(“er man, go to the bedside ‘of the patient, a] wok tata compas as regards his illness is the from the patient ‘i BEAR NOE onjeearee pa i gives clue to the correct diagnosis of the disease. Sympathetic attitude and keen obs ‘ essential to properly elici i es perly elicit the history and get tw the real malady of the patient. It is preferable to note down the history of the illness in the same way as expressed by the patient as far as practicable. Repetition of same complaint or irrelevant facts should be ignored intelligently. Leading questions are to be avoided during enquiry except where the patient is confused or is unable to express himself intelligently because of, say, mental dullness. It is impera- tive to exercise the restraint everytime a history is taken as leading questions suggest to the patient the symptoms the examiner expects to find or brings about an uncon- scious distortion of the patient’s history. Making bedside notes is very essential. The following points in a routine way : A. Name—This is as of the particular individual B. Age is a very impo as some diseases are prev: For example— arteriosclerosis, menopausal syndrome, malignancy et s acute rheumatic fever, older age group wherea! heart diseases, acute nephritic syndromes, Ihe history should be noted in ked as a rule for indentification for future references. rtant clinical data in history taking alent in particular age groups. ischaemic heart disease, c. are maladies of congenital congenitalpiaanosts like measles, haemolytic anaemias, infectious disease gnood: Chronic diphtheria are found in infancy and <7, ulcers are the leukaemias, gall bladder diseases; ep , diseases common in middle life. itatio™ cirthosis of C. Sex Diseases like mitral F847 oyymon in males liver, chronic duodenal ulcer are ™ S stitis, BYPO and whereas atrial septal defect, chronic cholera, are most hyperthyroidism: anaemia of nuustional Sang Duchenne commonly seen in females. HaemopP Live! in males. muscular dystrophy are found almost one cits ‘occupation D. Occupation—Enquiry about the pati “many diseases. may give some hints to the diag! Examples : . cinting Press (i) A person long employed 5 P efering from having blue line in the 80"! ne ne extremities abdominal colic, paraesthesias pane the periph- and revealing punctate basophilia 1" fferin eat blood smear bas certainly BOPH fetta from chronic lead poisoning: ; (ii) In an individual working in a coal mine and suffering from breathlessness, cough with expec- toration for a long time and clinically showing features of pulmonary emphysema,—the most possible diagnosis is coal miner’s pneuméconiosis. ‘A sewer or paddy-field worker who suddenly develops high temperature with rigor, muscle pi, ane an voiing wth jade, ev with leucocytosis. Positive an agi, episodes ‘tin test (with blood in the first week inocula- urine in the second and third weeks ree ing leptospira in smears from [iy ) and reveal- plood culture—is a patient of a kidney and eil’s disease, i Chances of coronai . e in businessmen, pee diseases are S Of sed more those with type A pers, lentary habj ing i it ‘abi (wy Men working in plastic aan it, and s Tubber ; er Industries are : ESSENTIALS OF CLINICAL nosis ii)GENERAL EXAMINATION 3 Prone to develop bronchial asthma and cancers of genitourinary tract, parti ularly those who handle chemicals like benzidine. Workers in mines (gold, copper, coal) pottery and sand blasting may develop silicosis, ‘a type Of pneumoconiosis. Pulmonary tuberculosis is Very often a complication of silicosis, (vii) Workers in printing industry who handle gum acacia often develop bronchial asthma. (vill) Asbestosis is a type of Pneumoconiosis that is Common in persons working in textile industries and in persons engaged in construction work, | Pleural plaques, bronchogenic carcinoma and : pleural mesothelioma are often associated with asbestosis. Persons suffering from these Occupational chronic de- bilitating illnesses may legally claim for compensation and Physicians are likely to be called in to diagnose the condition and assess the severity. E. Marital Status—The marital Status of the patient must be noted,—diseases like haemophilia A, nephrogenic diabetes insipidus, Duchenne muscular dystrophy, glucose ©—phosphate dehydrogenase deficiency are X-linked re- Cessive and hence are usually carried asymptomatically by females while male offsprings are unfortunate victims. Marriage in extremes of age results in babies with con. genital cardiac defects, abortion etc andsthis is exemplified by the common occurrence of Down’s syndrome (Trisomy 21) in children of elderly mothers and increasing frequency of Marfan’s syndrome with increasing paternal age. Psychiatric disturbances are sometimes precipitated by marital disharmony. ; Marriage between close relatives or consanguineous marriages result in more frequent expression of genetic defects in the offsprings. F. Address—Diseases like malaria, kala-azar, blackwater fever and filaria are common in West Bengal and parts of Orissa, whereas pernicious anaemia and subacute combined ~ la (vi) pesWa F ESSENTIALS OF CLINICAL Diacnog , degeneration are rerely encountered in the t commonly seen in temperate countries PS but gy ; " _ Intestinal and extraintestinal (e.g. hepatic) q giardiasis, ascariasiss, hookworm infection are yr" iy mon in West Bengal, and other regions of fac‘ Sm, jicularly along the Gangetic plains. G. Chief complaints—It is essential to note do or four most important symptoms of the patient ie three nological order along with their durations, —"” “M- H. History of Present illness—The patient shoug allowed to narrate the history of the present comply, from the beginning of its development in to without any leading questions being put in as fay practicable. & Unnecessary elaboration and repetition of symptom, should be tactfully avoided. Intelligent and educated tients sometimes narrate their complaints in medical a [e.g. acidity, rheumatism etc.] In such cases, they shoulg be asked to describe what discomfort they actually fee, Details of previous treatments stiould be enquired abou particularly the name and duration of drugs taken and ary Adverse reactions out of them (eg. hypersensitivity to penicillin), previous surgical procedures, irradiation’ or psychotherapy. These information may have influenced te presenting symptoms, or disease. For example, a female patient presenting with symptoms suggestive of diabetes mellitus may have history of long continued intake of corticusteroids for her rheumatoid arthritis. The patient should also be asked to produce the previous records, if possible. In case of children and very old o mentally sick partients, close relatives should be asked about the previous treatment. L. Past illness—The history of relevant diseases from which the patient has suffered in the past should be elaborated ; eg. (@ Rheumatic fever ; (ii) Malaria and Kala azar ; (i) Infectious diseases eg diphtheria, scarlet fever, small PO’ (iv) Infective hepatitis ; (v) Syphilis and gonorrhoea ¢ sem Ing,Re Wie Moedy, Very — “KEN Ing a down AL in. chro. t should be complaints sequences, as far as symptoms ducated pa- sdical terms they should ctually feel. quired about ken and any snsitivity (© radiquon or fluence! the ‘a female of diabetes od intake ° jous old of asked the prey : yery yd bE GENERAL EXAMINATION 5 LBNAMINATION There : igh be some o “— woMe correlation of the abow present clinical eae hepatosplenomegal cal signa—og bet galy, features of cee: couthaae, houmatie valvaar bout clears cadionyopaty, | easel tents cart disease, cardiomyopathy abes wt artic incompetence gonccoceal J. Family bi istory and on Y Ristors. and Personal history) Ena eng pom ter ai of death if they are Soot typertonsian, coronary ‘et SS ateae family and they are usually Aironet? (ii) As regards brothers and si see ast sine wecausetBy ere © : sisters, it is of value yypertersion, congenital heart di i mellitus, ischaemic heart disea: eee tomicie See oqeen sang ts 8 esc ‘of the same family. In suc a iy ace aoa Be yy. In such cases a family tee should be constructed. (iii) Food habit is very impor iron deficiency anaemia, avitaminosis ete a in the tropics. (iv) Chronic alcoholism may lead to diseases like cirrhosis of liver, coronary material disease, peripheral neuritis whereas ‘excessive smoking ™ Jead to chronic bronchitis with emphysema, Buerger's disease, bronchogenic carcinoma etc. tant because malnutrition, re very common habits of physical exercise may prevent y arterial disease _psychological 4 ete. (vy) Regular jisturbances the historyre 6 ESSENTIALS OF CLINICAL Diag Ne mig nations or false sensation oF percept ion: enquired about if severe mental disongg "4b nia is suspected. ders tke °° tet L. Menstrual History—tn {1 Ma females, * Mena, % nset of menstruation, duration « it tity of blood loss in each mena tatURtion ang te malities there of should be noted. Yele or ann Number of birth and complications duri hey afd birth (too carly birth, sectio, etc) or PreEnacy History of amenorthoca, if any, should tee be as” Onset of menopause or stoppage of eee as] symptoms attributed to premenopausal a x te enquired about in elderly females. TOME shouig Excessive blood loss due to gynaecological ca fibroid uterus or cancer cervix may be a clue to ioe like for a cause of anaemia. ‘Search, Perimenopausal bleeding, endometrial carcinoma, 4, functional uterine haemorrhage are sometimes ene with excessive bleeding. iateg History of taking oral contraceptives with its duratio be noted. Obesity, hypertension, deep ee jaundice, and sometimes breast carcirioma may ications of these drugs. e living condition should be should thrombosis, occur as comp! M. Social Background—Th noted = Patient is living on stree’ Patient has to climb eg t, ‘in a hut, house, flat. three stages to get at home, There is fresh water available, or not ; electricity, or not. Note, if necessary situation how pt is coming along with other people eg relatives, friends etc. Is there any other social pressure oF enviromental disorder which might cause unwell feeling or even disease (eg home near a big and busy street, Jot of noise, no proper sleep possible etc. There could be much more of interest, which you find out after a second or third talk with the patient. The social and enviromental sorrounding is one of the basic items. This conditions decides at last wether we were able to cure the patient or only “repair” a symptom. sdGENERAL WXAMINATION 7 ce PHYSICAL, EXAMINATION ENERAL s cies, anaemis, sunvay (Decubitus, build, nutrition, fa. lubbing, temperature, v,sAtMalee, pigmentation, sedemre 1. DECUBrTys * Fespiration, blood pressure) Definition, ie different types mn of the patient (i) (a) (b) in bed. The Decubitus of 4s" 60° 90° —S€vere dys, Noea orthopnoea), However even ie Perna Patient may be most Comfortable at 60° or even at 90° elevation. This is because dysponoea is a subjective Phenomenon and Patients vary from or endurance. Causes of propped up decubitus : Cardic—Left ventricular failure i incompetence. aortic valvular di sion, myocardial infarction/c: Patent ductus arterio: —mid dyspnoea —mModerate dyspnoea ue to mitral isease, hyperten- ‘ardiomyopathy, sus, Coarctation of aorta etc. Left atrial failure due to mitral stenosis, myxoma of left atrium, ball valve thrombus in the left atrium, mitral atresia etc, Massive pulmonary embolism pulmonale). Chronic cor pulmonale. Respiratory—Bronchial asthma, pleural effusion, Pneumothorax and hydropneumothorax. bronchogenic, carcinoma, chronic bronchitis with or without emphysema, pulmonary arteriovenous fistula, acute pulmonary oedema due to over transfusion, carbon monoxide poisoning etc. (acute cora x HANENTIAL OF CLINICAL, py, ONO, "4 Ww) camel Tipe Havin, wishin the ApheARAE Unger cavane VIAL CAPHEILY ang enny tite lhe hinge, ley, " lendy (Meg “, tag a? Gl) Newmlagicnl ANY THON eto, pons that cauNeN Paralysis of Fespirg cinteludint GUilAIN- Bare. gynge, Mlory tm laryngeal nerve palay Causing ne), recat mayathenias and myopathien CaUBin, Mido, ey muyele weakness or paralygiy & pia {i Depopnoea Patient feels comeorgy , the affected side and becomes yspn Ying i lies on the opposite side ©. pl ean ith, hydropneumothorax, pneumothorax te tin, (iv) Curled up decubitus is seen j acute ren, acute biliary colle meningitis e¢, "4! cog (v) Opisthotonos—seen in tetanus, Strychning soning spinal meningitis, maple syrup Po disease (leucinosis) or may occur as a hynes manifestation. lea (vi) Listless attitude—is seen in Unconsc; peritonitis, parkinsonism, hysteria, ‘COMMON CAUSES OF UNCONCIOUSNESS : Neurological @ Cerebral haemorrhage @ Cerebral embolism @ Subarachnoid haemorrhage @ Cerebral thrombosis @ Postepileptic coma and status epilepticus @ Encephalitis and encephalomyelitis @ Meningitis. Endocrine @ Diabetic coma (hyperglycaemic diabetic ketoacidosis or hyperosmolar nonketotic) @ Addisonian crisis © Hypothyroidism (Myxoedema coma) @ Pituitary Soma (Pituitary apoplexy) Cardiovascular @ Adams-Sjokes syndrome @ Syneopil attack due to severe aortic stenosis, pulmonary stenosis, sscmtic stenosis Fallot’s tetralogy etc. @ Hypertensive encephalopathy, Respiratory @ Carbon dioxide narcosis, respira failure, e I iousnes,Gastrointestinal @ ciated with hepatic f, GENERAL EXAMINATION ’ Hepatic coma (encephalopathy asso- failure) Ranai © Terminal stage of uraemia. Poisoning ‘© Barbiturate, morphin etc. Traumatic © Head injury. Psychogenic © ‘Hysteria, 2. BUILD Definition—Buila is the skeletal structure in relation to Be and sex of the individual as compared {a normal person. Build is short in those in whom it is below the 3rd centile of « normal population of same age and sex and tall when the height is above the 97th centile for normal population. Types—1) Short—The common causes are— (a) (b) (c (d) (e) @ (8) Normal genetic variation, Chromosomal abnormalities eg. Down’s syndrome, Turer’s syndrome, Noonan’s syndrome. Childhood diseases €g. marasmus, kwashiorkor, tickets, tuberculosis, fibrocystic disease, gluten, enteropathy, hook worm infestation, congenital cyanotic or acyanotic heart diseases, thalassaemia major, chronic renal disease, congenital syphilis glycogen storage diseases etc. Skeletal abnormalities, eg.. Achondroplasia, gargoylism, Ellis van Creveld syndrome, rickets, poliomyelities, Still’s disease. Endocrine disorders, eg, craniopharyngiomas or other pituitary tumours, idiopathic hypopituitar- ism. Frohlic’s syndrome, Laurence-Moon Biedl syndrome, hypothyroidism, sexual precocity, Cushing’s syndrome, congenital adrenal hyperplasia. Intrauterine maldevelopment eg foetal alcohol syndrome, progeria