By T. Ayitos. Liberty University. 2018.

Patients complain typical- ly of increasing back pain but this may be delayed Patients in whom there is evidence of regular opi- for several weeks so that the connection to the sur- oid use preoperatively generic fluoxetine 10 mg online, for example drug addicts purchase 20mg fluoxetine amex, gery and epidural may be missed generic fluoxetine 10mg line. Damage to nerves or the spinal cord include: during insertion of the needle and systemic toxi- • Liaison with the Acute Pain Team to inform it of city of the local anaesthetic are both unusual the patient’s admission. However, if a than normal may be required; small dose of opioid, for example morphine • explain that toxicity from high doses of opioid 0. Complications are the same as those due to opioids • Discussion with the patient to explain: given epidurally, and managed in the same way. Consensus guidelines for managing 88 Postanaesthesia care Chapter 3 postoperative nausea and vomiting. Asthmatics often develop bron- period that may be incidental or secondary to the chospasm that is resistant to treatment, and any anaesthetic and potentially life-threatening to the circumstance reducing the patient’s catecholamine patient. The inci- tinguishable from the above, but the release of his- dence of severe reactions to anaesthetic drugs is ap- tamine, etc. Of those reported to the Medicines Control Agency, 10% involved a fatality Causes of allergic reactions compared to 3. This probably reflects the frequency with which anaesthetic • Anaesthetic drugs: drugs are given intravenously. Clinical features in- • muscle relaxants (>50%): rocuronium, suxa- clude (in order of frequency): methonium, atracurium, vecuronium; • severe hypotension; • induction agents (5%): thiopentone, propofol. The possi- •Discontinue all drugs likely to have triggered the bility of a tension pneumothorax (secondary to reaction. Elevated • Ensure adequate ventilation: tryptase confirms anaphylactic or anaphylactoid • Intubation will be required if spontaneous reaction, but does not distinguish between them. In these circumstances a needle and do not forget to inform the patient and the pa- cricothyroidotomy or surgical airway will be tient’s general practitioner of the events, both ver- required. In the absence of a major pulse, of immunologically mediated reaction to anaes- start cardiopulmonary resuscitation using the thetic drugs. The greatest risk is during induction of anaesthe- sia, but some patients are also at risk during extu- Subsequent management bation and recovery. Reactions vary in sever- • intestinal obstruction or peritoneal irritation; ity, can be biphasic, delayed in onset (particularly • blood in the stomach; 91 Chapter 4 Management of perioperative emergencies and cardiac arrest • sympathetic stimulation, pain and anxiety; • After allowing the patient to recover, continue •afull stomach: using either a regional technique or a rapid- • an inadequate period of starvation; sequence induction and intubation. Signs suggesting aspiration include: (iii) Neuromuscular blocking drugs given: • coughing during induction or recovery from • Intubate with a cuffed tracheal tube to secure the anaesthesia; airway. Antibiotics should be given • Maintain the airway and place the patient head- according to local protocols. Failed intubation Anaesthesia for elective surgery The following plans concentrate on unexpected Assume that the patient is starved, minimizing failed intubation. The immediate management in the risk of aspiration, and a non-depolarizing these circumstances will depend upon: neuromuscular blocker given to facilitate tracheal • ability to maintain adequate oxygenation; intubation. Oxygenation and ventilation successful Failed intubation, failed ventilation Surgery essential: Whatever the surgical urgency, if intubation fails • Continue anaesthesia with inhalational agent in and the patient cannot be oxygenated via a face- oxygen. These patients should be admitted to an appropriate critical care area postoperatively and During anaesthesia may require endoscopy prior to extubation. Acute airway obstruction Management This may present in a variety of ways: Whatever the circumstances, the aim is to secure a patent airway to allow adequate oxygenation. Unconscious patient •W hen anaesthesia is adequate perform direct • Usually secondary to unrelieved obstruction laryngoscopy. The concurrent use of positive pressure ventilation will increase the rate at which the pressure rises Tension pneumothorax as gas is forced through the defect into the A pneumothorax exists when any gas accumulates pleural cavity, resulting in rapid cardiovascular in the pleural cavity. The nitrous oxide diffuses gas accumulates under pressure, then a tension into the air-filled space in a greater volume and at a pneumothorax exists. In addition to hypoxaemia, rate faster than nitrogen can escape, causing ex- the increasing pressure causes the mediastinum to pansion and a rise in the pressure. The conscious patient will be tachypnoeic and in • Insert a 14 or 16 gauge cannula in the second severe respiratory distress. There may also be: The insertion of a cannula has the effect of con- • surgical emphysema; verting the tension pneumothorax to a simple • tachycardia, hypotension; pneumothorax. This can then be treated by the •deviation of the trachea away from the affected insertion of a chest drain in the fifth intercostal side; space, midaxillary line on the affected side. Very rarely there may be bilateral tension •agradual rise in the inflation pressure, if the pneumothoraces. Severe hypotension Hypotension is a result of a reduction in either the Causes cardiac output or the peripheral resistance, alone Puncture of the pleura lining the surface of the or in combination (blood pressure = cardiac output lung (visceral pleura). Severe hypotension may 96 Management of perioperative emergencies and cardiac arrest Chapter 4 be defined as a systolic pressure 40% less than the usually the result of a combination of the above preoperative value.

