INFECTIOUS DISEASES AND INFECTIONS 1 DIPHTHERIA

INFECTIOUS DISEASES AND INFECTIONS 1 DIPHTHERIA Epidemiology - Age - Maximum incidence between 2-5 years Mode of spread - Droplet infection due to contact with person with active disease or more often with a carrier of virulent organisms Chronic sinusitis and diseased tonsils important predisposing factors Sub types of C diphtheriae - Three strains gravis, intermediate, and mitis usually related to the clinical severity of the disease, the other factors being host-resistance, site of infection and length of time elapsing before starting treatment Incubation period - 2 to G days Clinical types - 1 RESPIRATORY GROUP - includes majority Nasal diphtheria - Unilateral or bilateral nasal discharge, at first serous and often blood stained, later thick, mucopurulent and foul smelling Thick membrane may be visible on the mucosa of the anterior part of nasal septum Redness, excoriation, small follicular spots or pustules commonly present on upper lip round the nose Constitutional symptoms slight or absent Faucial diphtheria - Mild - Reddening of one or both tonsils with small membrane formation on one tonsil or in a tonsillar fossa Moderate - Membrane on both tonsils confined to tonsillar fossa Localised tonsillar lymphnode enlargement Severe - Spread of membrane to one of the faucial pillars and thence to palate on one side. The membrane has a characteristic oedematous margin and is spreading Tonsillar nodes enlarged with some oedema of surrounding tissues Very severe - Rapidly spreading filmy membrane on soft palate and roof of mouth with gross oedema of faucial and palatal tissue The membrane may be hemorrhagic. Gross swelling of neck (bull neck). Temperature in moderate to moderately severe cases seldom more than 38°C. Laryngeal diphtheria - More common in infants. Membrane involves larynx and also spreads to trachea and bronchi Initial symptoms are hoarseness, brassy cough and noisy breathing. Progressive laryngeal obstruction produces inspiratory stridor. Lower intercostal spaces are sucked in as not enough air flows in to fill the lungs If not relieved child dies of hypoxia 2 NON-RESPIRATORY GROUP - include vulva, vagina, umbilical cord, conjunctiva, auditory meatus, tongue and oesophagus Glans or coronal sulcus of penis after circumcision in infants Cutaneous diphtheria may present as a chronic ulcer or a persistent shallow ulcer with punched out areas. Diagnosis - Throat or laryngeal swab for smear (unreliable), or culture on glycerol-tellurite culture plate and Loeffler slope Complications - Aspiration of membrane can cause respiratory obstruction .1. Cardiovascular COMPLICATION Timing CLINICAL FEATURES Myocarditis Circulatory failure Acute onset Tough, ashy-grey uniform deposit Soft, yellowish white deposits in spots or patches with intervening areas of redness. Membrane very adherent, bleeding points Membrane easily removed leaving smooth when torn off surface. Pillars of fauces and uvula may be involved Deposit limited to tonsils Fever usually slight Fever high Cervical glandular enlargement rare. Cervical glands commonly enlarged 2 Moniliasis - Most common in infants, patches of soft deposit of fungus on buccal mucosa and tonsils. Exudate white and characteristically arranged as small linear membranes. Moniiia albicans will be seen on smear 3 Vincent's angina - Gingivitis with ulceration, no toxemia, marked foetor of breath, presence of fusiform bacillus and spirillum 4 Infectious mononucleosis - occurs usually in older children Exudate as a rule remains white Glands in neck enlarge but remain discrete Patient usually less ill .5 Agranulocytosis -

CENTRAL CONNECTIONS OF THE RETINA The axons of the ganglion cells

receptive fields are circular in shape. Kuffer and later Hubel and Weisel (who were awarded Nobel Prize) showed that, viewed from the functional point, the retinal receptive fields of the photoreceptors, or of the ganglion cells, can be divided info two classes: (i) on center, and (ii) off center In an 'on center' receptive field, when the center is stimulated by a beam of light, but the peripheral part of the field remains non illuminated, the ganglion cell (hence the optic nerve) is stimulated Conversely, in an 'off center' field, when the center is struck by light (the periphery remaining non illuminated) there will be strong inhibition of the ganglion cell (and hence the optic nerve fiber) Because of the presence of