etc. Drug induced eg, glucocorticoids, androgens,ESSENTIALS OF CLINICAL DIAGNos; NOSIS anabolic steroids, oestrogens, antith vitamin D ete. YFoig Tall—This is mostly inherited from and pathological causes are tall 5, Not comme? different causes are— Mon, Constitutional Overnutrition causing tallness before epiphyses sion Chromosomal abnormalities eg, Klinefe, drome (47 XXY). supermale ae al superfemale (XXX). Y) ang Miscellaneous causes include Marfan’s homocystinuria, cerebral gigantism, Tipogy oS and Beckwith Wiedemann syndrome, “Py 3. NUTRITION Definition—It means nourishment of the body which» assessed by ich ig (i) Subcutaneous fat, Gi) Bulk of muscle, (ii) Features of vitamin deficiency, if any. However in a recent study logistic regression analysis has shown that mid-upper arm circumference is as effective as other nutritional idices and combinations of differen ces have not been shown to be better especially ip ©) @ indi predicting death in malnourished children (BMI. 19% 293, 373) Types (1) Subnutrition—Body weight 10% less than that ( of a standard person in relation to age and sex, Ps It is due to quantitative dietary deficiency. t (2) Starvation—Body weight 25% less than that of } a standard person in relation to age and sex. a (3) Malnutrition Deficiencies of vitamins, miners and essential amino acids are characteristic. I ‘ ficiency. BY due to qualitative dietary de utrition. | overnutrition is also a form of maln (4) Cachexia—A cachectic shows anaemia, evide™ of vitamin deficiency and features of §GENERAL EXAMINATION i (5) Emaciation—Loss of subcutaneous fat and dim- inution of muscle bulk. (CAUSES OF PATHOLOGICAL SUBNUTRITION : @_ Pulmonary tuberculosis (due to anorexia as well as defective utilisation of untrients). Gi) Diabetes mellitus (loss of calorie due to glycosuria and malabsorption may be associated due to various gastro intestinal disorders). (iii) Thyrotoxicosis (iv) High fever ic to increased metabolic rate (v) Malignancy (6) Obesity—It means an excess of adipose tissue that imparts a health risk. The degree of excess ad- iposity is difficult to quantify; but the Framingham study has shown that a 20% excess over ideal weight imparts a definite health risk. Causes of obesity : These may be cither (a) primary or idiopathic where the Precise mechanism remains unknown, or (b) secondary, which may be due to (@ hypothyroidism, (ii) Cushing’s syndrome, (iii) hypothalamic disorders, (iv) pinealomas, (v) pseudohypoparathyroidism, (vi) pancreatic insulinomas, (vii) testicular hypogonadism, (viii) Polycystic ovarian disease, (ix) induced by drugs eg insulin, oral hypoglycaemic agents, glucocort coids, oestrogents etc. (x) abnormal distributions of fat eg lipodystrophies, (xi) or may be associated with syndromes or unknown aetiology eg Laurence- Moon-Bied! syndrome, Prader-Willi syndrome, Alstrom syndrome etc. ‘7) Nutritional oedema—This includes (i) Wet beriberi. i) Famine oedema with hypoproteinaemia i) Famine oedema without hypoproteinaemia (isohydraemic famine oedema) ) Epidemic dropsy.(g) Protein Energy Malnutrition (i) Kia, (ii) Nutritional marasmus : Here also infan, ESSENTIALS OF CLINICAL DIAGNOsis is a clinical condition characterised ey orhor a of growth, wasting, of muscles, grey o. |°"4atiog hair, pigmentation, desquamation ang strelen, of skin, oedema and signs of vitamin qi°ttion occurring in infants and children due to qir°i%cy of protein with adequate calorie intake, ca ly, it occurs due to prolonged breag, tm in, under one year of age suffer from rae Usual growth, loss of weight, wasting of musga" subcutaneous fats but the precipitating facto, | severe restriction of all foods, reproteins vitamins etc. One fifth to one third of thet weight is lost and the face is pinched ang poe curiously senile expression with sunken eyes n° thorax is particularly wasted with prominent sig Early weaning and rapid succession of pregnangi, are common causes in our country, (iii) Marasmic Kwashiorkor : In this variety, the children have some clinical features of both ty, above disorders. 4, FACIES Definition—Expression in the face of patient. Types—{i) Anxious—It indicates awareness or apprehen sion of the patient about the disease. It may be found in nervous individuals. (ii) Dull and vacant look of mentally retarded children Mongoloid facies is characterised by slanting eyes, epicanthic fold, small nose wih a smail oral cavity. This is characteristicaly seen in Down’s syndrome (trisomy 21). (iii) Masked facies—Parkinsonian syndrome, Ths facies is characterised by wide palpebral fy sures, infrequent blinking and spontaneo® ocular movements are lacking. This is # seen in bilateral facial paralysis. dg(iv) (vy) (vi) (vii) (viii) GUNERAL EXAMINATION Li MyOpAthien, systemic void of Hepatic Myasthenia Bravis, progressive SEleronin ote The face remains de- 'Y expression. : facies. This ig characterised by MTUnken yes, hollowed temporal fossa, Pinched up nove, parches lips, muddy com. Plexion, Seteric tinge. Tabetic facles—Fenturey kling of the forehead in an attempt to com- Pensate for the drooping of eyelids due to Prcudoptosis caused ‘by Paralysis of Muller's muscle, Thyrotoxic facies — exophthalmos are the oarse facial appeara wrinkling of eye- brows and thick tongue are the characteristic features Of cretinism, Apathy of hypothyroidism * should draw the attention of the clinician, ‘Moon’ facies The bloated 4ppearence of the face and rounding of the features are caused by— Are persistent wrin- Staring look and characteristic features, nce, Cushing’s syndrome and disease, Steroid therapy for a prolonged period, Acute (proliferative) glomerulonephritis, Minimal lesion and membranous glomerulone- Phritis, Myxocdema etc. Superior mediastinal syndrome and pulmonary stenosis, (In glomerulonephritis the lower eyelids become puffy because of less subcutaneous fat and ldw tissue tension.) (ix) Facies of bilateral facial palsy—a face devoid of any expression with loss of nasolabial and other prominent furrows (vide supra), The commonest cause ix Guillain-Barre syn- drome or acute infective polyneuritis (when bulbar nuclei are affected, Other rarer causes are sarcoidor leukaemias and lymphomas,Ww (xi) ESSENTIALS OF CLINICAL DIAGNO sig Melkersson’s syndrome. In infan is an important cause, f Flushed facies—(a) Malar flush—; of the cheek as seen in mitral with severe pulmonary jy S'S skinned individuals. Anotyer Pa delivery Hig) Steno, tic in fa myxoedema, Severe flushing of the cheeks hectic encountered in pulmonary tuberculosig flushing is characteristic of Patients Cushing's syndrome, polycythaemia sema (pink puffers) and carcinoid ye Postprandial facial flushing occurs in In congestive cardiac failure the chee] be red and high coloured and bluish tint be evident. (b) Generalised flush--May be causeg (i) High fever (ii) Severe hypertension Thyrotoxicosis (iv) Chronic alcoholism Carcinoid syndrome (vi) Pheochromog, (vii) Drugs like atropine, nicotinic acid acin) and percutaneus absorption gf monosulfiram, (viii) Systemic mastocytogis (ix) Toxic erythemas (x) Measles, Tubella, scarlet fever (xi) Lupus erythematosus tte, Localised flushing is seen in erythromelalga and also in systemic lupus erythematosus (SLE). Pallor—It is seen in shock where blood through the capillaries diminished, in pal attack, left heart failure, peripheral lar diseases like Raynaud’s phenome arterial spasm on exposure to cold gen pallor is found in severe anaemia. (i) Pallor with anaemia—found in all severe anaemia, infective endocarditis, theumatic fever etc.GENERAL EXAMINATION 6 (2) Pallor without anaeminn The eardiovateulae Causes are Tight mitral stenosis, Severe aortic Stenosis, Acute myocardial infarction, Acute 4 left ventricular failure, Acute peripheral cir culatory failure and other causes are () Nephrotic syndrome, (ii) Causalgia, (iii) Acute alcoholic coma, ene (iv) during paroxysm of vertigo in Meniere's disease, and (v) acute nephritic syndrome especially when there is anaemia, (xii) Risus sardonicus—The eyebrows are raised and the angles of the mouth drawn out due to tonic spasm of the muscles of the face in tetanus. Gait) Photophobia—in meningitis and also seen in meningisms. (xiv) Elfin facies—Found in supravalvular aortic stenosis (William's syndrome) that may be associated with hypercalcemia. 