When a parallel muscle has a central buy cheap fluoxetine 20mg line, large belly that is spindle-shaped order 20 mg fluoxetine overnight delivery, meaning it tapers as it extends to its origin and insertion generic fluoxetine 10 mg overnight delivery, it sometimes is called fusiform. Tendons emerge from both ends of the belly and connect the muscle to the bones, allowing the skeleton to move. When they relax, the sphincters’ concentrically arranged bundles of muscle fibers increase the size of the opening, and when they contract, the size of the opening shrinks to the point of closure. Consider, for example, the names of the two orbicularis muscles (orbicularis oris and oribicularis oculi), where part of the first name of both muscles is the same. The first part of orbicularis, orb (orb = “circular”), is a reference to a round or circular structure; it may also make one think of orbit, such as the moon’s path around the earth. The rectus abdomis (rector = “straight”) is the straight muscle in the anterior wall of the abdomen, while the rectus femoris is the straight muscle in the anterior compartment of the thigh. When a muscle has a widespread expansion over a sizable area, but then the fascicles come to a single, common attachment point, the muscle is called convergent. The attachment point for a convergent muscle could be a tendon, an aponeurosis (a flat, broad tendon), or a raphe (a very slender tendon). The large muscle on the chest, the pectoralis major, is an example of a convergent muscle because it converges on the greater tubercle of the humerus via a tendon. Pennate muscles (penna = “feathers”) blend into a tendon that runs through the central region of the muscle for its whole length, somewhat like the quill of a feather with the muscle arranged similar to the feathers. Due to this design, the muscle fibers in a pennate muscle can only pull at an angle, and as a result, contracting pennate muscles do not move their tendons very far. However, because a pennate muscle generally can hold more muscle fibers within it, it can produce relatively more tension for its size. In some pennate muscles, the muscle fibers wrap around the tendon, sometimes forming individual fascicles in the process. A common example is the deltoid muscle of the shoulder, which covers the shoulder but has a single tendon that inserts on the deltoid tuberosity of the humerus. Because of fascicles, a portion of a multipennate muscle like the deltoid can be stimulated by the nervous system to change the direction of the pull. For example, when the deltoid muscle contracts, the arm abducts (moves away from midline in 450 Chapter 11 | The Muscular System the sagittal plane), but when only the anterior fascicle is stimulated, the arm will abduct and flex (move anteriorly at the shoulder joint). For muscles attached to the bones of the skeleton, the connection determines the force, speed, and range of movement. These characteristics depend on each other and can explain the general organization of the muscular and skeletal systems. The handle acts as a lever and the head of the hammer acts as a fulcrum, the fixed point that the force is applied to when you pull back or push down on the handle. The effort applied to this system is the pulling or pushing on the handle to remove the nail, which is the load, or “resistance” to the movement of the handle in the system. Our musculoskeletal system works in a similar manner, with bones being stiff levers and the articular endings of the bones—encased in synovial joints—acting as fulcrums. The load would be an object being lifted or any resistance to a movement (your head is a load when you are lifting it), and the effort, or applied force, comes from contracting skeletal muscle. The educated class of subsequent societies studied Latin and Greek, and therefore the early pioneers of anatomy continued to apply Latin and Greek terminology or roots when they named the skeletal muscles. The large number of muscles in the body and unfamiliar words can make learning the names of the muscles in the body seem daunting, but understanding the etymology can help. Etymology is the study of how the root of a particular word entered a language and how the use of the word evolved over time. Taking the time to learn the root of the words is crucial to understanding the vocabulary of anatomy and physiology. When you understand the names of muscles it will help you remember where the muscles are located and what they do (Figure 11. Pronunciation of words and terms will take a bit of time to master, but after you have some basic information; the correct names and pronunciations will become easier. For the legs, superficial muscles are shown in the anterior view while the posterior view shows both superficial and deep muscles. These include naming the muscle after its shape, its size compared to other muscles in the area, its location in the body or the location of its attachments to the skeleton, how many origins it has, or its action. The skeletal muscle’s anatomical location or its relationship to a particular bone often determines its name. Similarly, the shapes of some muscles are very distinctive and the names, such as orbicularis, reflect the shape. For the buttocks, the size of the muscles influences the names: gluteus maximus (largest), gluteus medius (medium), and the gluteus minimus (smallest). Names were given to indicate length— brevis (short), longus (long)—and to identify position relative to the midline: lateralis (to the outside away from the midline), and medialis (toward the midline). The direction of the muscle fibers and fascicles are used to describe muscles relative to the midline, such as the rectus (straight) abdominis, or the oblique (at an angle) muscles of the abdomen. Other muscle names can provide information as to how many origins a particular muscle has, such as the biceps brachii. For instance, the sternocleidomastoid muscle of the neck has a dual origin on the sternum (sterno) and clavicle (cleido), and it inserts on the mastoid process of the temporal bone.

