weigh up the information given to reach a reasoned decision What types of consent do you know of? Standard consent form used for adults undergoing an operation under general anaesthetic. Consent Form 2 – Parental agreement to investigation or treatment for a child or young person. Consent Form 3 – Patient/parental agreement to investigation or treatment (procedures where consciousness not impaired). Consent Form 4 – Form for adults who are unable to consent to investigation or treatment (usually patients on the intensive care unit). The procedure and its potential risks are explained to the child and the parent or guardian. In some situations, consent for a child under 16 years of age may be obtained from the child, without their parents or legal guardian consenting on their behalf, if the child is deemed competent to understand the information and make an informed decision (termed ‘Gillick competence’). However, in practice, this is a situation that should be avoided if at all possible. In the case of an unconscious patient, the law recognises that it is in the patient’s best interest for such an emergency treatment to go ahead.

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In normal individuals cheap rosuvastatin line, the medial intcr- migration of the orbits in embryonic development purchase generic rosuvastatin. Orbital canthal distance is equivalent to the palpebral length rosuvastatin 10mg visa, and hypertelorism is present in several hundred syndromes and the ratio between the medial inter-canthal distance and the disorders order on line rosuvastatin, such as Waardenburg syndrome and Crouzon lateral inter-canthal distance is approximately 1:3. Normal values head malformations such as the morning glory disk anomaly, of this index for infants, children, and adults are around 0. Telecanthus is believed to result from overgrowth in width of the fronto-nasal process. Telecanthus is present in a number of multisystem malformation syndromes/’ Surgical repair of telecanthus consists of separate approaches to the three soft tissue elements responsible for creating the deformity: the cpicanthal fold, underlying subcutaneous tissue, and the medial canthal tendon. Ihe subcutaneous tissue, which is often abnormally thick, is excised under direct visualiza­ tion, and the medial canthal tendon can be shortened by a tuck, resection, or transnasal wiring, as described below. It is often useful to excise the fibrous band of tissue that runs beneath the skin and muscle and contributes to the fold. Note gray hair, increased inter-inner canthal distance (telecanthus) with lateral displacement of the Figure 3. The tendon is then secured with a 30-gauge stainless steel wire, which is passed transnasally. For bilateral cases, the wire will exit a similarly created hole in the bone on the opposite side; for unilateral cases, the wire passes through two small holes drilled just above the opposite medial canthal tendon and lacrimal sac. Abnormal insertion of the lateral canthal tendon may be due to deficiency of the tendon itself or to an abnormal position of an otherwise normal tendon. Lateral dystopia of moderate severity (congenital leukoderma), iris (heterochromia irides and requires a tarsal strip procedure. In more severe cases, the hypo isochromia irides), and hair (white forelock and lateral canthal tendon or lateral tarsal strip should be premature graying) (Fig. After reflecting the lacrimal sac, an opening is and skin extends continuously from the forehead to the aterial corr cheek, passing in front of the orbit, where it forms a small depression (Fig. In the second, incomplete, atypical or partial form of cryptophthalmos, there arc rudimentary eyelid structures and a conjunctival sac may be present temporally. There is localized corneal to the eyeball, does not carry lashes, and continues over opacification. Cases such as those reported by Key1-’ and Sugar," where there is typical cryptophthalmos on one side and abortive cryptophthalmos on the other, indicate that the two anomalies are equivalent. Cases have been reported with typical cryptophthalmos on one side and a dermoid, microphthalmos, or eyelid coloboma on the other side. Л fourth type of isolated cryptophthalmos exists where the eyelids are formed with a full complement of adnexal accessories. The eyelid fissure is displaced inferiorly close to the inferior orbital rim, but the conjunctival sac is rudimentary and the globe is not visible. The skin of the upper [ Ж eyelid is elongated, adheres to the underlying globe with a dimple over the cornea, and fuses with the shortened lower eyelid. True ano­ toes and/or fingers, renal anomalies, and malformations of phthalmia is the total absence of the tissues of the eye and the genital organs, especially in females. Other less common can be distinguished from extreme microphthalmia only malformations include anal atresia and umbilical hernias by histologic examination. Renal malformations such as renal term “clinical anophthalmia” when referring either to cases agenesis or dysplasia may occur, resulting in spontaneous of true anophthalmia or to extreme forms of microphthal­ abortions, stillbirths, or neonatal deaths. It is our belief, however, that identified causative mutations