Children under 5 years of age - Single dose of 0.5gm. Older children -Single dose of 1.0 gm.

may prove fatal. DIAGNOSIS - Larvae of S. stercorails may be found in sputum of in lung and jejunal biopsy samples, as also duodenal contents and faeces. TREATMENT - Thiabendazoie 25 mg/kg b.d. for 5 days (maximum dose 3g/day) after meals. The tablets must be chewed. Side effects • Nausea, anorexia, vomiting, diarrhoea and giddiness. Rarely drowsiness. pruritus, xanthopsia, bradycardia and hypotension. Urine often smells of asparagus. Albendazole 400 mg/day for 3 days in adults, teptomeninges). Myelogram showing multiple tilling detects. Positive immunological tests (serum immunoblot and CSF enzyme-linked immunosorbent assay) for detection of anticysticercal antibodies. Plain radographs showing 'cigar-shaped' calcifications in (high and calf muscles TREATMENT - Nictosamide - Adults - Single dose of 2.0 gm. Children under 5 years of age - Single dose of 0.5gm. Older children -Single dose of 1.0 gm. The tablets should be given on empty stomach, chewed thoroughly and washed down with a little water. A purgative e recommended if the dead. segments are not passed out within a few hours. Praziquantel - Single dose of 5-10 mg/kg after a light breakfast (all age groups). For cerebral cysticercosis - Praziquantel 50 mg/kg/day for 15 days, or Albendazole 15 mg/kg/day for 30 days. Treatment is considered successful when the sacolex is found, no proglottids appear within 4 months of tharapy in case of T. saginata. faecal examination ramains negative for 3 months after treatment incase of T. solium Enterobiasis -is caused by the pinworm (thread worm) E. vermicularis. The adult threadworms live in the colon and rectum. and the gravid female emerges from the anus to deposit the eggs on the surrounding skin. These eggs if swallowed liberate the contained larvae which mature as they pass down the intestine. CLINICAL FEATURES - Minimal except for anal and parianal itching. Heavy infestation may cause insomnia due to pruritus. anorexia and abdominal discomfort. COMPLICATIONS -Appendicitis is a known intestinal complication. Non-intestinl complicaitions- include vulvo-vaginitis inyoung girls and occasionally endometritis and chronic pelvic poritonitis due to granulomas formed round staying enterobius worms. invasion of the urinary tract, which faciliates bacterial infection may cause enuresis. Some patients with pritected or recurrent infection have psychological problems DIAGNOSIS - Adult female E. vermicularis can be seen in perianal area, in faeces. or during proctoscopy or vaginoscopy. Presence of eggs can be demonstrated by applying adhesive cellophane tape to the perianal skin for microscopic inspection at night. removed and examined the next morning. TREATMENT Mebendazole - Single dose of 100 mg (all ages). Pyrantel - Single dose of 10mg/kg (maximum 500 mg) Pyrivinium - Single dose of 5 mg/kg (maximum 600 mg). Piperazine citrate - 85 mg/kg or 7 days (maximum 2 5 mg) Sporadic infections are usually cured by one treatment. In internsive and symptomatic infections, drug therapy snould be rapeated after 2 weeks, and then if necessary every 2 months. Adjuvant measures - to prevent reinfection. Nails should be cut short and gloves and close-titting sleeping drawers should be worn at night. Childs hands must be scrubbed will brush before meals. All infected members of the family should be treated simultaneously. Strongyloidiasis - is caused by the nematode Strongyloides stercoralis. Infection is acquired in the same way as hookworms and thereafter it is self-perpetuating. CLINICAL FEATURES - (a) Asymptomatic. (b) Skin - Penetration of larvae causestranslent linear, itching erythema, (c) Respiratory - Pneumonitis and Loeffier's syndrome (during lung migration). (d) Intestinal - Ufcerative and/or hemmorrhagic enteritis due to superficial inflammation of jejunal mucosa, resulting in savere hypoproteinamia and anemia. (e) Acute disseminated stronglyloidisis - may develop during pregnancy, puerperium. or in immunosuppressed subjects when it may prove fatal. DIAGNOSIS - Larvae of S. stercoralis may be found in sputum or in lung and jejunal biopsy samples, as also duodenal contents and faeces. TREATMENT - Thiabendazole 25 mg/kg b.d for 5 days (maximum dose 3 g/day) after meals. The tablets must be chawed. Side effects - Nausea, anorexia, vomiting, diarrhoea and giddiness. Rarely drowsiness, pruritus, xanthopsia, bradycardia and hypotension. Urine often smells of asparagus. Albandazole 400 mg/day for 3 days in adults, TREATMENT - Praziquantel in three equal doses of 20 mg/kg at 4h intervals with meals. Apart from mild sids-effects of drowsiness, headache, dizziness, etc. a syndrome of severe abdominal pain followed by bloody diarrhoea may occur. PREVENTION -1. Protection of small habitats from infection by provision of clean water and toilet facilities, and health education 2 Mass therapy with oxamniquine. metriphonate or praziquantel to reduce amount of egg excretion 3 Snail destruction by improved irrigation methods and use of moIluscicides. 4. Prevention of infection by wearing protective clothing 18. HYDATlD DISEASE : Defination - Hydatid disease of man is zoonosis caused by infection with tapeworm larvae of the genue Echinococcus. There are two forms -(a) Cystic: The much more common E. granulasus causes unilocular hydatid cysts and is