Phosphatase Nucleotides Nucleoside + Phosphate Nucleosidases (Nucleoside phosphorylase) The nucleosides obtained above either absorbed or degraded into bases and sugars by nucleosidases 20mg fluoxetine amex. Mechanism Transcription involves 3 stages i) Initiation ii) Elongation iii) Termination Three phases of transcription 1 purchase 10mg fluoxetine visa. This complex enzyme buy fluoxetine 20 mg with mastercard, called the holoenzyme is needed to initiate transcription since the s factor is essential for recognition of the promoter. It is common for prokaryotes to have several s factors that recognize different types of promoter (in E. The holoenzyme binds to a promoter region about 40-60 bp in size and then initiates transcription a short distance downstream (i. With in the promoter lie two 6 bp sequences that are particularly important for promoter function and which are therefore highly conserved between species. Using the convention of calling the frst nucleotide of a transcribed sequence as +1, there 2 promoter elements 98 lie at position -10 and -35, that is about 10 and 35 bp respectively, downstream of where transcription will begin. The most common termination signal is a G ≡ C rich region is a palindrome, followed by an A = T rich sequence. Those that lack such a structure require an additional protein, called rho protein (r) to help recognize the termination site and stop transcription. The product of transcription in eukarryotes are called as primary transcripts and they undergo modifcation by a process called post transcriptional modifcation. Okasaki fragments are present in i) both the parental strands ii) both the daughter strands iii) leading strand iv) lagging strand c. G-C rich region followed by A-T rich region is a signal for i) initiation ii) elongation iii) termination iv) primer formation d. One among the following is not a modifed base i) pseudo uridine ii) isopentyl adenine iii) methyl guanosine iv) deoxy thymine e. The metabolism of our body comprises two major balanced activities: anabolism (synthesis) and catabolism (degradation). Whether the metabolic changes are exergonic or endergonic, most of them have to be catalysed by enzymes. If one particular enzyme is defcient or absent then that leads to a block in the pathway of biochemical reactions leading to metabolic abnormalities which are present throughout the life and handed over to the progeny. The absence or defciency of an enzyme will cause an abnormal accumulation of the intermediate products of metabolism in the body and increased excretion in urine as such or their degradation products. For example, in the following reaction a c b d R B C D P R is the reactant, B, C and D are intermediates and P is the product and a, b, c and d are enzymes catalyzing various steps of the reactions. In this reaction pathway, if any one of the enzyme is defcient or absent, the previous intermediate accumulates and produces toxicity. It also affects the amount of product (P) formation which may be essential biologically and there by leads to pathological diseases. Beadle and Tatum put forth their theory of one gene one enzyme hypothesis which states that one gene controls the synthesis of a single enzyme. Galactosemia, Von-Gierke’s disease, hemophilia, albinism, alkaptonuria and Tay-Sach’s disease are some of the important diseases due to inborn errors of metabolism. Due to the enzyme defect galactose accumulates in blood and is reduced by aldose reductase in the eye to the corresponding galactitol which causes cataract. The general condition is more severe if it is due to a defect in galactose 1 - phosphate uridyl tranferase, since galactose 1- phosphate accumulates and depletes the liver of inorganic phosphate. After 2 - 3 months of age the liver may show fatty infltration and lead to cirrhosis (non functioning of liver cells). Galactosemia at this age is associated with mental retardation due to accumulation of galactose and galactose 1 - phosphate in cerebral cortex. In this, the enzyme which is defcient is glucose 6-phosphatase that converts glycogen to glucose 6-phosphate and then to glucose. Massive enlargement of the liver, pronounced hypoglycemia in between meals, failure of blood glucose to rise on administration of glycogen and convulsion are seen in this condition. Since glucose 6- phosphate cannot leave