5. ANAEMIA Definition—Qualitative or quantitative reduction of cir- culating RBC and /or of the percentage of haemoglobin concentration in relation to standard age and sex. Normal blood count— RBC— Male —S5 to 6 million/emm Female — 45 to 5.5 million/emm WBC— Male 4,000 — 11,000 cmm Femate.] Haemoglobin— Male-14.6 to 15.5 gm per 100 ml (10.11%) Female-13.3 to 14.6 gm per 100 mi (90.100%) (100% = 14.6 gm per 100 mi} Reticulocyte— 0 to 1% Platelet — 1.5 to 4 lacs/emm. Anaemia is said to be severe when heamoglobin is less than 40% moderate when 40.50%, mild when 50.60%ESSENTIALS OF CLINICAL DtAcne oats 16 Siteftto be looked for— (Lower palpebral conjunctiva Gi) Tip and dorsum of tongue, Gii) Soft palate, (iv) Nail beds— (v) General skin, palm and sole, Colour of the mucous membrane of the conjuncs the tongue is more reliable than the aan a Estimaion of percentage of haemoglobin and examin, of stained films indicate the severity and actioign ™ anaemia. "BY ‘Symptoms referable to anaemia : General—Fatigue and lassitude. Neurological—Giddiness, vertigo. dimnes of visip headache. insomnia, tingling and numbness of extremities Cardiovascular—Palpitation, dyspnoea, anginal attack Gastrointestinal—Indigestion, diarrhoea, anorexia. Signs due 10 anaemia : General —Pallor, oedema. Cardiovascular—Water-hammer pulse, pistol shot sound, capillary pulsation forceful apex, haemic murmur over the pulmonary area in left second or third space or in the apical region. ejection click and nonrumbling soft diastolic murmur in mitral area. This is due to relative stenosis of mitral or tricuspid valve secondary to greatly increased blood flow. This murmur 15 encountered in sickle cell anaemia where the anaemia is very severe and chronic. (Noncardiac causes of water-hammer pluse ae thyrotoxicosis, high fever, Paget's disease, arterio- venous fistula, wet briberi, chronic annoxic cor pulmonale, hepatic coma etc.) Respiratory—Crepitations in lung bases. Neurological Features of polyneuritis or subacute com- bined degneration of spinal cord and papilloedema Renal—Albuminuria. Gastrointestinal—Enlarged liver and spleen due (0 prolif eration or reticuloendothelial cells.FRM ae & Bo (b) (c) (d) tl. Iv. Vv. VIL @ GENERAL £XAMINATION Types of anaemia Iron deficiency (Hypochromic Haemorrhagic acute post haemorrhagic anaemia following trauma or intestinal bleeding and chron- ic post haemorrhagic anaemia in bleeding from haemorthoids, from peptic uleer, due to hook- worm infestation or chronic menorrhagia; Nutritional deficiency: After gastrectomy; Malabsorption syndrome. Megaloblastic—This is due to vitamin B12. and/ or folate deficiencies leading to arrest of matura- tion of the cells. The causes are Nutritional; Pregnancy; Liver diseases; Malabsorption syn- drome; Drugs eg (a) Folate antagonists eg methotrexate and pyrimethamine, (b) Anticonvul- sants eg phenytoin, (c) Cytosine arabinoside by interfering with DNA synthesis. The causes that are rare in our country are (a) Pernicious anaemia (b) In leukaemias and haemolytic anaemias—due to excess utilisation of folate; (c) Diphyllobothrium latum infestation. Dimorphic anaemia—Presence of the pictures of both iron deficiency and megaloblastic anaemia in peripheral blood. This type is quite common in our country. The causes are—{i) Hookworm infection with nutritional deficiency state. (ii) Pregnancy. Anaemia of scurvy. Anaemia of hypothyroidism. Haemolytic anaemias— Hereditary disorders of PBC : (a) Congenital spherocytosis ; (b) Haemoglobinopathies like sickle cell anaemia, thalassaemia, haemoglobin C disease and haemoglobin E disease; (c) Glucose-6 phosphate dehydrogenase (66PD) and other enzyme deficiencies in RBC. microcytic) (a)me < OF CLINICAL btm HoRnNTIALS Q) Due te antibody formation cyles ARaing (1) Haemolytic disease of newborn "the, Gi) Autoimmune (acquired) haemoty, (iil) Symptomatic. haemolytic ansemig, "4 (iv) Paroxysinal haemoglobinuria $ ‘ (v) Rh incompatibility (vi) Mismatched blood transfusion (3) Due to infective or toxic factors ; (i) Organisms like haemolytic streptococ, ylococei, Clostridium welchii etc ws Staph, Gi) Malaria ; Blackwater fever ; , (iii) Arsenic, lead and other heavy meta), drugs like sulphonamides, potassium er ang methyl dopa and chemicals like itsoteaet etc. alene VI. Anaemia due to bone-marrow. depression_ pancytopaenia or aplastic or hypoplast, ic causing anaemia. (a) Idiopathic (b) Secondary to : . (i) drugs like chloramphenicol, trinitrotoluene gold, anticonvulsants (troxidone), arsenic, following use of cytotoxic drugs—due 10 idiosyncratic reaction. (ii) Idiosyncrasy to certain chemicals and insecticides—benzol and its derivatives like trinitrophenol. (iii) Repeated exposure to X-rays and radioactive substances. Vil. Myelosclerosis, myelofibrosis, myelophthisic anaemia, multiple myeloma Jead to simulta nd normoblasts ence of myelocytes a! ood and is re ood picture and i ferred (0 % s due neous pres in the peripheral’ bl leucoerythroblastic bl to bone marrow infiltration.if oo ag Ylig. semi ng GENERAL RAMINATION Ud by i VET Anaemia at uncertain origin lon (4) uraemia (partially due to deficieney ef envi lo. Fopotetin in chrante penal failure) ott, (OH) malignancy, chronic lnfwetions, hepatic elt hte. thosis, chuemataid-artheliie ete tend to iL Me, anaemias of chronic divardere Ste hay, IX. Sideroblastic anaemia~ tie a type of uy th, dyshacmopoietio anamia where periphers! avy blood picture is hypectramie micrueytie oF lass Mew, dimorphic in lype but the hone marrow tains rigned sideroblasts, Sideroblaste are Hucleated red blood cells having exeeas iron Pthay ‘, containing granules in the eytoplaam, Here a Wilisation of iron ix impaired due to defect in erythropoiesis, These are either hereditary (sexlinked partially recessive) or acquired Pople, The latter may be (i) primary (idiopathic) oF (ii) secondary, The secondary anaemias may be duc to—-(a) Druge like antictuboreutous, Paracetamol, phenacetin; (b) nutritional dis. order eg chronic alcoholiam, nutritional megaloblastic anaemia, malabsorption, (e) One), Arsenic increased haemopoietic cell proliferation eg TUBS—due 4, myeloproliferative disorders, leukaomiax haemolytic anaemiay, Nearly one-third of the sideroblastic anaemias respond to | Be (og 100 mg) daily doses of pyridoxine, In all cases of severe-anaomia apart from routine exam: ination