on center and off center receptive fields some well known phenomenon can be explained It is known that when a light which is uniformly bright (so that it produces an uniform illumination of retina), falls on the eye, the vision becomes poor The explanation is, that concomitant stimulation of on center and off center receptive fields (due to the uniformity of brightness) results in mutual cancellation of their effects The presence of on center and off center retinal fields help us to make sharp delineation of the objects CENTRAL CONNECTIONS OF THE RETINA The axons of the ganglion cells are collected as the optic nerve, and they make exit from the eye through the optic disc and continue to proceed to their destination as optic nerve (fig 10B2. 3.1) (a) Fibers of the each optic nerve partially decussate at optic chiasm, the fibers from the nasal half of each retina cross to the opposite side but those of the temporal halves do not cross [fig 10B2. 3. 1 (a)] After decussation, what is formed is called optic tract Each optic tract contains fibers from nasal half of the opposite side and fibers from the temporal half of the same side It is to be remembered, that the image that is formed on the nasal half of the retina is from the object at the temporal half of the visual field of the same eye whereas the objects on the nasal half of the field of the vision are focussed on the temporal half of retina of the same eye The right optic tract, for example, therefore, brings information from the left temporal region and right nasal region of visual field that is, left halves of the visual fields of each eye 10B2. 3. 1b). The optic chiasma is in close relation to the pituitary gland. Tumor of the pituitary gland therefore causes compression of the central part of the optic chiasma The optic tract fibers end in the following regions: (i) Lateral geniculate body, LGB, (fig. 10A. 1. 1. C. ) (also called lateral geniculate nucleus, LGN,), this is the most important relay station This is a part of the thalamus (n) Pretectal area, which is just in front of tectum of the mid brain (N B Tectum is the dorsal portion of the midbran) (iii) Superior coliiculi, a pair of elevations, one on either side on the dorsal side of the midbrain (fig. IOA. 1. 1 C). Fig 10B23. 1 (a) Central connections of the optic nerve Note the individual sites, where a lesion produces -(i) blindness of one eye (ii) binasal hemianopia (in) bitemporal hemianopia (iv) homonymous hemianopia (v) scotoma Fig 10B.2.3.1(b) Besides these three mam stations, the fibers from the optic tract also end in the (iv) suprachiasmatic nucleus of the hypothalamus, (v) pulvinar of the thalamus (fig 10A 1 1 C) and (vi) other areas of the thalamus as well as in the brain stem Lateral geniculate body (LGB/LGN) The most important group of fibers from the optic nerve ends in the LGB. LGB is a part of the thalamus LGB itself has six layers Fibers arising from the nasal half of the contralateral retina end in layers, 1,4 and 6 whereas those arising from the ipsilateral temporal half of the retina end in layers, 2, 3 and 5 The cells of LGN also have receptive fields, which are of different sizes and which are also (like those of the photoreceptors), rather circular This is due to obvious reasons Informations of ganglion cells of the retina are thus faithfully transmitted to the LGB cells From the LGB, further order neurons arise and proceed as geniculocalcarme tract also called ('optic radiation'), to terminate on the visual cortex Visual cortex On the occipital lobe, near its posterior pole, lies the visual cortex, popularly called (Brodmann's) area 17 (fig 10A. 1. 1B and fig. 10D. 6. 2) The area is concerned with the integrated vision The neighbouring areas, area 18 and area 19 are visual association areas Visual cortex receives fibers from the LGB The area representing the macula densa lies in the pole of the occipital lobe For a small area of the retina like the fovea centrals, the representative area is rather disproportionately big (the student may recall the sensory homonculus, fig 10B1 3 2) Hubel and Wiesel showed that there are some peculiarities associated with the functions of area 17 Thus, the area 17 cells are readily stimulated when the light (or the object) is (i) in the form of straight lines, (n) the lines are moving, and (in) the lines have a particular orientation Therefore, when one looks at a featureless flat non motile object (e g a featureless