liver cells, there is compensatory increase in glycolysis leading to increased levels of pyruvic acid and lactic acid. If any one or more of these factors are not synthesised adequately and properly that results in defect in blood clotting and thereby hemorrhage. A number of inherited defciency of the blood clotting factors are found in human and are collectively called as hemophilias. Causes Hemophilia is an inherited disease, where clotting occurs at an abnormally slow rate due to the absence of one or more of the blood clotting factors. These individuals should be extremely careful not to contract even minor injuries like trauma or extraction of tooth, since this may result in severe hemorrhage ( blood loss ). The defect is in the enzyme tyrosinase which is responsible for the biosynthesis of the pigment and hence the individual appears bleached. In this condition, melanin is not synthesized in the melanocytes and affects the skin, hair, sclera and choroids etc. Cause The disease is characterised by the defciency of homogentisate oxidase which catalyses the conversion of tyrosine to acetyl coA and acetate.

Specific laboratory tests Qualitative test Specimen Urine generic 20mg fluoxetine mastercard, stomach contents order fluoxetine 20 mg online, scene residues generic fluoxetine 20mg overnight delivery. B- To test for acetylsalicylic acid or methyl salicylate in stomach contents or scene residues, and to test for 77 Toxicology salicylamide in urine, stomach contents or scene residues, first boil 1 ml of sample with 1 ml of aqueous hydrochloric acid (0. Azide preservatives react strongly in this test, and weak false positives can be given by urine specimens containing high concentrations of ketone bodies. This test is sensitive and will detect therapeutic dosage with salicylic acid, acetylsalicylic acid, 4-aminosalicylic acid, methyl salicylate and salicylamide. Measure the absorbance of the supernatant at 540 nm against plasma blank Results Calculate the plasma salicylate concentration from the graph obtained on analysis of the salicylate standards. Some salicylate metabolites interfere, but plasma concentrations of these compounds are usually low. Oxalates, for example, from fluoride/ oxalate blood tubes, also interfere in this test. Toxic manifestations of barbiturates vary with the amount of ingestion, type of drug and time elapsed since ingestion. Phenobarbital) generally cause toxicity, but fatalities are more common with the latter. Moderate intoxication is characterized by greater depression of mental status and severe intoxication causes coma. Phenobarbital) levels are helpful for making a diagnosis but of little value when predicting the severity of the over dose. Specific laboratory tests Quantitative assay Specimen Whole blood, plasma or serum (5 ml) Reagents (see annex I) 1. Standards (see annex I) Solutions containing barbital at concentrations of 5, 10, 25 and 50 mg/l in blank human plasma 80 Toxicology Procedure 1. Add 5 ml of sample, 2 ml of hydrochloric acid and 60 ml of diethyl ether to a 250-ml separating funnel. Lubricate (with purified water) and insert the funnel and shake gently for 2 minutes. After standing for 5 minutes, and then discard the lower aqueous phase, add the diethyl ether extract to 10 ml of borate buffer in a second separating funnel and mix for 1 minute. Allow to stand for 5 minutes and again discard the lower, aqueous phase through the funnel tap. Wash round the funnel with 5 ml of purified water; allow standing for 5 minutes and again discarding the lower, aqueous phase through the funnel tap. Add about 4 g of sodium sulfate/charcoal mixture to the ether extract in the funnel, shake to disperse, and filter the extract through phase-separating filter-paper into a 150-ml conical flask. Add a further 20 ml of diethyl ether to the separating funnel, shake and add to the extract in the flask through the filter funnel. Evaporate the extract to dryness on a water-bath at 40°C under a stream of compressed air or nitrogen. Check the spectrophotometer zero at 240 nm using purified water in both sample and reference positions. Add 4 ml of filtrate from the test-tube to a clean, dry cell, add 50 µl of concentrated ammonium hydroxide and mix using a plastic paddle. If necessary, accurately dilute a portion of the extract with purified water to bring