of blood, bone marrow study should be carried Sion Tinitrototuae hemicals and lerivatives like ' out, Coomb's test may have to be done in some forms of and radioactive haemolytic anaemia. In hereditary spherocytosis, the text is negative; it is positive in immune haemolytic anacmias, myelophthisic ad to simula 6. CYANOSIS aa Definition—Bluish discolouration of the skin and mu: nd normoblass cous membrane due to excessive amount of reduced referred (0 © haemoglobin in the blood (more than Sgms/100 ce) re and is Clinical cyanosis is present when oxygen saturation is below 85%. Types :2» ESSENTIALS OF CLINICAL DIAGNOsig 1. Peripheral cyanosis—This OCCUTS in the normal arterial oxygen saturation sn ate 10 pro oxygen unsaturation of the venocapillary ang i f rs of nose, fingers and toes, ear lobule, : and sole lechanism— . pails (peripheral), (b) Low cardiac output, _ (©) Stuggish circulation in extremities, Causes— @ Accute left ventricular failure OF acute lef, atiy failure .with peripheral stasis. (i) Shock from severe burns or severe haemorrhage Gii) Exposure to cold, (iv) Cryoglobulinaemia—Cryogobulin is an abnormay Plasma protein (globulin) which forms Bet at low Causes— (@) Pulmonary—co; pulmonale, pleura) ffusi Pneumothorax.tespiratory failure, Pneumon;, WO" sorption collapse etc,, : (b) Cardiac—Congenital Cyanotic heart gi, right to left shunt—eg Fath O'S tetra vith Eisenmenger complex and syndrome. Tye By,GENERAL EXAMINATION a @rome is characterised by pulmonary hypertension with reversal of shunt, the term Eisenmenger's complex is used when the reversed shunt is at the ventricular level. Cyanosis tardive or late cyanosis may be found in AS D_ with reversal of shunt due to increased pulmonary and nght ventricular resistance because of heart failure or pulmonary 7) Chemy red colouration of skin is produced in oxide poisoning. ing. Clinical effects of Conse om a) # of and bleeding Yo @ Recurrent arthritis, gout and tophi form (3) Pulmonary * 2 Sooondary polyeyhacmia—ex n cr pumontle (4) tal heart diseases. . monary embolism. (5) Embolic manifestation—< Lise oma 2 MTL OF cane i 4 Ohany , "Onn Otte. With feversal of 'YPettension ok 7 JAUNDICE > Definition—Yettowi Sitesi) Upper (i (iv) w) Latent jaundice [1 ™E—1.5m ran be detected only by sean my) bulbar conjunctiva, Soft palate, Undersurface of tongue, Skin, Palm and Sole, Internal tissues are also stained when the jaundice is Types—(a) Obstructive, (b) Haemolytic, (©) Toxic atocellular or combination of any of tye Obstructive Jaundice : This is due to a block y Pathway between the site of conjugation of pin, in the liver cells and entry of bilirubin ig the intestine. Clinical effects— @ Gi) (iii) (iv) Ww) wi Greenish-yellow bulbar conjunctiva, Petechial haemorrhage (due to Vit K deficiency’ which being a fat soluble vitamin is not absorbed from the intestine and hence the bleeding disor. der). Sinus bradycardia—increase in the vagal inhibi tory tone due to circulating bile salt. Marks of scratching due to pruritus-possibly + reflex; bile acids acting as irritants on the nerve endings. Enlarged liver. Gall bladder may or may not be palpable ee pon the cause. (According to Coury gt bladder is usually not palpable in joundie iGENERAL EXAMINATION 3 due to a stone in the common bile duct whereas in carcinoma of the h cad of pancreas gall bladder _. becomes distended.) (ii) Splenomegaly due to associated biliary cirrhosis (rarely), (viii) Mustard oil coloured urine. Gx) Clay coloured stool. ()_ Xanthelasma, xanthoma tuberosum ete in about 20% of cases. Liver function tests which are mainly dependent upon the Patency of the bile ducts are impaired. In obstructive Jaundice, serum alkaline Phosphatase level varies between 30 and 100 KA units. [Normal serum value in adult is 3 to 13 King-Armstrong (KA) Units per 100 ml or 40—100 iulj Causes of obstructive jaundice + (A) Intrahepatic— @) Viral infection—infective hepatitis; (b) Drugs like (i) Chlorpromazine, (ii) Para aminosal- icylic acid, (iii) Sulpha drugs—sulphadiazine, (iv) Chlorpropamide, (v) Methyl testosterone and oth- er anabolic steroids, (vi) MAO inhibitors, (vii) oral contraceptives, (viii) Alcohol, (ix) INH etc. (c) Active chronic hepatitis; (d) Cirrhosis of liver (e) In pregnancy—due to cholestasis; () Lymphoma (eg Hodgkin's disease); (g) Secondary carcinoma of liver; (h) Sometimes in severe bacterial infection; (i) Pericholangitis in chronic ulcerative colitis. (B) Extrahepatic— (i) Impacted gall stone ; (ii) Enlarged glands at porta hepatis; (iii) Carcinoma of head of the pancreas; (iv) Carcinoma of ampulla of Vater or bile duct; (v) Carcinoma of gall bladder;cad ESSENTIALS OF CLINICAL piacnosis olving the common (vi) Rarely a duodenal ulcer inv’ bile duct; Cuil) Sticeure of common ite duct. 32 (viii) Sclerosing cholangitis complicating © colitis. i Haemolytic Jaundice : This is due © excessive Sear of red blood cells resulting i” # a " load on the liver. Clinical features : (i) Lemon-yellow bulbar conjunctiva: vith the (ii) Anaemia, the degree of which eee of bone severity of haemolytic P! marrow to regenerate: . ly—due to excessive activil yr surgery; Icerative d po ty of the Gi) Splenomegal, reticuloendothelial syste™- ini unt of (iv) High-coloured stool containing large amount! sterco-bilinogen and stercobilin- ; (v) Freshly voided urine is of normal colour sing® ee bilirubin is present but oxidation ee kes urobilinogen [0 urobilin quickly turns the unne dark. ; | (vi) Examination of plood reveals reticulocytosis. — (vii) Liver function tests dependent upon metabolic activities of the parenchymal cells are normal. Causes :— @ Congenital (a) Hereditary spherocytosis: (sickle cell anaemia, (b) Haemoglobinopathies thalassaemia etc.); (©) Glucose-6-phosphate_ dehydrogenase (G6PD) and pyruvate kinase deficiencies. (ii) Acquired (a) Mismatched blood transfusion; (b) Rh-incompatibility; (c) Following poisonous snake bite; (d) Drugs (eg primaquin. phenacetine, sulphonamides)puc.c-Hom. M ‘Access! Date. (e) wo (g) (h) Ww ad College & Hospital 2137 -GRNERAL EX AMINATION 2s causing haemolysis due to G6PD deficiency in RBC; Infection by Parasites—malaria and kala azar: Acquired immune haemolytic anaemia Marchiafava Micheli syndrome or paroxysmal noc- turnal_ haemoglobinuria (PNH)—due to unusual Sensitivity of RBC to complement; Paroxysmal cold haemoglobinuria (PCH) second- ary to syphilis (congenital syphilis); March haemoglobinuria—due to external trauma to small vessels. Toxic or Hepatocellular Jaundice : This is due to damage of liver cells by toxic or infective agents. Causes : (A) Infective i) (ii) Gii) (iv) Viral—Hepatititis A, B, C, D, E, Cytomegalovirus, EpsteinBarr and Yellow fever viruses. Spirochaetal—Leptospira icterohaemorrhagia (Weil's disease). Protozoal—Toxoplasma gondii. Rickettsia—Coxiella burnetti (Q fever agent). (B) Toxic1) Drugs : @ Gi) (iv) (vy) (wi) (vii) (viii) Chlorpromazine and other phenothiazine deriva- tives; MAO inhibitors; Imipramine, amitryptiline; Erythromycin, tetracycline (in high doses partic- ularly in pregnancy and in impaired renal func- tion), rifampicin. Isoniazid and para aminosalicylic acid; Methyldopa Phenylbutazone, indomethacin overdosage of paracetamol. Halothane, the anaesthetic agent (idiosyncratic reaction). and grossESSE! (2) Poisons and Toxins (i) Carbon tetrachloride, (iy Yellow phosphorus: (ii) Copper sulphate, {iy) Alcohol. ; . A fungal toxin used as poison (amanita | 7 Other conditions—In " plestasis) jaundice may oxacmias or hyperemesis, both causes. 