big white wall) the cells of the area 17 are not very stimulated, but if on the same wall there are lines, the area 17 cells will be stimulated However, the cells of area 17 which correspond to the demarcations between the individual lines and the wall are particularly stimulated It follows that (i) contrast phenomenon, (n) demarca­tion and (iii) delineation are some of the main features of area 17 Some further issues may also be noted 1 Sup ri singly, even if the area 17 be destroyed still then the person can at least recognize objects to some extent (Recall, pain continues to be perceived even after destruction of sensory cortex) This recognition, however, is so incomplete that it cannot be termed, 'seeing' This 'residual vision' may be due to the activities of superior colliculus or some other area 2 Both the

procrastination, stubborness, dawlling, deliberate inefficiency or a pretence of forgetfulness.. Treatment: of personality disorders

for example, procrastination, stubborness, dawlling, deliberate inefficiency or a pretence of forgetfulness.. Treatment: of personality disorders: 1. Drugs - have little part to play. Anxiolytic or neuroleptic drugs may have to be given for short periods, especially during times of undue stress. 2. Supportive psychotherapy - is often beneficial in some personality disorders. 3. Psychoanalysis. 6. PSYCHOSEXUAL DISORDERS This group of disorders is characterised primarily by disturbances of sexual function. Classification: 1. Gender identity disorders: TRANSSEXUALISM - Here the individual desires to be of the sex opposite to that indicated by his normal external genitalia. In addition, the person feels estranged from his body, has an overpowering desire to live as a member of the opposite sex and seeks to alter the body appearance and genitalia to confirm to those of the opposite sex. This gratification, or (b) abnormality in the manner of sexual gratification. ETIOLOGY - (1) Psychogenic factors are probably the only causes in all perversions. (2) Primitive people and persons with low intelligence show perversions more often. (3) Psychoanalytical schools regard perversions as the result of regression or arrested emotional development at earlier stages of psychosexual development. (4) More common in men than women. TYPES - Some examples of sexual deviations: Homosexuality (lesbianism in women) - Sexual gratification through persons of own sex. Varying degrees exist. According to some, heredity plays an important role: others believe in psychogenic basis - disturbed emotional relationship between child and parents like overattachment to mother, and poor identification with the father. Homosexuality is designated as asexual deviation only if a person is disturbed by, and wants to change his homosexual orientation. Bestiality - Sexual gratification with animals. Exhibitionism - Sexual gratification through showing of genitals by men to the members of opposite sex. Fetishism - Sexual stimulation obtained by men from inanimate objects, e. g. underclothes, shoes of women. When the object is a - statue, it is called pygmalionism Gratification is obtained by masturbation, while looking at these articles. Voyeurism - Sexual gratification by watching other people nude or having sexual intercourse. Sadism and masochism - Sexual gratification through inflicting or suffering pain either during sexual intercourse with the member of the opposite sex or totally replacing the urge for heterosexual relations. Transvestism - Sexual gratification through putting on clothes of other sex. Paedophilia - Repeated sexual activity with pre-pubertal children, as a preferred or exclusive method of obtaining sexual excitement. TREATMENT: On the whole unsatisfactory. Psychotherapy helps in better social adjustments rather than in changing the sexual orientation. Behaviour therapy has been used with some success. Hormonal treatment, to reduce the sexual drive, is of limited value. 