the reading on to the scale, and record the magnitude of the dilution. Results 1) To perform a quantitative measurement, measure the difference between absorbance at pH 10 and at pH 2, construct a calibration graph by analysis of the standard barbiturate solutions, and calculate the barbiturate concentration in the sample. Alternatively, use the following formula: ((absorbance at pH 10) - (absorbance at pH 2)) × Dilution factor (if any) × 25 = barbiturate (mg/l) 2) Sample volumes of less than 5 ml may be used, but there will be a corresponding loss of sensitivity unless "micro"- volume fused silica spectrophotometer cells are available. Environmental toxicants Exposure of biological systems to chemicals may occur through environmental pollution of the atmosphere, water or soil. Food born toxins derived from different microbes also can contribute in causing environmental intoxication. The possibility of carbon monoxide poisoning is obvious for the victim of fire and smoke inhalation; but accidental and suicidal exposures are also common. The gas is readily absorbed across the alveolus and combines with hemoglobin with high affinity than oxygen. This displacement of oxygen from hemoglobin leads to a decrease in oxygen transport and causes tissue hypoxia. Elimination of carbon monoxide is predominantly through respiration; only about 1% is 83 Toxicology metabolized to carbon dioxide. Laboratory analysis - Carboxyheamoglobin level – should be measured as early as possible to establish the diagnosis of carbon monoxide poisoning. Carboxyheamoglobin should be measured from blood sample using spectrophotometric methods. Although not as accurate, carboxyheamoglobin levels can be estimated from expired air using a breath analyzer for carbon monoxide. The PaO2 is often normal, as it is a measure of oxygen dissolved in plasma, not a measure of oxygen bound to hemoglobin.

C ascades ofch em icals and enz ym es are released from intracellular granules Th ese cascades also appearto prom ote th e synth esis and release ofch em icals knownas cytokines fluoxetine 10mg low cost. C h em icals em itted by activated m astcells and th eirneigh bours intissue m ay induce basoph ils generic fluoxetine 20mg free shipping, eosinoph ils purchase 20mg fluoxetine amex,and oth ercells flowing th rough blood vessels to m igrate into th attissue. Th e ch em icals facilitate m igrationby prom oting th e expressionand activity ofadh esionm olecules onth e circulating cells and onvascularendoth elialcells. Th e circulating cells th enattach to th e endoth elialcells, rollalong th em ,and eventually,cross betweenth em into th e surrounding m atrix. Th ese recruited cells secrete ch em icals ofth eirown,wh ich cansustainim m une activity and dam age tissue. N eonatal & infant im m une system s S erialinfections Im m une response Th 1 Th 2 Th 2 A ge B alanced Th 1/Th 2 Th e intrauterine environm entis powerfully Th 2 – at~2yr th is im prints Th 2 dom inance uponth e neonate D elayed m aturation of Th1 capacity F ew serialinfections – h ygiene,sm allfam ily siz e etc Im m une response Th 1 Th 2 A ge U nbalanced Th 1/Th 2 Th 2 dom inance at~2yr L ongerperiod oftim e inwh ich to m ake and establish Th 2 responses to environm entalantigens (i. This m ay have resulted in m ore w idespread clinical expression of atopic disease" Itcanbe interpreted interm s ofa failure to m icrobially m odulate default Th 2 responses inch ildh ood Fam ily history for asthm a and cum ulative incidence of allergic diseases in offspring. G enetics Clim ate change im pact on the ecosystem of pollen‐producing plants Environm ent Cutaneous exposure to a food allergen, especially to inflam ed skin,m ay be a sensitizing route. W ith a concom itant lack of oral exposure to induce tolerance, the effect could N utrition be prom oting food allergy The com plex interplay betw een hostand environm entalfactors leading to allergic diseases A llergic R hinitis • R hinitis ‐ definition: Inflam m ation of the m em branes lining the nose • Characterized by nasal congestion, rhinorrhea, sneezing, itching of the nose, and/ or post nasal drainage, dry cough, ocular sym ptom s • A llergic rhinitis ‐ definition: Rhinitis that is caused by an IgE‐m ediated reaction to an aeroallergen. C opyrigh tElsevier2002 Food A llergy A dverse food reaction ‐ any aberrant reaction