. RENAL DISORDERS 1. INVESTIGATlONS IN RENAL DISEASE. The Urine I. GENERAL CHARACTERS

leucodystrophy Cockayne's syndrome (b) Paraproteinemia Myeloma Waldenstorm's rnacroglobulinemia (c) Drugs Amidarone (d) Chronic inflammatory damyelinating neuropathy. Autonomic neunopathy - 1. Diabetes melitlus. 2. Uramia 3. Guillain-Barre syndrome. 4.Alcoholic liver disease. 5. Amyloidosis. 6. Idiopethic Congenital Riley-Day syndrome. Acquired Shy-Drager syndrome. 7. RENAL DISORDERS 1. INVESTIGATlONS IN RENAL DISEASE. The Urine I. GENERAL CHARACTERS - A. Volume - varies with amount of fluids ingasted, perspiration,etc. Normal average for adult 1,200-1,500 ml. (40-50 oz.) Polyuria -A. Transient polyuria -(1) Induced or therapeutic- (a) ingestion of large amounts of fluids. (b). Alcohol, tea, coffee, acidifying salts like citrates or tartrates, spices, large amounts of sugar (c) Diuretics. (d) High protein diet. (2) Spontaneous- (a) Due to nervousness or after a nervous attack, e.g. examination, neurasthenia, after an attack of epilapsy. migraine. asthma, angina pectoris or paroxysmal tachycarda. (b) Hydronephrosis with periode emptying of renal sac. (c) Attack of malaria, during the cold stage. (d) During convalescence from fevers like enteric. (e) Diminution or disappearance of oedema, e.g. recovery from acute naphirtis, cirrhosis of Iiver. (f) Post-anuric duresis. (g) Crisis of chronic nephrosis. B. Continued polyuria - (1)Cranial diabetes insipidus. (2) Nephrogenic diabetes insipidus. (3) Primary polydypsia - (See Chapter 5). Oliguria - Diarrhoea, fever. decompensated heart disease. glomerulonephritis, during accumulation of fluid in serous cavities, uremia Nocturia - 1. Prostatism. 2. Oedematou states. 3 Polyuric states - Diabetes mellitus/insipidus, primary polydipsia. Post-ATN 4. Salt-losing naphropathies - Analgesic nephropathy, medullary sponge kidneys, sickel call disease 5. Bladder disease - Tumour, infection (TB, fungal, schistosoma), loss of reflex inhibition (e.g. MS), vesicoureteric reftux ('double micturition') in children B Transparency - Freshly passed normal urine is clear and transparent. Cloudiness - (a) Amorphous phosphates - form white sediment in neutral or alkaline urine which disappears on addition of acid, (b) Amorphous urates -White or pink cloud which disappeare on heating (c) Blood - Bright red blood from lower urinary tract, dark red or brown from upper tract. Dipstick testing for haemeglobin is a sensitive method of detecting sigfuficant microscopic haematuria particularly when the Sp gr of urine specimen is low. (d) Bacteria - Uniform cloud or opalescence. (e) Chyluria or milky urine - due to blocking of thoracic duct by filaria or inflammatory or naoplastic conditions, with consequent rupture of lymphatics of the bladder. (f) Spermatozoa and prostatic fluid. C. Colour - Depends on volume of urine voided and varies roughly with specific gravity. (a) Colourless -in polyuria and diabetes insipidus. (b) Dark colour - concentration as in fevers. (c) Dark yellow - bile, riboflavin. carotene containing foods. (d) Red -Drugs. (1) Excretion products - Rifampicin, matronidazole, sulphasalazinsr doxrubicin. desferrioxamine. (ii) Drug toxicity -Barbiturates (acute intermittent porphyria), clofibrate, heroin (rhabdomyolysis), wartarin, urokinase (hematuria) (2) Beeturia. (3) Favism (e) Red brown - Urates. porphyria. rnyoglobinurla. (f) Dark brown to black - Alkaptonuria, tyrinosis. melanosis (g) Green to greenish blue - Methylene blue, Ps. aerginosa infection, indigo compounds (h) Cloudy - Laucocytes, bacteria, urates (acid urine), oxalates (alkaline urine), (i) Smoky - Trace of erythrocytes. (j) Bloody - Frank hematuria. D. Odour - Characteristic 'aromatic' odour most marked in concentrated urine. Odour becomes ammonical during decomposition, a cloudy urine with an ammoniacal odour suggests cystitis or pyelitis, usually with obstruction in the urinary tract. Fruity odour in diabetes. Urine containing cystine may develop odour of sulphuretted hydrogen during decomposition. Articles of diet and drugs impart peculiar odour.e.g. asparagus and turpentine E. Reaction - of fresh urine usually acidic (blue litmus paper turns red) with an average pH about 60 pH paper range is from 4. 