7. SUBSTANCE USE DISORDERS (Drug dependence) Definition: Substance use disorders are characterised by the consumption of certain drugs or substances at those dose levels and under those circumstances and settings that significantly augment the potential for harm, whether or not such use is legal, and whether it is intended to be therapeutic, pleasurable or physician-prescribed. The term 'drug-dependence1 is sometimes used synonymously. This term refers to a state arising from repeated administration of a drug on periodic or continuous basis. Two kinds of dependence are described - (a) Psychological dependence - which is defined as the development of a craving for a drug because its effects are perceived as pleasurable. (b) Physical dependence - which implies occurrence of a physiological or biochemical change produced by drugs due to which the body requires the continuous presence of the drug if a withdrawal syndrome is to be avoided after discontinuation of the drug. Central to the concept of drug dependence or abuse, is the phenomenon of tolerance i. e. on repeated administration of the same dose of a drug, there is a declining effect of the drug. Drugs on substances liable for abuse: and which can produce dependence are - 1. Ethyl alcohol. 2. Opiates such as morphine, pethidine. heroin. 3. Sedative-hypnotic drugs - Barbiturate, methaqualone and benzediazepines. 4. CNS stimulants -amphetamine. 5. Cannabis preparations - Charas, ganja. 6. Hallucinogenic substances - LSD. 7. Other substances like tobacco, caffeine, phencyclidine and organic solvents. Etiology: Several factors have been suggested - 1. Genetic factors - especially in alcoholism, but the exact mode of inheritance is not known. 2. Biochemical factors - Deficiency of endogenous opiates (endorphins) has been incriminated as a possible etiological mechanism in opiate dependency Similarly, abnormalities in alcohol dehydrogenase have been postulated for the etiology of alcoholism. 3. Learning factors - e. g. relief of withdrawal symptoms by ingestion of a drug may act as a re-inforcer for further dependence on the drug. 4. Personality factors - Many alcohol and drug users appear to have some degree of an underlying personality disorder. A number of them possess self-indulgent tendencies or a sense of inferiority which makes them incapable to face stresses of daily life. 5. Psychiatric disorder - Many alcoholics or drug

appendicitis due to inflammatory changes in the right rectus abdominalis muscle, or to inflammator

prominences. Sign of virulent process. Occur relatively late (G weeks-G months) in the course of the disease and remain for several weeks. (ii) Rheumatic tendinitis, tenosynovitis, myositis and bursitis may seldom occur. Nodules indicate chronicity and associated with significant heart disease. G. Respiratory - (i) Epistaxis may be an atypical manifestation. ii) Rheumatic pneumonia - uncommon and almost always occurs in patients with severe carditis: Chest X-ray may show changing areas of pulmonary infiltration which do not respond to antibiotics but respond dramatically to steroid therapy. 7. Gastro-intestinal- (i). ild gastro­enteritis may be one of the prodromal features. Occasionally signs of acute appendicitis due to inflammatory changes in the right rectus abdominalis muscle, or to inflammatory changes in the mesentery, or to enlargement of abdominal lymph glands. (ii) Repeated vomiting spells. 8. Nutrition - Loss of weight or failure to gain weight. 9. Central nervous system - Rheumatic chorea late manifestation. Psychic disturbances like insomnia and delirium. Occasionally acute rheumatic fever is ushered in by headache, nuchal rigidity and meningism, or with high fever and delirium, convulsion or coma. 10. Polyarteritis - rare, may affect vessels in brain, lung, heart and mesentery. Laboratory findings: 1. EVIDENCE OF PRECEDING STREPTOCOCCAL INFECTION - Antistreptolysin-O (ASO) determination useful in 80 per cent of cases. Titre <250>

- Prednisolone 40-80 mg/day tapering slowly over several months. Iritis - Atropin

reactions - Prednisolone 40-80 mg/day tapering slowly over several months. Iritis - Atropine 1 % drop plus Hydrocortisone 1 % drops 4-hourly, plus prednisolone 10-20 mg ay p. o. (ii) Type 2 reactions - Thalidomide 100-400 mg daily (contraindicate in premenopausal women), or Clofazimine 300 mg/day tapering slowly, or Prednisolone 20-40 mg/day tapering over several weeks. C. Surgical treatment - (a) Excision of small lesions Large nodules touched with strong carbolic or nitric acid. Removal of necrosed bones and splitting of nerve sheath if a nerve is constricted by dense fibrous tissue. (b) For persistent localized severe nerve trunk pain, infiltration of the thickened nerve sheath or the nerve itself with 10 ml. 1 % procaine, or with the latter solution to which 25 mg of hydrocortisone and 1,500 units hyaluronidase have en added.. The injection may be repeated..