after ingestion of a food or food additive • Toxic reactions — due to toxin (bacterial, other) present in a food • N ontoxic reactions ‐ depends on individual susceptibilities • Im m une ‐ allergy or hypersensitivity (Type I) • N onim m une – intolerances: D ue to pharm acological properties of the food (caffeine or tyram ine), U nique susceptibility of the host (lactase deficiency), E. The English version serves two purposes: as a learning aid for international students and to encourage German-speaking students to familiarize themselves with medical English; the lectures are delivered in German. The translation from the original German version is my own; I am afraid it will occasionally sound appalling to native English speakers, but it should at least be intelligible. Over the course of evolution, this has led to the development of highly sophisticated defense systems in multicellular organisms. To maintain the integrity of our organism, it is essential to distinguish between biological structures that have to be fought off –ideally, everything that poses a danger to our organism—and structures that must not be attacked, e. This problem is not at all trivial, as dangerous attackers from the worlds of viruses, bacteria and parasites consist of largely the same molecules as the human body. Early in evolution, simple multicellular organisms developed a defense system activated by sensing typical molecular patterns associated with pathogens or distressed cells. In the best case, it nips an incipient infection in the bud; in the worst case, it keeps an infection in check for a few days. We are all absolutely dependent on this "old" system: infectious agents propagate so fast that we would be dead long before the second, evolutionarily younger system had a chance to kick in. Our most efficient defense mechanisms mount a custom-made counter-attack against the specific infectious agent invading our organism. Bespoke work takes time, meaning the system is simply not ready for use during the first days of an infection. This is because our immune system is able to learn what constitutes "self"; everything else is viewed with suspicion. As additional criteria to assess the level of danger, activation of the first, innate system is taken into account. While these molecules in fact cause inflammation, their ultimate goal is of course not inflammation, but defense. The drawback: if we would like to inhibit unwanted inflammation, we are usually able to alleviate it, but not to suppress it completely. It has a basic recognition function for many bacteria, can alert and recruit phagocytes, enhance visibility of bacteria to phagocytes and sometimes even lyse bacteria. The third pathway, which is mainly antibody-activated and hence part of the adaptive immune system, developed much later, but was identified first. The alternative pathway of complement activation starts with the spontaneous hydroysis of an internal thioester bond in the plasma complement component C3 to result in C3(H2O). The changed conformation of C3(H2O) enables binding of the plasma protein factor B which is in turn cleaved into fragments Ba and Bb by the plasma protease factor D. If C3b binds to the membrane of one of our own cells, the process of activation is inhibited by one of several different protective proteins, preventing damage to the cell. Facilitated by the bacterial surface, factor P (properdine) stabilizes the membrane- bound C3bBb complex. This complex, the C3 convertase of the alternative pathway, subsequently works as an amplifying tool, rapidly cleaving hundreds of additional C3 molecules. Soluble C3a diffuses into the surroundings, recruiting phagocytes to the site of infection by chemotaxis. This function, making the bacterium a "delicacy" for phagocytes, is called opsonization, from the Greek word for goody. The complement cascade does not stop at this point: further activation of components C5 through C9 ultimately result in the formation of membrane pores that sometimes succeed to lyse the bacterium. The smaller cleavage products C3a, C4a, C5a, sometimes called "anaphylatoxins", have additional functions in their own right: apart from attracting phagocytes, they cause mast cell degranulation and enhance vessel permeability, thereby facilitating access of plasma proteins and leukocytes to the site of infection.