5-7 F. Specific gravity -Generally varies with quanlity of urine. Normal range 1.017ti 1,020. Diseased kidneys lose partially or campletely their ability to respond to the need of the body with the result that the urine has about the same specific gravity throughout the day II. CHEMICAL EXAMINATION - 1 Proteins - Urine may contain mostly albumin (selective proteinuria) or may contain larger molecules as well (non-selective proteinuria). Excretion mainly of albumin signifies a glomerula lesion. Causes of proteinuria-(1) PHYSIOLOGICAL- Amount of protein excreted is small and the condition is temporary (a) Orthostatic benign - usually in older children and adolescence (i) Urine sample passed on waking is negative for proteinuria while urine passed after 2 hours ambulation is positive. Usually increased by exercise (ii) Proteinuria 'tubular' in character i.e it contains small molecular weight proteins which normally pass through the glomerulus and are reabsorbed by (the proximal tubule. (iii) <1g/day. No increase with time (b) Prolonged exposure to cold, (cj After a meal rich in proteins (alimentary proteinuria) (d) Pregnancy. (e) Pre-menstrual (f) During first 10 days after birth (2) PATHOLOGICAL (a) Glomerular lesion -(i)

. RENAL DISORDERS 1. INVESTIGATlONS IN RENAL DISEASE. The Urine I. GENERAL CHARACTERS

leucodystrophy Cockayne's syndrome (b) Paraproteinemia Myeloma Waldenstorm's rnacroglobulinemia (c) Drugs Amidarone (d) Chronic inflammatory damyelinating neuropathy. Autonomic neunopathy - 1. Diabetes melitlus. 2. Uramia 3. Guillain-Barre syndrome. 4.Alcoholic liver disease. 5. Amyloidosis. 6. Idiopethic Congenital Riley-Day syndrome. Acquired Shy-Drager syndrome. 7. RENAL DISORDERS 1. INVESTIGATlONS IN RENAL DISEASE. The Urine I. GENERAL CHARACTERS - A. Volume - varies with amount of fluids ingasted, perspiration,etc. Normal average for adult 1,200-1,500 ml. (40-50 oz.) Polyuria -A. Transient polyuria -(1) Induced or therapeutic- (a) ingestion of large amounts of fluids. (b). Alcohol, tea, coffee, acidifying salts like citrates or tartrates, spices, large amounts of sugar (c) Diuretics. (d) High protein diet. (2) Spontaneous- (a) Due to nervousness or after a nervous attack, e.g. examination, neurasthenia, after an attack of epilapsy. migraine. asthma, angina pectoris or paroxysmal tachycarda. (b) Hydronephrosis with periode emptying of renal sac. (c) Attack of malaria, during the cold stage. (d) During convalescence from fevers like enteric. (e) Diminution or disappearance of oedema, e.g. recovery from acute naphirtis, cirrhosis of Iiver. (f) Post-anuric duresis. (g) Crisis of chronic nephrosis. B. Continued polyuria - (1)Cranial diabetes insipidus. (2) Nephrogenic diabetes insipidus. (3) Primary polydypsia - (See Chapter 5). Oliguria - Diarrhoea, fever. decompensated heart disease. glomerulonephritis, during accumulation of fluid in serous cavities, uremia Nocturia - 1. Prostatism. 2. Oedematou states. 3 Polyuric states - Diabetes mellitus/insipidus, primary polydipsia. Post-ATN 4. Salt-losing naphropathies - Analgesic nephropathy, medullary sponge kidneys, sickel call disease 5. Bladder disease - Tumour, infection (TB, fungal, schistosoma), loss of reflex inhibition (e.g. MS), vesicoureteric reftux ('double micturition') in children B Transparency - Freshly passed normal urine is clear and transparent. Cloudiness - (a) Amorphous phosphates - form white sediment in neutral or alkaline urine which disappears on addition of acid, (b) Amorphous urates -White or pink cloud which disappeare on heating (c) Blood - Bright red blood from lower urinary tract, dark red or brown from upper tract. Dipstick testing for haemeglobin is a sensitive method of detecting sigfuficant microscopic haematuria particularly when the Sp gr of urine specimen is low. (d) Bacteria - Uniform cloud or opalescence. (e) Chyluria or milky urine - due to blocking of thoracic duct by filaria or inflammatory or naoplastic conditions, with consequent rupture of lymphatics of the bladder. (f) Spermatozoa and prostatic fluid. C. Colour - Depends on volume of urine voided and varies roughly with specific gravity. (a) Colourless -in polyuria and diabetes insipidus. (b) Dark colour - concentration as in fevers. (c) Dark yellow - bile, riboflavin. carotene containing foods. (d) Red -Drugs. (1) Excretion products - Rifampicin, matronidazole, sulphasalazinsr doxrubicin. desferrioxamine. (ii) Drug toxicity -Barbiturates (acute intermittent porphyria), clofibrate, heroin (rhabdomyolysis), wartarin, urokinase (hematuria) (2) Beeturia. (3) Favism (e) Red brown - Urates. porphyria. rnyoglobinurla. (f) Dark brown to black - Alkaptonuria, tyrinosis. melanosis (g) Green to greenish blue - Methylene