in 17 of the 40 families, and outward appearance greatly affects social interactions. The eyelid fissure forms in the sixth month of gestation, increased as needed with a dermis fat graft (Fig. As a last resort, craniofacial surgery may be neces­ often malformed both in its anterior and posterior segments, sary to expand the bony orbit to permit adequate soft tissue rendering visual prognosis very guarded even if a good expansion. Visual potential may be estimated with the aid of ultrasound, computed tomography, magnetic resonance imaging, visual evoked response, and electroretinography. Procedures should be aimed at obtaining a clear visual axis in addition to creating some form of functioning Eyelid colobomas are full-thickness notch defects of the eyelid structures. Surgical from a nearly complete abscncc of the eyelid to only a incision in the area of the palpebral fissure, for instance, may small notch in the lateral aspect of the lower eyelid, as seen open directly into the anterior segment of the eye. Eyelid colobomas absence of a conjunctival sac and hence of a normal ocular may be triangular or quadrilateral (Fig. Upper eyelid defects (the majority of colobomatous viable option for this severe deformity in some cases. In par­ eyelid defects) are usually nasal and occur between the tial or abortive cryptophthalmos, surgical intervention may inner and middle third of the eyelid. Colobomas of the upper eyelids arc seen in 12% to 20% of patients with Goldenhar syndrome, a variant of the oculo- auriculo vertebral dysplasia syndromes. The coloboma usually overlies an epibulbar dermoid, and patients may have preauricular skin tags, microtia, deafness, facial asym­ metry, macrostomia, microstomia, and vertebral anomalies (Fig. Goldenhar syndrome results from faulty devel­ opment of structures derived from the first and second branchial arches and the first branchial cleft between the sixth and eighth week of gestation. Patient was extensively investigated and did not have any associated malformations. Defect was repaired by primary approximation with excellent cosmetic and functional result. Lower eyelid colobomas are usually temporal, located between the middle and outer thirds. Colobomas of the eyelid may be due to failure of the mesodermal folds to fuse completely during devel­ opment. Additional fairly common findings include a tendency toward macrostomia, maloc­ clusion, high palate, and a high nasal root. The hair growth patterns are unusual, often showing tongue-like extensions of hair onto the cheeks, There may be grooves, clefts, or pits on the cheek between the mouth and the ear. This syndrome represents the most extensive abnormality of A the first branchial arch. When there is a positive family history, the gene is almost 100% penetrant, although there is wide variability in expres­ sion of the disorder among family members. Ihe ophthalmic features are among the most consistent and diagnostic in this syndrome. In addition to lateral downward sloping of the palpebral fissure, lower eyelid colobomas are present in 75% of patients, with partial to total absence of the lower eyelashes. There was an associated atypical retinal coloboma/ 1 and defects of the orbital rim are occasionally scen. Note microphthalmia and right lower Goldenhar syndrome by the rarity of lower eyelid colobomas eyelid defect near the inner canthus. The inner canthus is not Upper and lower eyelid defects may also be seen in the displaced outwards as in telecanthus. Sliding or rotational flaps are preferred upper and lower eyelids by strands of fibrovascular tissue techniques. In some cases the Ankyloblepharon filiforme adnatum has been associ­ coloboma can be converted to a pentagonal defect, which ated with multiple conditions, most commonly disorders is then repaired in the same way as an eyelid margin lac­ of orofacial clefts. This technique can be used to correct up to 50% of may be seen, for instance, in popliteal pterygium syndrome, eyelid margin defects if combined with a canthotomy and an autosomal dominant cleft syndrome characterized by cantholysis (Fig. Internal ankyloblepharon refers to by cleft lip/palate, paramedian pits or mucous cysts on the fusion of the eyelids from the inner canthus outwards with lower lip, and hypodontia. The outer half of the lower eyelid appears to sag inferiorly and is not well apposed to the globe. This widens the palpebral fissure and gives the appearance of lower eyelid ptosis. Frequently, the palpebral fissure also has a downward slant because of an inferiorly displayed attach­ ment of the lateral canthal tendon. There are three small string-like (filiform) attachm ents between the upper and lower eyelids families with an autosomal dom inant syndrome o f anky­ temporally. There is Euryblepharon is a horizontal widening of the palpebral separation between the lids and the globe temporally, with downsloping of fissure, usually due to horizontal lengthening of the the fissure and exposure of the outer canthal conjunctival area. Other common systemic of microblepharon is seen in the ablepharon-macrostomia abnormalities include cardiovascular anomalies, cleft lip/ syndrome/*"9Ablepharon (no eyelids) should not be used palate, and kidney or urinary tract anomalies.