1 causes of 1 bilirubin transport particularly in poy ESSENTIALS OF CLIMEAl, Din NOY 2). Poisons and Toxins ; a) ai) Gi) (iv) (vy) (c) Some (a) (b) (c) “d) Jaundice in cardiovascular disorders (a) Carbon tetrachloride, Yellow phosphorus, Copper sulphate, Alcohol, A fungal toxin used as poison (am, Other conditions—In pregnang cholestasis) Jaundice may be due ie liver; toxaemias or hyperey anita Phat, ‘ Mess, both we ta being rare causes. the other important causes of Jaundice “ Primary defect in bilirubin transport, tion in the liver cells particularly js, i infants is known as physiological ;,,. newborn. The defect in onica, iti ant | immaturity of the enzyme mechanism, fo Gilbert’s syndrome—the fault is in the # bilirubin by liver cells and a partial deq tt ot glucuronyl transferase enzyme. This is an nud autosomal dominant disorder. w inbeieg Dubin-Johnson syndrome is an autosomally jg ited benign defect in the transport of (it glucuronide from the liver cells into canaliculi. Rotor syndrome is somewhat 4; Crigler-Najjar syndrome—An autosomal rece, condition, consists of the two types Type I—Total absence of the enzyme gh transferase. It is the severe form. Un hyperbilirubinaemia may lead to kemi new born and ultimately to death. Type Il—Partial deficiency of the glucuronyl transferase is present. The pati survive to adult life. Congestive cardiac failure—hepatic co! and hepato cellular hypoxia in congestive ess failure are associated with disturbance isGENERAL EXAMINATION z function of the liver. This may give rise to icteric tinge. (b) Recurrent and/or multiple pulmonary infarctions. () May be associated with repeated myocardial infarction. (d) Iatrogenic. 8. PIGMENTATION Usual sites that are to be examined are— @ Face, (ii) Inside the cheek, Gii) Creases of palms, (iv) Skin particularly pressure points and areas ex- Posed to light Causes of pigmentation— (A) Physiological @ ~~ Pregnancy—eg chloasma, linea nigra. secondary areola etc. Racial. Gii) Bluish black pigmentation of the mongols_ (B) Pathological Congenital—{a) Von Recklinghausen’s discase— typical cafe-au-lcit pigmentation. ON. B.—other causes of cafe-an-lait Pigmentation are—{i) mberous scle- Tosis or epiloia (ii) Polyostotic fibrows dysplasia— Albright’s syndrome: (iii) Watson syndrome—pulmonic stenosis with cafe-au-lait patches, (iv) normal- ly in 10% of all people, (v) infective endocarditis etc. (b) Xeroderma pigmentosum. (c) Peutz-Jeghers syndrome. (d) Multiple polyposis of colon. (e) Acanthosis nigricans juvenile variety. ( Blooms syndrome-characterised by28 ESSENTIALS OF CLINICAL. | DIAGNO gis, 4 typical faci ind photesenmnetton © erythema on face. ‘*!*"Riec"™ (g) Nevus. "Setay, Acquired —(a) Physical agents : 1 (i) Exposure to radiation. (ii) Exposure to sun-rays and heat ii) Erythema ab igne—Caused by domestic conditions. ¥ local hea (b) Skin diseases : a . @) Lichen planus, (i) Exfoiative Pityriasis versicolor, (iv) Demis he tits, iy if (vy) Patchy pigmentation m Tpeti patches in leucoderma, mane with oo Chronicus, (vii) Psoriasis, (viii) ‘chen simple erythematosus, (ix) Acanthosis eae sociated with diabetes mellitus, roe me internal malignancies eg carcinoma pars (c) Poisoning : (i) Chronic arsenical poisoning (ii) Argyria—diffuse slaty grey colouration deposition of silver in the skin. toe z (d) Endocrine = a Addison’s disesae—increased pigmentation skin and mucous membrane varying from to dark brown in colour. Gi) Pituitary tumours—particularly ACTH MSH producing tumours; Nelson's sy! ii) Thyrotoxicosis; (iv) Diabetes mellitus; (v) Prolonged steroid therapy. (e) Parasitic—Chronic malaria, Kala-azar. (f) Nutritional deficiency : @ Malabsorption syndrome, chronic chronic liver disease, kwashiorkor, (ii) Pellagra >GENERAL EXAMINATION 2 (g) Metabolic : (i) Haemochromatosis (bronze diabetes)—gener- alised, bronze colouration; (i) Prophyria (congenital, variegate and cutanea tarda); Gi) Willson’s disease (Hepatolenticular degener- ation). (h) Drugs : Busulphan, fixed drug eruption as may Occur with sulphur drugs; steroids etc. Causes of hypopigmentation - Congenital— (a) Albinism—Congenital absence of pigment in the skin either localised (piebaldism) or generalised; (b) Vitiligo ; (©) Fanconi’s syndrome; (4) Phenylketonuria. Acquired— (a) Infections; (@_ Hypopigmented anaesthetic patches in tuber- Culoid leprosy (associated nerve thickening confirms the diagnosis); Gi) Pityriasis alba; Gii) Tinea versicolor—a fungal infection; (iv) Eczematous dermatitis; (v) Psoriasis. (b) Endocrine factors : () Hypopituitarism; (ii), Hypogonadism. (c) Others : (i) Alopecia areata; (ii) Chloroquine. Varieties of skin eruptions : (a) Macule—Abnormal colour of the skin in a localised area without elevation or depression, eg haemorrhages into the skin, rose spots of typhoid fever, secondary syphilis. (b) Papule—A raised area from the surface, size about 5 mm. eg acne, lichen.w ESSENTIALS OF CLINICAL DIAGNOsig (ec) Vesicle—Raised from the surface 4, milky or serous fluid (size about Sm) « Comin pox, small pox. B chit (a) Pustule—Raised from the surface, sing », mm, contains pus eg chicken pox, sman tt $ (c) Bigger than papule involving epiderm;, = mis eg leprosy. dep, Diets : () Wheals-Raised from the surface of the Tm a pale centre and red periphery. Mainty Mit (g) Blebs—Area of the epidermis raiseg fre surface, size more than 5mm; contains yp; serous fluid, eg herpes, impetigo, Pep vulgaris. "Bus Haemorphagic spots (Purpura) :— (1) Petechiae : The spot is less than 1 mm and does not disappear on pressure by a (2) Suggillations : These are larger mac than 2 em, in diameter and does not disap pressure. oy. in di Blass stigg. ules, (3) Eechymoses: These are extensive purpuric (4) Haematoma: These are large haemorth, skin causing elevation of the skin, Causes of haemorrhagic spots (purpura) in (A) Capillary endothelial defect : (a) Vascular purpura (Sympatomatic)— @ Anaphylactoid purpura eg Henoch— Schoenlein, purpura simplex. (ii) Infections : infective endocarditis, septicaemia, meningococcal meningitis, typhoid fever ete ii) Chemical agents and drugs (eg phenylbutazone, aspirin, indomethacin. phenobarbitone, peti. cillin, sulphonamide, snake venom.) (iv) Metabolic : uraemia, hepatic failure, (v) Other symptomatic Vascular purpura Cushing's diseases, scurvy, dysprotein ™Macules, AES in the the skin ; |wn GENERAL EXAMINATION like cryoglobulinaemia multiple myeloma, ete) iscellaneous = ” Dyan disorders like collagen diseases (4 polyarteritis nodosa, allergy); (ii) Mechanical; (iii) Orthostatic. Congenital = ° @) Heredity haemorrhagic telangiectasia (Osler- Ze Rendu Weber disease); (ii) von Willebrand’s disease ; (iii) Hereditary capillary fragility; (iv) Ehlers Danlos syndrome. (B) Due to deficiency of blood platelets: (1) Primary, idiopathic thrombocytopenic purpura (2) Secondary :— () Common causes = @) Drug and chemicals—Cytosin arabinoside, busulphan, methotrexate, vincristine—all cause purpura by depressing the bone marrow. (ii) Aplastic anaemia (iii) Leukaemias, Lymphomas, myelofibrosis. dis- seminated carcinomas—cause thrombocyto- penia by infiltrating the bone