blue, Ps. aerginosa infection, indigo compounds (h) Cloudy - Laucocytes, bacteria, urates (acid urine), oxalates (alkaline urine), (i) Smoky - Trace of erythrocytes. (j) Bloody - Frank hematuria. D. Odour - Characteristic 'aromatic' odour most marked in concentrated urine. Odour becomes ammonical during decomposition, a cloudy urine with an ammoniacal odour suggests cystitis or pyelitis, usually with obstruction in the urinary tract. Fruity odour in diabetes. Urine containing cystine may develop odour of sulphuretted hydrogen during decomposition. Articles of diet and drugs impart peculiar odour.e.g. asparagus and turpentine E. Reaction - of fresh urine usually acidic (blue litmus paper turns red) with an average pH about 60 pH paper range is from 4. 5-7 F. Specific gravity -Generally varies with quanlity of urine. Normal range 1.017ti 1,020. Diseased kidneys lose partially or campletely their ability to respond to the need of the body with the result that the urine has about the same specific gravity throughout the day II. CHEMICAL EXAMINATION - 1 Proteins - Urine may contain mostly albumin (selective proteinuria) or may contain larger molecules as well (non-selective proteinuria). Excretion mainly of albumin signifies a glomerula lesion. Causes of proteinuria-(1) PHYSIOLOGICAL- Amount of protein excreted is small and the condition is temporary (a) Orthostatic benign - usually in older children and adolescence (i) Urine sample passed on waking is negative for proteinuria while urine passed after 2 hours ambulation is positive. Usually increased by exercise (ii) Proteinuria 'tubular' in character i.e it contains small molecular weight proteins which normally pass through the glomerulus and are reabsorbed by (the proximal tubule. (iii) <1g/day. No increase with time (b) Prolonged exposure to cold, (cj After a meal rich in proteins (alimentary proteinuria) (d) Pregnancy. (e) Pre-menstrual (f) During first 10 days after birth (2) PATHOLOGICAL (a) Glomerular lesion -(i)

Elasticity of blood vessel and BP. The Windkessel vessels are elastic vessels.

ty and the end diastolic volume (i. e venous return to the heart), affect the BP. Peripheral resistance. Recall, the peripheral resistance. R= 8 rl. From this, we have 1. If the viscosity rises (i.e. in polytythemia) the BP rises, and vice versa. 2 But the most important factor is the radius of the blood vessel 'r' as BP varies inversely as r4. The radius in turn, varies according to the tone of the vascular smooth muscles. Greater the tone smaller the lumen of the vessel and greater is the resistance. As described in chapter 8 of see. V, the tone of the smooth muscle depends'upon the following: 1. Sympathetic discharge. This in turn depending upon the VMC activity. [The VMC activity, in turn, is influenced by, - (a) raflexes from the periphery (e. g. baroreceptors from the arterial tree) ,(b) impulses from higher center (e.g. emotion) and (c) PaO2 etc. (see fig. 5.8.1 for de-tails)]. In short, the sympathetic stimulation causes vasoconstriction, which leads to increased resistance and thus the BP rises. 2. Chemicals, like the angiotensm, adrenalin etc. (chap. 8 sec. V, for details), which act directly on the smooth mus-cles. The actual process of regulation (that is, maintenance of BP homeostasis) is usually divided into two groups viz (A) short term and (B) long term controls. A Short term control is achieved via neural mechanism. It includes the sinu aortic reflex (for details, see chaps. 4 & 8. sec V) principally and some other reflexes like reflexes from atrial receptors, stretch reflexes from left ventricle etc. (fig. 5.8.1). In short, baroreteptors of the heart and artenal tree are the kingpin of the homeo static mechanism of short term reflex. The sinu aortic mechanism is the principal short term reflex in maintaining the BP homeostasis. In abnormal circumstances, like, a sharp fall of BP (say due to massive hemorrhage or severe diarrhoea) or a sharp rise of BP (say due to uncontrolled anger causing severe sympathetic stimulation) it begins to act immediately, and tries to bring back the BP to the normal value ("buffer nerves"). The other reflexes also maintain the BP homaostasis to some extent. Thus, hypervolemia causing elevation of BP stimulation of atrial volume receptors suppression of ADH loss of extracellular fluid via urine restoration of blood volume and thus of BP. Some other reflexes like the J receptors from lung affect the BP and work towards the benefit of the body. But they are not called into action in day to day life. [The VMC is also stimulated when the limbic system is stimulated (fig. 5.8.1.) as in rage. But this is not aimad towards the maintenance of BP homeostasis. Rather, the elevation of BP is an associated feature of the emotions like rage. The