(c) Reconstructive surgery is required for paralysed fingers, foot-drop, and hammer toe, and plastic surgery can correct facial disfigurement caused by loss of eyebrows, facial palsy, saddle-nose deformity, ectropion, pendulous ear lobes. PREVENTION - Child contacts may be given BCG vaccination, especially infants born in leprous families Children who have been in close contact with lepromatous leprosy can be given prophylactic dapsone for a minimum of three years. Now that quantities of M. leprae are available from experimentally infected armadillos, a specific vaccine becomes a possibility. 9. RICKETTSIAL DISEASES Etiology and Epidemiology - Organisms - Small bacteria varying in size from coccoidal to bacillary. They are morphologically indistinguishable from each other, contain both RNA and DNA and are Gram-negative. Transmission - is by arthropods (tics, mites, lice and fleas). Direct man-to-man spread of infection does not occur naturally. Humans become infected when they move into an environment inhabited by infected vectors, or when ecological conditions permit large number of vectors to move into man's environment. The clinical syndrome results from disseminated focal perivasculitis and is similar in all ricketssial diseases, though it varies in severity. MAJOR RICKETTSIAL DISEASES OF MAN - 1. Typhus fever - 1. LOUSE-BORNE OR EPIDEMIC TYPHUS -Caused by R. Prowazeki and transmitted from man to man by human body louse. Incubation period - 10-14 days. (a) Stage of invasion - Abrupt onset with rigors and fever, severe headache, muscular pains and conjunctival injection. Active delirium, insomnia common, severe attack may commence with vomiting, rigor or convulsion. Temperature is high at onset, rises steadily to maximum on 5th day. (b) Stage of eruption and nervous excitement - (i) Rash - usually on 5th day. Pink macules varying in size and shape, disappearing on pressure. Generalised but face rarely involved. In a day or two lesions become dull red and finally slate blue or grey before disappearing. Petechiae may occur. Following eruption of macules, paler subcuticular lesions appear between the macules - subcuticular mottling or mulberry rash. (ii) Temperature - high till the 6th day. (iii) Delirium -replaces headache and stupor. Mostly at night. (iv) Spleen may be palpable. (c) Stage of prostration - Patient appears exhausted and stuporose, this may progress to delirium or coma. Hypotension may result from myocarditis and peripheral vasodilatation .Features of grave prognostic significance include - progressive fall of B. P , gangrene of fingers or toes, pressure areas and genitalia, urinary and faecal incontinence, renal failure and secondary infection. (d) Stage of defervescence- In favourable cases about the 12th or 14th day striking improvement occurs. Patient becomes quieter. Fever becomes remittent and drops to normal in a few days. Complications - (a) Bronchopneumonia. (ii) Myocarditis. (iii) Thromboembolic complications. (iv) Peripheral failure. (v) Suppurative parotitis. (vi) Gangrene of areas of skin. 2. BRILL-ZINSSER DISEASE - is a recrudescent form of epidemic typhus. Intense frontal headache and low B. P. are prominent features. Scrub typhus-caused by R. tsutugamushi and transmitted by larval mites. Eschar at site of mite feeding. Lymph nodes draining the eschar swollen and tender with generalised lymphadenopathy, fever, chills, headache, malaise and orbital pain. Maculopapular rash in about 50% may appear between 3rd and 7th day. Lymphocytosis in blood (large lymphocytes). Convalascence prolonged. Diag. - (a) Serology. Detection of antibodies by microimmunofluorescence (MIF). A tit re of 1: 128 in diagnostic. (b) Weil Felix reaction- Louse and flea or tick borne typhus agglutinate with strain OX-19 and OX-2, scrub typhus with OX-K alone. Tr. - Doxycycline 200 mg/day for 10 days. II. Spotted fevers-ROCKY MOUNTAIN SPOTTED FEVER - is the most severe form. Caused by R. ricketsii and carried by ticks. Abrupt onset of fever with chills, severe headache, photophobia, prostration and muscle and joint pains. Temperature 40°-41 °C with irregular morning remissions. Rash on 3rd or 4th day, maculopapular, first on extremities then spreading to the trunk, the rash becoming petechial. In severe cases rash becomes confluent, deep red or purple and may necrose. CNS manifestations include restlessness, confusion and delirium. In severe cases coma and peripheral vascular collapse precede death.