marrow. (iv) Hypersplenism—platelets are sequestered in the spleen (v) Systemic lupus erythematosus—autoimmunity (vi) Liver diseases; (vii) Infective eodocarditis ; (viii) Deficiency of Vit B, —defective maturation; (ix) After massive blood transfusion. (x) Disseminated intravascular coagulation— excessive consumption of clotting factors. Il) Rare causes : (i) Wiskott-Aldrich syndrome—hereditary defect in maturation of platelet ;ENTIALS VP SMALL DIAG +; BSSENTIAL Te PIAGNO gs Gy Thrombotic thrombocytopenic Gi) After prosthetic valve Feplacenna "ty, (iv) Food allergy etc. rent, . OEDEMA ; ° Definition—A local Or generaliseg (hich the body tissues and/or the “Rd contain an excessive amount of tissue up Fostricted sense it means an increas” "vig travascular component of the extraces” thy fluid. Nulag Sites— td qd) Dependent oedema or pitting oedema i found in congestive cardiac failure in Steg ients; kle (b) patients; (a) at the an on th, the foot, (c) and gradually ascends N dor the leg, thigh and trunk with increasin srt at of the failure. ig In patients confined to bed, examine the the sacrum (small of the back). Other Plags,”* eyelids, abdomen (parietal oedema) shoulg looked for. Oedema of the face, particy, aso, iness of the lower eyelids is foung , Pt nephritic and nephrotic syndromes. * (1) Solid oedema of myxoedema of ce, ; lymphostatic disorders eg filariasis does not nie pressure. _s Method of demonstration— Firm pressure for 5 seconds over the malleolus, medial surface of lower end of tibia a sacral region will produce a relatively pep dimple. ° 2 Types of oedema : (A) symrpetrical and (B) asymmet Symmetrical oedema may be either genei localised. Causes of generalised symmetrical oedema : (a) Congestive cardiac failure—Possible are— Fez ‘2. #:qi) (ii) EXAMINATION Impairment * tena} fall in the pt flo f © glomeryy : ading to a in excessive Teabsy tation rate Tesultin, bs Fenal tubules Water and sar by 2 formal renal bloo, vi omerular filtration estminue which 1 Sate exer, Wesiday of Incteased ¢, ins S pI (iv) wy) terstitial fluid accumulation, (>) Renal : ) Lymphatic factors 4; I S like | nerompetent valve , Poor Ho important roles. Chronic Passi. tion of albumii 'whangiectasis, rainge also play d wane cause hypoalbuminaemia leading to in @_Nephrotic syndrome—Due to excessive loss of protein in the urine leading to dimin- ished colloidal oncotic pressure (ii) Acute nephritis—inflammatory swelling of the glo- meruli causes fall of glomerular filtration rate leading to relative increase in tubular reabsorption with consequent reduction in urine volume and expansion of intravascular fluid volume. Hypoproteinaemia ; Oncotic Pressure is most- ly maintained by serum albumin, fall in con- centration of which predis poses to oedema etc. The causes are—(i) Inadequate proteinj se \ | | ESSENTIALS OF CLINICAL HENS on, famine, Pfloric A 9 (ii) Failure A Siges labsorption syndrome, intake—(eg kwashiork struction with vomiting. tion or absorption eg malabsorPeo” A . chronic pancreatitis, resec#o” siderable length of small intestine ST cali ra thesis in liver diseases i chronic active hepatitis. GV) Excess ve A protein in the gastro intestinal tract (ee — enteropathy. ulcerative colitis, Crohn's ie ease, chieaic gastrointestinal infection) 2 Excessive loss of protein in urine (eg nephactic syndrome.) ue Generalised symmetrical oedema may eee be a to—(d) angioneurotic oedema, (©) idiosyncratic action a aspirin, potassium iodide, (f) excessiv© arsenic ingestion, Obstruction of the superior vena cava oF its ™ : by mediastinal neoplasms, chronic mediastinal fibrosis, thoracic aneurysms, thrombosis etc. (ii) Erysipelas, cellulitis, Ludwig's angina, (iii) Angioneurotic oedema, (iv) Dermatoses of various aetiologies, (v) Inferior vena cava obstruction of various aetiologies, (vi) Milroy’s disease (vii) Pretibial myxoedema, (viii) Epidemic dropsy etc. ‘Asymmetrical oedema is mainly due to (a) Local causes eg—{i) arteriovenous aneurysms, (ii) Milroy’s disease, (iii) superficial or deep tissue infections, (iv) venous obstruc- tion, (v) lymphatic obstruction (eg by filariasis, metastatic carcinoma etc), (vi) Stings, bites and other causes of local inflammatation; and rarely due to (b) General causes eg toxins, drugs, angioneurotic oedema etc. 10. TEMPERATURE Normal—98°F to 99°F, (normal body temperature shows a diurnal variation of 1.5°F with an increase towards evening, reaching the paek betw and 10 pm). ae sa ¢ pm Subnormal—Below 98°F. (36-7°C)GENERAL EXAMINATION 35 Pyrexia—Above 99°F, .(3:2°C). An increase in the diurnal variation of more than 1-5°F is the rule, but the pattern of diurnal variation is commonly main- tained, Hyperpyrexia—Above 106°F (41-1°C) Hypothermia—Below 95°F (35°C). Causes of hyperpyrexia’ : (1) Septicaemia (2) Lobar pneumonia (3) Heat stroke (4) Malaria (5) Pontine haemorrhage (6) Encephalitis (7) pyelitis' (8) Thyroid storm (9) Malignant hyperthermia (eg caused by halothane or succinylcholine) (10) Neuroleptic Malignant syn- drome or NMS. (caused by potent neuroleptics in therapeutic. doses). Causes of hypothermia : (1) Myxoedema coma. (2) Peripheral circulartory failure, congestive car- diac failure. (3) Enteric fever, when there is haemorrhage of perforation. (4) Accidental prolonged exposure to cold. (5) Hypoglycaemia. (6) Acute respiratory failure. (7) Renal failure. (8) Extreme wasting as in malignancy or starvation (9) Coma due to alcohol, barbiturates, chlorpromazine, tricyclic antidepressants, mor- phine etc. Types of fever : Continuous—The daily fluctuation is less than 1-5°F and temperature does not touch the baseline. This is commonly encountered in pneumococ- cal pneumonia, in second week of entric fever, lobar pneumonia, rheumatic fever, miliary tw- berculosis, meningitis etc. Remittent—The diurnal fluctuation exceeds 2°F and| 6 ESSENTIALS OF CLINICAL DIAGNOSIS does not touch the base line This is commonly found in pulmonary tuberculosis, amoebic liver abscess, urinary tract infection etc. Intermittent—Fever continues for several hours (usy. ally 104° 105°F), and returns to normal some. | time during the day, as occurs in vivax malaria, Types—(a) quotidian, (b) tertian, and (c) quartan, Quotidian—The paroxysm of intermittent fever occurs daily, as in septicaemia, double infection with P. vivax etc. Tertian—The paroxysm occurs on alternate days as in benign tertian malaria due to P. vivax or malignant tertian due to P- falciparum. (c) Quartan—The interval between the two consec- utive paroxysmal attacks is two days as in quartan malaria due to P. malariae. A combination of the above three types of fever may be found in a case of typhoid ie, remittent in the first week, continued in the second week and fluctuation of 3° or 4°F in the third week. Hectic—Temperature is characterised by a great swing a rise by 5°F during the night returning to normal in norning accompanied by sweating. This type is com- found in septicaemia, empyema, advanced tubercu- (a) ) , commonly referred to as rigor (due to con- skin vessels) occurs in infection by parasites ©E coli infection, occasionally following ions due to some pyrogen reaction, and and perpetuated by intermittent admin- ‘other effective antipyretics. in acute E coli pyeltis and in eas in typhoid fever and in ya gradual one. In typhoid ies to steps classically