hypothalamus is stimulated during exposure to cold (chap 1, Sec. XD); this too is an associated feature. Motor and premoter cortex are stimulated during exercise, causing tremendous redistribution of blood (by dilatation of skeletal muscle vessels and constriction of splanchnic and cutaneous vessels) but this is to meet the demands arising, out of a particular situation and not aimed towards achieving BP homeostasis)] B. Long term control. This is achieve a through the renin-angiotensin - aldosterone axis as well as via ANP and work through adjustment of blood volume as described below. Blood volume and BP. In the foregoing discussion (neural control) it has bean assumed that the volume of blood has been kept constant throughout. Blood pressure homeostasis however, can be achieved by adjusting the blood volume also. Thus, fall of blood volume release of renin from the kidneys production of angiotensin production of aldosterone sodium retention retention of body fluid so that blood volume expands restoration of BP. In short, fall of BP due to hemorrhage can be tackled by increasing the blood volume, via renin angiotensin axis. This mechanism is however slow to appear and of prolonged duration. Conversely, if there is hypervolemia of blood. the atria are distended ANP (atrial natriuretic peptide. for details, see chap 2 sec VIII) secreted from atrium — diuresis hypervolemia corrected hypertension corrected. Elasticity of blood vessel and BP. The Windkessel vessels are elastic vessels. As already stated (chap. 7, sec. V) if they lose their elasticity, systole hypertension develops, where the SBP is raised but not the DBP. In systolic hypertension the mean BP does not change so much [Compare Ihe effects of systolic and diastolic hypertension on the mean BP. from a pressure of 120/3C mm Hg, let the BP rises to 170/80 mm Hg in one person or to 140/110 mm Hg in a second person. In the first instance, the mean BP is 110 bul in the second it becomes 120 mm Hg although the rise of SBP + DBP together, is 50 mm in both the cases ). A predominant rise in DBP indicates rise m penpheral resistance and is characteristic of essential hypertension whereas a systolic hypertension indicates atherosclerotic degeneration of Windkessel vessels. In the past, rise of DBP used to be regarded as more ominus of the two types (systolic versus diastolic) of hypertension but the leaching was not wholly correct. Effect of velocity on BP If the velocity of blood is very high, the BP determined by sphygmomanometer (henceforth to be mentioned at BP) will give a low value. Thus, (i) in aortic stenosis, the BP is very low. (ii) LowBP is also found in cases of coarciation of aorta, beyond the narrowing. In both the instances, the narrowing increased the velocity of the blood as explained earlier (fig. 5.7.1) and this partly explains the sharp fall of BP. Conditions affecting BP A. Physiological 1. The effect of age on BP has already beena

The static compliance is what has been described above. Obviously, the compliance also depends upon

graph do not coincide. In plain words. at identical intrapleural pressure, the volume of lung is Iess in inspiratory phase than that in expiratory phases. This type of curve is called hysteresis curve by mathematicians (GK hysteresis = to lag behind). So, the difference in the stretchability between inspiratory and expiratory phase accounts for the hysteresis loop of the compliance. The compliance increases in emphysema. but decreases in fibrosis of the lung and pulmonary edema (see applied physiology, later in the chapter for furthe details). Two Items an used. The static compliance and the specific compliance. The static compliance is what has been described above. Obviously, the compliance also depends upon volume of the lung (at low volume, the compliance is high). When the compliance, is determined and values are expressed with reference to the lung volume, it is then called 'specific compliance'. Specific compliance. There is a term, 'relaxation volume. The point at the end of a quiet expiration is called ralaxation volume. At this,point, intrapulmonary and mtrapleural pressures are zero i.e. exactly atmospheric . At ralaxation volume. the lung still contains some air called functional residual capacity (normally about 2500 Ml). On either side of the ralaxation volume point, upto limited range, the pressure volume curve more or less linear (fig 4.2.3). Fig 4.2.3. To illustrate the principle of specific compliance. Specific compliance is the compliance of the lung at ralaxation volume expressed per liter of the functional residual capacity, that is specific compliance - compliance/ functional residual capacity. For example, let the (static) compliance of a man is 0-21/ cm of H2O and his functional residual capacity is 2500 ml. his specific compliance will be 0.08 liter/per cm H2O/liter (0.081 cm H2O-1 liter -1) Compliance of the chest wall and of the excised lung. In experimental animals. lungs can be taken out of the thoracic cavity