Diffuse endothelial proliferate glomerulonephritis - Light microscopy reveals hypercellular glomerular tufts

deposits and C3 (type I) or electron dense material incorporated into the membrane (type II, dense deposit disease). 4. Diffuse endothelial proliferate glomerulonephritis - Light microscopy reveals hypercellular glomerular tufts with proliferation of endothelial and mesangial cells which have neutrophilic and mononuclear cell infiltrate and perhaps crescent formation. IgG containing complexes seen on immunofluorescence along the GBM and in the mesangium. The lesion often occurs in association with acute infections, producing an acute nephritic illness (e.g. post-streptococcal GN) but healing completely .5. Anti-GBM disease - Linear deposition of IgG along GBM with variable inflammatory response Most destructive, hence neutrophilic cell infiltration, heavy fibrin deposition and extensive epithelial crescent formation Circulating anti-GM antibody attaches to the basement membrane and initiates damage. Goodpasture's syndrome - Anti-GBM disease associated with pulmonary hemorrhage. It is strongly associated with cigarette smoking G Crescentic glomerulonephritis - results from proliferation of epithelial cells. It may occur particularly in SLE, anti-GBM disease and the vasculitides (Wegner's granulomatosis and microscopic polyarteritis), but often occurs in absence of underlying disease. This pathological term is used synonymously with classical term 'rapidly progressive glomerulonephritis' Investigations in glomerular disease: Baseline measurements: 1. Glomerular filtration 2. 24-hr protein excretion 3. Plasma albumin and creatinine Diagnostically important tests: 1. Urine - RBC casts indicate glomerular disease 2. Anti-DMA antibodies - positive in SL E 3. Antinuclear factor - positive in SLE 4. Blood glucose - excludes diabetes 5. CXR -detects pulmonary oedema, malignancy, pulmonary hemorrhage, cavitation in Wegner's granulomatosis G Hepatitis B antigen -excludes hepatitis B 7 Rheumatoid factor - positive in RA 8. Serum and urine electrophoresis - excludes paraprotein 9 Anti-neutrophil cytoplasmic antibodies - positive in most cases of microscopic polyarteritis and Wegner's granulomatosis 10. Anti-glomerular basement membrane antibodies - Diagnostic of antiglomerular basement membrane disease 11. Serological tests for syphilis - excludes syphilis Clinical manifestations ACUTE NEPHRITIC SYNDROME Definition - A disease most common in children, characterised pathologically by diffuse inflammatory changes in the glomeruli and clinically by usually abrupt onset of macroscopic hematuria, proteinuria (usually moderate), oedema, hypertension and impaired renal function with or without oliguria Not all features may be present at the same time. Causes - 1. Infective agents - (a) Viral- Hepatitis, HIV, mumps, echovirus, varicella, cytomegalovirus, (b) Bacterial - Hemolyic streptococcus, pneumococcus, klebsiella, staphylococcus spp , salmonella, brucella, gonococcus, yersinia, syphilis, tuberculosis, leprosy. (c) Parasitic - Malaria, filaria, schistosomiasis, mycoplasma 2 Multisystem diseases - SLE, polyarteritis, Henoch-Schonlein purpura, Goodpasteur's syndrome, hemolyticuremic syndrome 3 Primary glomerular disease - Membranoproliferative glomerulonephritis, Berger's disease, mesangial proliferative glomerulonephritis. 4. Miscellaneous - Acute inflammatory demyelinating polyneuropathy, serum sickness, irradiation of Wilrrfs tumour Clinical features - Modes of onset - (a) Oedema - puffiness of face. (b) Urinary symptoms - Scanty and smoky orfranky bloody urine. (c) Symptoms of acute infection - Fever, bodyache, vomiting. (d) Cerebral symptoms - Headache, convulsions (e) Insidious onset - Weakness, pallor, loss of appetite. (f) Accidental discovery - on routine urine examination SYMPTOMS AND SIGNS -. 