Growth monitoring is particularly important for follow-ups for children under 3 years of age fluoxetine 20mg with visa. Weighing a child regularly on a growth chart and understanding the direction of the growth line are the most important steps in detection of early malnutrition purchase fluoxetine 20 mg line. Gomeze classification of Nutrition Status Weight for age/reference Edema present Edema absent weight 60-80% Kwashiorkor Underweight < 60% Marasmic Marasmus Kwashiorkor It is very important to follow subsequent measurements and plotting order 20 mg fluoxetine otc, to watch the direction of the line showing the child’s growth. Table 4 Interpretation and the findings of growth charts Indication Child’s Danger sign Very Dangerous condition Stagnant Losing weight Good gaining weight Indication of the growth Monitoring chart Interpretation Child is growing Not gaining Losing weight may well weight Find out be ill, needs care why Poor nutrition infection Intervention Complement the Instruct the Careful counseling mother mother, support return soon, admit her or refer 90 Pediatric Nursing and child health care 7. The side effects of malnutrition include hypoglycemia, hypothermia, hypotonic and mental apathy. Severe malnutrition (Kwashiorkor and Marasmus) contributes to high mortality and morbidity of children less than five years in developing countries and to mental and physical impairment in those who survive. A) Kwashiorkor: The most acute form of malnutrition is generally found in a child of 10-14 months who has had an excessive carbohydrate diet containing relatively little protein. Coldness of the extremities is well marked and the child is miserable but apathy when anorexia and/or diarrhea set in, there is loss of weight in spite of edema. This marsmic stage may be due to mal absorption rather than deficiency in caloric intake. Chronic cases show depigmentation of skin and hair, with the hair losing its luster, becoming straight, dry and sparse. Marasmus: This condition, seen in children whose weight is markedly 91 Pediatric Nursing and child health care below normal for their length is described as state of starvation. A general deficiency of protein and energy has occurred, leading to severe wasting of subcutaneous fat and muscle tissue. The marasmic child appears as a wizened old man in appearance, with loss of most fatty tissue, shriveled buttocks and emaciated limbs. Many of the signs of kwashiorkor, such as edema, skin rash and hair discoloration are absent. If a child is to be cured, he must be able to eat high protein and energy diet and his family must have enough food for him. If he does not want to eat, we have to feed him through a tube in health facilities. The danger signs that show that a malnourished child needs treatment quickly are edema, apathy and not eating well. Prevention of malnutrition The following are some of the important approaches in prevention of malnutrition in children. Classification of malnutrition: Signs classification Severe visible wasting or Severe palmer pallor or severe malnutrition/severe Edema on both feet anemia Some palmer pallor or Very low wt. Since the body doe not manufacture vitamins small amounts must be included in the diet. Some are soluble in fat and are ingested in dietary fat (vitamin A, D, E and K), and some are water soluble (Vitamin B complex and Vitamin C). Vitamin A Normal growth, normal vision, normal reproduction Maintenance of epithelial cell structure and function Immunity to infection 95 Pediatric Nursing and child health care Deficiencies results in: • xerophthalmia, (night blindness, conjunctiva dryness, Bitot spots, Keratomalacia, and even eyeball perforation and blindness) • Increased risk of infections (Viral is more). Excess results in: • Raised intracranial pressure, irritability,dry skin, hair loss, brittle bones 2. Parasthesia, weakness, gastrointestinal symptoms • Dry beriberi (peripheral neuropathy, mental confusion,nystagmus) • wet beriberi ( biventricular cardiac enlargement, systemic venous hypertension, bounding pulse) • Infantile beriberi (acute cardiac failure) 3. Riboflavine (B2) • Coenzyme in oxidative –reduction reaction 96 Pediatric Nursing and child health care Deficiency results in; • Angular stomatitis, cracking and fissuring of lips • Glositis, papillary atrophy • Scrotal or vulvae dermatitis • Photophobia, corneal vascularisation • Anaemia, hair loss , ataxia • Personality changes, retarded intellectual development 4. Niacin (nicotinic Acid) • Oxidative –reduction reactions , fat synthesis, glucolysis • Deficiency results in: Pellagra (dermatitis, diarrhea, dementia) • loss of weight, poor appetite, sore mouth, indigestion • insomina, confusion • skin erythema, pruritus, discoloration, flaking 5. Pyriodoxine (B6) • Coenzyme in amino acid metabolism and • Muscle glucogen phosphorylase Deficiency results in: Infants: hyperirritability, convulsions, weakness anemia, and dermatitis 6. Ascorbic Acid (vitamine C) • Formation of collagen, amino-acid metabolism • Iron and copper metabolism • Protection against free radicals (oxidents) Deficiency results in: Scurvy • ulceration ,poor wound healing, anemia • Scurvy: irritability , unproductive cough, bone tenderness, sub-periosteal hemorrhages 8. Vitamin D: • Calcium and phosphate homeostasis • Normal mineralisation of bone and teeth Deficiency result in: • Rickets, Osteomalacia Excess result in: • Hypocalcaemia, ectopic calcification • Failure to thrive 98 Pediatric Nursing and child health care 9. Vitamin E (tocopherol): • Antioxidant (protects against free radicals) • Preserve cell membrane integrity Deficiency result in: • Hemolytic anemia, skin changes • Encephalomalacia 10. Vitamin K Synthesis of coagulation factors Deficiency results in: • Coagulophathy: haematuria, hematomas, and heamorragic disease of newborn • Hemolytic anemia may be caused by the water soluble form of vitamin K Iron deficiency Anemia: Anemia refers to a deficit of red blood cells or hemoglobin in the blood. Nutritional deficiency • Iron deficiency • Folic acid deficiency 99 Pediatric Nursing and child health care Vitamin B12 deficiency b) Decreased erythrocyte production: • Pure red cell anemia • Secondary hemolytic anemia’s associated with infection, renal disease, and chronic disorders Aplastic anemias Invasion of bone marrow by A, Leukemia B, Tumors 3. Assessment of the child’s condition Building resistance to infection Administering blood transfusion as ordered Nursing management: 1.