and stretchability or compliance of the lungs alone can be measured. lt is seen that the excised lung has a rather low compliance (i.e. it is rather stiff). On the other hand, in experimental animals , the compliance of the thoracic wall minus the lungs also can be seen. It is seen that the thoracic wall alone (minus the lungs) has a high compliance. Stated simply. this means that, if not opposed, the lungs try to collapse whereas the chest wall tends to expand out. The compliance of an intact man or animal (i.e. chest wall plus the lungs), is the resultant of these two opposing forces. In amphysema the lung considerably loses its elastic recoil, (i.e. the tendancy to collapse is Iost), leaving the tendency of the chest wall to expand. unopposed. In emphysema, therefore chest wall remains expanded. Loss of elasticity causes increase of static compliance in emphysema. Factors influencing compliance These are (a) factors present in the pulmonary tissue, (b) factor presents in the chest wall. The factors residing in the pulmonary tissue are - These are (a) factors present in the pulmonary tissue, (b)factors present in the chest wall i) elastic fibers of the lung (ii) surface tension within the alveoli, (iii) interdependence These three factors taken together constitute the the 'elastic recoil' of the lung. Elastic recoil, opposes the streaching of the lung Hence, reduction of elastic recoil = rise in compliance and vice versa Elastic fibers of the lung is a major cause of its elastic recoil. One property of the elastic fiber is that like a strip of India rubber, it elongates when stretched but recoils back to its original (resting) length when the stretch is with draw. During inspiration these elastic fibers are elongated but because of their tendency to -ecoil, it oppooses the expansion (for further details, see 'emphysema chap 6, sac IV). Surface tension within the alveoli is due to the fact that alveoli contain a very thin film of fluid lining their inner side (fig 4.2.4) Fig. 4.2.4. To illustrate the effect of surface tension. If the intraalveolar surface lension rises sufficiently the alveolus collapses. The individual molecules of this fluid, because of the surface tension. try to come closer to each other and the result is that the alveolus tends to collapse as shown in fig 4.2.4. This force too, ultimately opposes the expansion of the lung. Following Laplace's law (see also fig 5.12.1). it can be shown that in a spherical body. Iike alveolus, P=2( EMBED Equation 3 V r where. P is the
Pressure that causes the alveolus to collapse, (EMBED Equation 3) is the surface tension and r is the radius.that is P is pressure
high (and the alveolus collapses) when y is high or r is low. It follows in conditions (i) where the surface tension of the fluid Iining the interior of the alveolus is high (as in 'hyaline membrane disease'), or (ii) where the radius of the alveoli becomes very small, the lung, as a whole strongly resists its expansion (It should be noted that there is another effect of rise of surface tension of the intra alveaolar fluid. if raised sufficiently, it overcomes the colloidal tension of plasma (of the blood of surface capillaries of the lung) and draws fluid from the capillary to alveoli (pulmonary edema)] [N. B. P in the above equation may be called, trans alveolar pressure ] Surfactant. Within the alveolus, there is a material, called surfactant, which reduced surface tension exerted by the alveolar fluid As early as in 1929, von Neergard suspected the presence of a sort of such thing but it was Pattle 1956 who proved the existance of surface tension radusing agent in the alveolar fluid. The surfactant is chemically a mixture of phospholipids (chiefly dip almity "lecithin) and protein. it is secreted by the

SOME COMMON FOODS Common articles of food may be divided as follows:

may cause harm to the body. The following should be noted. The calorie requirement varies from person to person and in the same person from time to time. To adjust this, carbohydrate (rice, wheat, potato, sugar jaggery and so on) and fats and oils (butter, ghee, cooking oil) should primarily be adjusted whereas ordinarily protein should not be considered for adjustments of calories. SOME COMMON FOODS Common articles of food may be divided as follows: I Meat, fish,egg. Sources of animal prtein (meat about 20% fish same as meat. egg about 14%). Proteins are of very high quality. Disadvantage is high cost. However because of the Government policy of encouraging poultry in most states of India, priced egg is not