1. Oedema - may come on suddenly or gradually. Puffiness of face and whitish pallor constitute "nephritic fades", swelling of face usually in morning Generalised anasarca may occur. Oedema may be absent in mild cases and also in very severe cases. 2. Hypertension - occurs in majority of cases, the diastolic pressure being 90 to 120 mm usually, and as a rule persists for at least one week, returning to normal a few days after patient has had diuresis In 5 to 10 per cent cases hypertensive encephalopathy develops, the clinical features being severe headache, vomiting, fits, hemiparesis and other focal signs such as aphasia Associated mental changes such as confusion, disorientation and coma. The rise of pressure may give rise to pulmonary oedema. JVP is commonly elevated and with peripheral oedema presents a picture of CCF Renal retention of salt and water is responsible for the circulatory disturbance in acute nephritis. 3. Impaired renal function - Oliguria. Acute renal failure develops in some. Laboratory findings - 1. Urine -Volume reduced, dark in colour or smoky when fresh, tea-coloured after haemolysis. Proteinuria variable, rarely more than 2. 5 gm per day. Red cells and red cell casts. Also white cells, white cells casts and granular casts. 2. Evidence of streptococcal infection - in post-streptococcal GN. Demonstration of presence of A beta-haemolytic streptococcus of nephritogenic M-protein type in throat or skin lesion, and of an immune response to one or more of streptococcal exoenzymes. 3. Haematology - Polymorphonuclear leucocytosis, raised ESR 4. Biochemical - Blood urea and

Antihypertensive drugs should be given only to those with renin-angiotensin

Antihypertensive drugs should be given only to those with renin-angiotensin hypertension, after reducing fluid overload. 5. Anemia
- is a complication of uremia which is partly corrected by dialysis. Recombinant human erythropoietin can be given but is ineffective in presence of iron deficiency, severe deficiency of other erythropoietic factors, chronic or acute infections, aluminium intoxication, bone marrow suppression or uncontrolled hyperparathyroidism. G. Osteodystrophy and derangement of calcium and phosphate metabolism - Main cause of osteodystrophy is failure of hydroxylation of vitamin D in the kidneys. Low vitamin D activity associated with hypocalcemia and increased phosphate concentration. High doses of 1,25-dihydroxycalciferol 1-3g as bolus two to three times a week are more effective than daily small doses to prevent and reverse advanced hyperparathyroidism 7 Dialysis amyloidosis - is a common complication of long-term dialysis but may also occur with conservative treatment Clinical features are carpal tunnel syndrome and osteo-arthropathy. 8. Type II hypehipedemia - is a feature of chronic renal failure and often persists in dialysis patients. If diet is not effective, HMG CoA reductase inhibitors may be given . 9. Cardiovascular complications - Myocardial infarction, cardiac failure and CVAcan occur. 'Uremic'cardiomyopathy is characterised by concentric or more often, septal asymmteric LV hypertrophy, hyperparathyroidism may contribute to its development. 10. Infections - are generally the result of impaired immune response caused by uremia and malnutrition, associated with the risk of microbial contamination of the vascular access and extracorporeal circuit. Hepatitis B and C infection are not uncommon. 