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When resuscitation fails and the patient dies buy cheap rosuvastatin on-line, attention should be focused on comforting the grieving family and also the medical team should analyze the course of events and understand how and why their efforts did not succeed purchase rosuvastatin 10mg with amex. Resuscitation is not indicated either in the emergency department or in the field for patients with rigor mortis or dependent lividity purchase cheapest rosuvastatin. Stabilization of the critically ill child generic rosuvastatin 5 mg on-line, chapter 57, 17th edition, Nelson Textbook of Pediatrics 2003;279-96. A study of chest compression rates during cardiopulmonary resuscitation in humans; the importance of rate directed chest compression, Arch Intrn Med 1992; 152:145-49. Pediatric resuscitation: An advisory statement from the pediatric working group of the international Liason committee on resuscitation. Treatment of paroxysmal supraventricular tachycardia in the emergency department by clinical decision analysis. Textbook of pediatric intensive care, 3rd edition, chapter 1, cardiopulmonary resuscitation, Charles, L. A prospective population based study of the demographics, epidemiology, management and outcome of out of hospital pediatric cardiopulmonary arrest Ann Emerg Med 1999;33:174-84. While basic priciples of physics and gas flow apply to all age groups, anatomical and physiological differences play a significant role in selecting the type of ventilator as well as the ventilatory modes and settings. Upper airway in children is cephalad, funnel-shaped with narrowest area being subglottic (at the level of cricoid ring), as compared to adults where the upper airway is tubular with narrowest part at the vocal cords. Respirations are shallow and rapid due to predominant diaphragmatic breathing, and inadequate chest expansion due to inadequate costovertebral bucket handle movement in children. Therefore a child tends to get tachypneic rather than increasing the depth of respiration in response to hypoxemia. Oxygen consumption/kg body weight is higher therefore tolerance to hypoxemia is lower. Susceptibility to bradycardia in response to hypoxemia is also higher due to high vagal tone. Pores of Kohn and channels of Lambert (bronchoaveolar and interalveolar collaterals) are inadequately developed making regional atelectasis more frequent. Other important factors for choosing ventilatory settings include the primary pathology, i. Therefore, a balance between elastic recoil of the chest wall and the lung determines lung volume at any given time. Normal inspiration is actively initiated by negative intrathoracic pressure driving air into the lungs. Oxygenation Partial pressure of oxygen in alveolus (PaO2) is the driving pressure for gas exchange across the alveolar-capillary barrier determining oxygenation. Shunt (Perfusion of an unventilated alveolus, atelectasis, fluid in the alveous) d. V/Q mismatch can be corrected by increasing the amount of lung that is ventilated or by improving perfusion to those areas that are ventilated. In the pediatric age group one time constant that fills an alveolar unit to 63% of its capacity is 0. It takes three time constants to achieve greater than 90% capacity of the alveolar unit filled. Time constant = Resistance (Pressure × Time/Volume) × Compliance (volume/pressure) This signifies that a certain minimum inspiratory time is required to fill the alveoli adequately which is generally two to three time constants, i. This is important when selecting the inspiratory time on the conventional ventilator. Indications of Mechanical Ventilation4 Indications remain essentially clinical and may not be always substantiated by objective parameters such as blood gas analysis. Modes of Ventilation Control Modes In this mode every breath is fully supported by the ventilator. In classic control modes, patients were unable to breathe except at the controlled set rate. In a conventional controlled mode, weaning is not possible by decreasing rate, the patient may hyperventilate if agitated leading to patient/ ventilator asynchrony. Patients on control modes will need sedation and or paralysis with a muscle relaxant. In newer control modes, machines may act in assist-control, with a minimum set rate and all triggered breaths above that rate are also fully supported. There is a potential for increased work of breathing and patient/ventilator asynchrony, if the ventilator interferes with the patient’s effort to breath or if there is