high. The associated fat (in ordinary butcher's cut of meat) is however saturated and its ingestion predisposes to atherosclerosis. II Milk. milk product (excluding ghee butter) : Milk is almost a complete food. very high quality protein (though not as high as in Gr I : for details, see later. III. Grains (cereal) : Rice and wheat. Rich in starch and contain between 7 to10% protein. Protein is of good quality. Deficient in fat, cheap. Table 7.16.1: Balanced diet (for non rich and moderately working main. Food Vegetarian Non vegetarrian lacto vegetarian gms/day gms/day. Cereals rice/wheat 350 350 Pulses (dal). gram 90 60 Meat/fish - 50 Milk 300 100 Vegetables (pulbul, ladies finger, cauliflowers, 100 100 carrot, brinjal etc. Potato 75 75 Green leafy vegetebles 100 100 Egg one (about 60 gms) Fats and oils cooking oil butter/ ghee, fat 50 40 associated with meat Sugar and jaggery 40 40 Lemon one.Seasonal fruits some helps some helps N. B. Values are approximate only. Important, See that (i) there is enough fibers in the diet (to prevent colorectal cancer, breast cancer, atherosclerosis diverticutosis (ii) plenty of caroteinoids are taken (to prevent cancer lung, breast cancer). (iii) fat, particularly saturated fat intake is low (iv) NaCl is restricted and finally (vi) sugar intake is low. IV. Pulses (dal) and legumes: Dal. Rich in protein but poor in fat. Protein is somewhate less digestible and of tower quality. It is the most important protein supplier throughout whole of India excepting marginal areas of North East India. because of its importance to the nation, the Government of India is trying very hard to improve the national yield of dal. Protein content of the dry dal is between 20% to 25% cheap. Byumas usually the dried peas and beans are meant. Soyabean is also a kind of legume. They contain high amount of vegetables protein. The major protein supplier in Latin American countries is, kidney bean. which they consume in large quantity Soyabean contains approximately 40% protein and 17% fat V. Nuts (peanute. almonds, walnuts, ground nuts, etc): Very rich in fat (about 40%) and protein (about 25%) content is almost equal to dal. IV. Roots and tubers: Potato and sweet potato are examples of tubers. They are rich in starch but poor in fat. Carrots and beet roots are examples of roots. Beet is a rich source of sugar like sucrose but not of starch. Protein content is very low. Carrot has protective effects against lung and breast cancers. VII. Green Vegetables: Green leafy vegetables are primarily taken to increase the bulk of food and to avoide constipation. Other vegetables like brinjal. pulbul lady's finger etc. are low in calories. MILK Milk is almost a complete food containing protein. carbohydrate and fat as well as the important vitamins and minerals. Milk however, is deficient in iron. Old people living in isolation and depending mostly on milk and bread (not fortifed with iron) can thus develop anemia. which is sometimes called 'milk injury'. The protein of milk is of very high biological value i. e high quality protein). The composition of milk varies from species to species. Thus the protein percentages of human and cow's milk are 1.3 and 3.5 gm 100 gm. respectively.Buffalo's milk contains higher percentage of fat but same percentage of protein as that of cow. Goat's milk con-tains lesser amount of fat and hence it is better digestible. Proteins of milk are casein and whey piotem. whey proteins are a mixture of lactalbumin and lacto globulin. Fat milk is chiefly bulyrates m fine emulsion. Carbohydrate of milk is lactose. Milk is rich in calcium and phosphorus. The deficiency of iron usually does not matter to the new born as it is born (provided it is not premature. see also metabolism of iron chap. 2.2) with some store of iron. Table 7.16.2 gives the composition of bovine milk and mother's milk. Table 7.16.2: Composition of milk (approx) Article Buffalo Human Effects of boiling Boiling of milk as is commonly done in Indian households destroys the vit C. Pasteurization also causes destruction of some (about 25%) via C content of milk. [ NB. Recently, some American nutritionists are showing same drawbacks of cow's milk ] APPLIED PHYSIOLOGY Obesity Introduction. Every healthy person has some fat in his adipose tissues, which can be mobilized when there is lack of energy input (starvation) to provide energy. Teleotogically. therefore some extra fat is desirable, particularly for our primitive ancestors (who, sometimes, had to face acute shortages of food) or in a comatose patient who might have to remain without food for days together. Normally however, in todays society, with food, supply usually assured obasity is a major health hazard. This is because, obesity is associated with a number of diseases, notably.