11. Malnutrition -due to Gl tract changes, loss of amino acids and peptides in the dialysate, sodium restriction, poor payability of the diet land hypercatabolism induced by the dialysis. Peritoneal dialysis Here the patiens peritoneum is used as the semipermeable membrane between capillary blood and dialysis fluid which is introduced into the peritoneal cavity through a permanent catheter Methods of peritoneal dialysis : 1. CONTINUOUS AMBULATORY PERITONEAL DIALYSIS (CAPD) is the most common technique Three or four exchanges of about 2 litres dialysis fluid are required every day. Complications - (a) Mechanical effects of increased abdominal pressure and leakage of dialysis fluid - abdominal hernia, hemorrhoids, back pain, oedema of external genitalia, hydrothorax. (b) Infections - peritonitis, infection of skin at exit site. (c) Metabolic complications - Obesity, hypertriglyceridemia and diabetes following glucose loading from dialysis fluid, protein and amino acid losses. Advantages - Can be performed at home without any specific equipment, lower cost than hemodialysis, continuous fluid removal with better hemodynamic stability. Disadvantages - Complications as stated above, high failure rate, psychological problems related to indwelling catheter, fatigue from continuous treatment. 2. INTERMITTENT (PERIODIC) DIALYSIS - 8-12 hrs of dialysis with 12-16 hrs of interdialytic phase. 3. CONTINUOUS CYCLIC PERITONEAL DIALYSIS - A single day of exchange, plus 4-6 exchanges during the night using automatic equipment. Renal transplantation - is the treatment of choice for ESRD, as it enables the patient to resume a normal life, with no restrictions in diet and fluid intake. Types of renal transplantation - (a) LIVING DONOR TRANSPLANTATION - Renal transplantation between identical twins is the only situation where immunosuppression is not required , following grafting. First degree blood relatives may be suitable donors but most transplant units require the donor to be both ABO compatible and to have close matching particularly of HLA class II loci. (b) CADAVERIC TRANSPLANTATION Contraindications - (a) Old age. (b) Associated conditions that might deteriorate with immunosuppression e g bronchiectasis or severe cardiovascular disease. (c) Presence of high titres of cytotoxic antibodies to transplant antigens Immunosuppression -Cyclosporin is the drug of choice. Immunosuppression with cyclosporine can be achieved without long-term steroid treatment Many immunosuppressive drugs produce side-effects. Complications of transplantation - (1) Rejection - Identification of rejection -(a) Serum creatinine is the most common marker. (b) Renal biopsy - may also be used to detect rejection and to assist in determining presence of cyclosporin toxicity. Cl.Fs. - (i) Acute cellular or vascular rejection occurring in first 3 months may be reversible by short-term high-dose corticosteroids. Additional regimens such as ant i lymphocyte immunoglobulin and plasmapheresis may be necessary. (ii) Chronic vascular rejection is usually unresponsive to treatment and may lead to progressive graft deterioration (2) Complications of immunosuppression - Side-effects associated with immunosuppressive drugs - (i) General - Susceptibility to infection, increased risk of neoplasia (ii) Corticosteroids - Hyperglycemia, Gl bleeding, cataracts, avascular necrosis of bone, Cushings habitus. (Complications now reduced with low dose regimens). (iii) Azathioprine
- Generalised or selective marrow hypoplasia, jaundice (iv) Cyclosporin - Nephrotoxicity, hirsutism, gingival hyperplasia, tremor..