insufficient flow for the spontaneous breaths. Ventilators would have an inbuilt latent period of about 25% of the inspiratory time in which to recognize the patient’s effort in order to synchronise the mandatory breath in order to reduce asynchrony. Support Mode Pressure support:5 Ventilator supplies pressure support (flow) at a preset level but rate is determined by the patient, expiration begins passively when inspiratory flow decreases below a certain level preset in the vntilator (flow cycled). Volume support is also available in Servo 300 ventilators following the principle of pressure suport (delivery of the set volume over the patients natural inspiratory time duration keeping the pressure to a minimum. Pressure support can decrease work of breathing by providing flow during inspiration for patient triggered breaths. If volume is set, pressure varies; if pressure is set, volume varies according to the compliance. Compliance = ΔΔΔΔΔ volume/ΔΔΔΔΔ pressure Chest must rise no matter which mode is chosen Following are three main expectations from the ventilator 1. Ventilator must not interfere with patient’s efforts (synchrony) Whenever a breath is supported by the ventilator, regardless of the mode, the limit of the support is determined by a preset pressure or volume. Important requirements include adequate movement of the chest and minimal barotrauma or volutrauma. One must have a set up of high/low pressure alarms in volume cycling and, low expired tidal volume alarm when using pressure cycling. Volume Limited Ventilation Ventilator stops the inspiratory cycle when set tidal volume has been delivered. Volume is lost if there is a circuit leak or significant leak around the endotracheal tube, therefore, an expired tidal volume needs to be monitored and set. Some ventilators will alarm automatically if the difference between set inspired tidal volume and expired tidal volume is significant (varies between the ventilators). Ventilators have a negative pressure sensor which can be set at various levels of sensitivity to initiate a breath usually based on patient effort (negative pressure) or elapsed time before the next breath in the event of respiratory depression or apnea. The patient’s effort can be “sensed” as a change in pressure or a change in flow in the circuit (flow triggering). A setting of greater than 0 makes it too sensitive (meaning the triggered breath from the ventilator will be too frequent). Too negative setting will increase the work of the patient (to generate a negative pressure) to trigger a ventilator breath. It delivers the breath with a decelerating flow pattern that is thought to be less injurious to the lung. Volume Support Volume support is in principle equivalent to pressure support where a “goal” tidal volume is set and machine delivers that volume at variable pressure support, but within the set limits of pressure support. The machine watches the delivered volumes and adjusts the pressure support to meet desired “goal” within limits set. Initial Ventilator Settings One should always have the general idea regarding, what initial ventilatory settings to chose when initiating the ventilation. Normal I:E ratio = 1:2-1:3 • Higher I-times may be needed to improve oxygenation in difficult situations (Inverse ratio ventiation) increasing the risk of air leak. Gas Exchange Related Problems Inadequate oxygenation (hypoxemia) Inadequate ventilation (hypercarbia) Inadequate Oxygenation Important guidelines: 1. Inadequate tidal volume delivery (hypoventilation) will occur with endotracheal tube block, malposition, kink, circuit leak, ventilator malfunction. If volume limited: Increase tidal volume (Vt), Increase frequency (rate) (f) If asthma: Increase expiratory time, may need to decrease ratio achieve an I:E ratio >1:3. Change endotracheal tube if blocked, kinked, malplaced or out, check proper placement 6. Measures to Reduce Barotrauma and Volutrauma: Folowing concepts are being increasingly followed in most pediatric intensive care units. Permissive hypoxemia: PaO2 of 55-65; SaO2 88-90% is acceptable in exchange for limiting FiO2 (<. Patient ventilator dysynchrony:Incoordination between the patient and the ventilator: Patient fights the ventilator!! If patient fighting the ventilator and desaturating: Immediate measures Use Pnemonic: D O P E D—displacement, O—obstruction, P—pneumothorax, E—equipment failure 1. Check tube placement: When in doubt take the endotracheal tube out, start manual ventilation with 100% oxygen.

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