FACTORS INFLUENCING RESPIRATORY CENTER (RC

somewhere in the medulla ( it should be noted that usage of anesthesia causes some distortion. Therefore,there is no wonder (that the picture which emerges from anesthetized experimental animals, to some extent differs from what is in conscious man. L FACTORS INFLUENCING RESPIRATORY CENTER (RC) Three sets of factors. as indicated in the beginning of this chapter, influence the RC These are, (i) peripheral reflexes, (ii) chemical control and (iii) influences from the higher center. PERIPHERAL REFLEXES I. HeringBreuer reflex. According to the classical concept, the picture is as follows Receptors are present in the smooth muscles of the finer bronchioles. When the lung is inflated these (stretch) receptors are stimulated impulse generated these impulses are carried by the vegal (afferent) nerve fibers which emerge from these receptors impulses ultimately cause inhibition of the inspiratory center (I neurons) inspiration stops and expiration starts no stretching of these receptors now therefore, no inhibition on the neurons now inspiratory center again begins to send impulse the next cycle begins, his is called Hering-Breuer inflation reflex. According to the classical view, the Hering-Breuer
inflation reflex is an important cause of rhythmicity of the respiration, importance of the Hering-Breuer reflex. For a long time, it (the Hering-Breuer reflex) used to be thought to be of great importance for the maintenance of tha rhythmicity of the respiration. In absence of Hering-Breuer reflex, it was thought, respiratory frequency will diminish but the individual respirations would be deeper. The position has changed in recent times. It is now believed, that the Heing-Breuer reflex does not play a significant role, at least in man. m ordinary tidal volume breathing of the heathy resting individual (eupnea). It becomes important only when the respiratory excursions become violent as in hyperpnea ( = excessive breathing) of muscular exercise. In a case of hyperpnea. the Hering-Breuer reflex becomes active and the excessive prolongation of contractions of the inspiratory muscles are prevented; this causes rise in the rate of respiration but fall in the amplitude of individual excursions. Question arises, how the body is benefited by reducing the period of contraction of the inspiratory muscles in excercise hyperpnea, when the need of the air is great? The answer seems to be that towards the end of a deep inspiration, stretchability of the lung is reduced, as explained earlier while discussing the compliance of the lung (fig 4.2.3.), so that a stage comes, when the inspiratory muscles are working but there is no real entry of air into the lungs. In this stage the contraction of the muscles produces only expenditure of energy but no (or little) gain in respiration. Thus the body prevents excessive cost for the breathing during muscular exercise. Also, during enercise, it is necessary that excess CO2 produced should be removed, by expired air. Activation of Hering -Breuer reflex ensures increased frequency of expiration increased washing out of CO2. In short. Hering-Breuer reflex is weak in resting adult human beings. It becomes active when the tidal volumes exceed one liter (normal. 500 ml). Hering Breuer deflation reflex. If the lungs are greatly deflated, impulses are set up in another type of receptor which travel up via vagus to stimulate inspiration. This is Hering-Breuer deflation re-flex. In ordinary tidal air volume breathing (eupnea) this is not called into action but in such conditions like collapse of the lung (atelectesis) this reflex is activated and inspiratory drives are increased. The teleology is obvious. In a case of collapse of the lung, increase in inspiratory drive will cause more air entry into the healthy parts of the lung, and will thus compens ate for the functional loss of lung tissue. II. Propnoceptors in the chest wall ( "load detecting mechanism") if the compliance of the lung is decreased (eg. in lung fibrosis), the expansion of the chest wall becomes difficult Or. if the airway resistance increases (e.g. emphysema) air flow becomes difficult. In such conditions, there is an intrinsic mechanism [which involves the mechanoreceptors like muscle spindles, joint receptors and tendon receptors of Golgi (for details of them see chap 2, sec XC)] by which the thoracic cage detects that the thoracic cage expansion, ie , tidal air volume is not adequate (ie, the needs of the body are not fully satisfied) and the muscles of inspirations work harder (= contract more vigorosly) this state (= muscle contraction) continued until the filling of the lungs is adequate. It appears that afferent nerve fibers from the mechano receptors of these muscles of inspiration reach the cerebral cortex. (The organs Iike muscle spindles detect the fact that contraction of the muscles of inspiration is not adequate (i.e. the spindles detect the load), send the information to the anterior horn cell of the spinal cord (fig 10C. 2. 1). Collaterals arising from these nerve fibers go to the cerebral cortex). It is possible, one of the mechanisms by which we become conscious to the need of more sustained effort to inspire (dyspnea) is the firing of these collaterals to the cerebral cortex. In short, activation of these corticopetal (= cerebral cortex seeking) fibers is one of the mechanisms of dyspnea. III. J. receptors. J. reflex. In 1955 A.S. Paintal established the existence of another kind of receptors, the j receptors, which when stimulated produce widespread changes in the respiratory. cardiovascular and skeleto muscular system. These receptors are situated in close relation to the pulmonary capillaries