Growth monitoring refers to the regular assessment of the growth of children under two years old to detect deviation from normal growth and the application of appropriate interventions discount fluoxetine 20 mg otc. In the following section you will learn how you can counsel mothers and caregivers about the growth and nutritional status of their children purchase fluoxetine 20 mg free shipping. To measure individual health and to instigate effective action in response to growth faltering (slowing down) cheap fluoxetine 20 mg on line. Teach mothers, families and health workers how diet and illness can affect child growth and thereby stimulate individual initiative and improved nutrition and healthcare practices. Poor linear growth (underweight and stunting) usually occurs in the first 24 months of life. If the child is not optimally fed during this time, they could lose 11cm from the potential height that they would have reached as an adult. By the time a child is two or three years old, catch-up growth is less likely to occur; such children have probably failed to grow and are potentially stunted for the rest of their lives. You learned how to assess whether a child is stunted in Study Session 4 of this Module. Age of malnourished child Determinant factors Birth Maternal factors (including nutrition), gestational age Four-six months Infant feeding practices, maternal ability to care for the child Six months to two years Complementary feeding practices, exposure to infections, disease and poor household food as the child gets older Two-five years Inadequate access to household food; infections and social deprivation In Ethiopia we use underweight for monitoring growth, as it indicates acute changes in the nutritional status of the child. If you determine that the child is malnourished (underweight), you should be able to analyse the causes, identify resources, suggest alternative solutions and arrive at decisions together with the mother or caregiver as to what should be done about the child. This process of assessment analysis and action is known as the ‘triple A’ cycle which is described below. Assess This stage involves weighing a child on a regular basis, and comparing the child’s growth with the standard and with their previous weight. This helps to identify any nutritional problems and will help you reflect on and review the child’s situation with the mother or caregiver. Analyse This requires exploration of any nutritional problem of the child in order to understand the root causes of any difficulties. You should identify gaps in feeding or care practices and think about different alternative solutions and resources that you can suggest to the mother or caregiver. Action This stage involves counselling the mother or caregiver about relevant actions. It involves decision making and resource identification as well as deciding on individual and collective doable actions. After thorough discussion with the mother or caregiver, you should be able to decide on the specific actions they need to do. Ideally these actions are feasible and can realistically be done by the caregiver and the household. Each time the child is weighed again, re- assessment is done, followed by new analysis and new action as necessary. The most important issue in growth monitoring is not the position of the child ThetripleAcyclemeasuresthe on the growth curve at one particular time, but the direction of his or her direction of the child’s growth. A single point on the line of growth could be reached from different directions (that is, the child’s weight could go down to the single point or could move up to that point on the chart). Normally the child’s measurements are expected to fall between the lines indicated on the graph by -2 and +2 Z-scores (see the right hand side of the graph). It gives you information you need to be able to advise the mother and caregiver what they need to do for their child. You need to find out the problem together with the mother or caregiver and counsel them on what to do. So you should encourage the mother to continue feeding the child in the way she has been doing. Knowing the rate and direction of growth will help you when you are counselling the mother or caregiver. You should always employ nutrition counselling as a tool to help you achieve this objective. Nutrition counselling is a process of finding the solution to the child’s nutritional problem together with their mother or caregiver. Unlike nutrition education, nutrition counselling is a two-way process during which the mother is actively involved in describing the child’s problems as well as participating in analysing the causes and identifying the available resources and solutions. Working together in this way with the mother or caregiver will help them reach a decision about the doable actions. Analysing causes and identifying 156 Study Session 11 Nutrition Education and Counselling actions are an important part of the overall process. Once you weigh the child and determine their nutritional status you need to share this information with the mother and negotiate with her what actions she can take. Follow-up is also very important and you should always recommend to the mother that she makes an appointment so you can see whether she has carried the agreed actions or whether she has had some problems with these. Counselling is an important skill, and as you have seen, a key element of the triple A cycle.