erisis or by lysis.GENERAL EXAMINATION 7 The temperature falling quickly within 6 to 12 hours is known as a crisis and is found in lobar pneumonia. Alternately the fever subsides gradually over several days by lysis infections untreated by antibiotics (as occurred in typhoid fever before the introduction of chloramphenicol) and in bronchopneumonia. The course of fever may be regular (as in lobar pneumonia and malaria) or irregular (as in tuberculosis or bronchopneumonia). Regular alternation of recurrent bouts of pyrexia with a period of apyrexia is known as. Pel-Ebste in temperature and is sometimes seen in lymphomas (eg Hodgkins’ disease) and an irregular alternation may sometimes be noticed in infective endocarditis. Relapsing .fever—This comprises a group of acute infectious diseases clinically characterised by cyclic peri- ods of fever and apyrexia, Malaria is a good example, but the term is classically used for the fever caused by spirochaetes of the genus Borrelia recurrentis. Pyrexia of unknown origin : (PUO or FUO) I. Definition : When a fever of more than 101°F, persists for 2-3 weeks with the cause remaining obscure despite intensive study for 1 week, the fever is called pyrexia of unknown origin. II. Causes : Some of the common calises are Hodgkin's and non-Hodgkin’s lymphoma, carcinoma of lung, liver and other sites with or without metastasis, connective tissue disorders like systemic lupus erythematosus, polyarteritis nodosa, infections like tuberculosis brucellosis, subacute infective endocarditis, subphrenic abscess, pyelonephritis and hypersensitivity to a drug. Ill. Investigations : PUO requires systematic and thor- ough clinical examination and intensive laboratory inves- tigation to detect the cause. Preliminary investigations (Step )— (i) History (including drug history) and thorough clinical examination etc.ESSENTIALS OF CLINICAL PIAGNosis Routine haemogram includin leucocyte count and ESR to ¢ a Gitte, . mononuclear cells suggestive of ela © abn Ndy| ot leucopenia for enteric fever. vita) brucellosis, high ESR for Collagen, ven, Paraprotinacmia, tuberculosis erg” ‘lea, (iii) Midstream urine for routine exam; croscopy, culture and sensitivity test tion, : secutive days. for ¢ i, (iv) Liver function tests (v) Plain X-ray of chest, (both Pa views)—to exclude tuberculosis, garg" bey other chest infections, Midosis (vi) For female patient—a high Vaginal G culture and sensitivity test, Swab foy (viii) Venous blood culture, 3, taken at interye, > I hour, when temperature is >101,3°F a of or more usually suffice, but for those wl received antimicrobials within the Iac;"t® Me and in whom endocarditis Temains a possi. a total of 6 cultures should be taken oe day period. And in emergent Conditions f tures are to be taken simultaneously from dig ferent anatomical sites. The femoral vein should Preferably be avoided, (viii) Plain X-ray of abdomen—so exclude subphrenic abscess enlargement of organs like kidney, jj spleen, appendicular abscess etc. (ix) Mantoux test. (x) Throat swab for culture and sensitivity. { (xi) Routine examination of stool—for Entamosht | histolytica etc. (ii) Step I : ea i vet (i) Stool culture and sensitivity for enteric fe other salmonella infection. (ii) Widal test—for enteric fever. (iii) Intravenous pyelogram—when pathology(iv) (vy) (vi) (vii) (viii) (ix) &) (xi) (xii) Step I: di) Gi) ww) —" GENERAL, EXAMINATION w Ney is suspected NO Of Where size of the enlarged (etinepic abou oe hidney is faut Bunnelltest—for i 5. cytomegalivirus complement fixation test and test for toxoplasmosis —if atypical lymphocytosis or mononucleotis found in. pe ripheral blood. Test for lupus erythematosus or LE cell, anti- nuclear factor, rheumatoid factor or Jatex fixation tests if ESR is above 50 mm in first hour and Clinically collagen disease is suspected, Antistreptolysin (ASO) titer—if throat swab shows B-haemolytic streptococci and rheumatic fever is suspected. Study of plasma proteins patriculary immunoglobulins—when ESR is >50 mm and multiple myeloma or paraproteinsemia is sus- ted. Liver scan-—for primary of secondary Iie a cer or amoebic liver abscess. If primary cancer . ted it can be confirmed by alpha is suspect lod. tein (AFP) level of blood. , fetoprot toimmune haemolytic Coomb’s test for aut ia. iis. anaemi: postsin tor secondary syphi Wasserman cent fixation est ‘Amoeba complemé test for Q—fever Complement fixation infectious mononucten. shown 10 have 00 fous blood cultures ip (when bl ents with je is, deep mycoses ure have rial blood culture Th : ) sinuses ColecystOF yy and Patna ery Plain X19 0 primary Nver iver biopsy— oe of miliarywo ESSENTIALS OF CLINICAL DIAGNOg, is (Y) Screening of diaphragm 4 when py abdomen suggests a subphrenic “ay x, (v1) Bone marrow—stained film tg exe Ney, myeloma and marrow culture tat Brucella, ARR (vu) Kveim test—when plain X-ray chy ative Mantoux test suggest sarcoignt ang (viii), Biopsy of lymph gland—fo, ie lymphoma ete. “be rey, Step IV: The following tests are to be done Only for rk and for unusual presentation of commo, (i) Dental X-ray—for dental abs, painless and is overlooked, (ii) Bipedal Lymphangiogram—for te disease. CESS Which Pe h Gi) Fibrin degradation product i. urine—for disseminated intravascular a tion. (iv) Weil-felix-reaction—for Rickettsia} dise, Step V: (i) Laparotomy—This is done when Procedures fail and when factitiou: excluded. Lympo: granuloma, rej i abscess or arterivitis may be confirmed staged if required after biopsy. the aj Ss fe 3 MALARIA ji Malaria is the most common infections disease j world (300-500 Mio newly infected People per year 2.3 Mil in 1991) There are three different types of m all transmitted by female anopheline mosquitos feverperiod pages before) : Benign type (1/3): @ malaria quartana (Plasm malaria) @ malaria tertiana (Pl. vivax ovale) Malignant type (2/3)@ malaria tropica (PI. falci Double infections are possible, too.GENERAL EXAMINATION Female mosquito zygote form in midgut oocysi divides asexual Human liver : Preerythrocytic shizogony bursting liver cells dis liberates sporozoites charging merozoites; migrate in salvary gland liverperiod=incubation Period r—-- v gametocytes, relatively inert | in the bloodstream L Erythrocytes shizogony (asexual Clinical feature : Malaria is an acute febrile illness with a periodic picture. The dangerous, life threatening malaria is caused by Pl. falciparum, with the shortest incubation period of about 7 days. Relapses may occur in malaria tertiana as a result of reactivated liver hypnozoites. The general development is shown below : Cold stage : feeling of cold and apprehension, chills, malaise, headache, fatigue, shakes of the whole body (15 min-1h). chest, back, abdominal and joint pain, nausea vomiting clinically anaemia possible, rhild jaundice with soft hepato/splenomegaly, skin cold, cyanotic and dry, pulse, low volume tachycardia. Hot stage (2-6h) flush fever >40°C (> 104°F). tachypnoea, nausea, vomiting weakness, confusion, delirious skin, dry, burning and flushed; pulse: high volume tachycardia. Sweating stage (2-4h) : immense swaeting. temperature weak and sleepy, but more or less 0.K. —tropica irregular; sub-/bi-tertian, (24/36/48h), Fever periodicity quotidian 4“ESSENTIALS OF CLINICAL PIAGNOS iy Thrombocytopenia is a marker of the S€Venip, Complications duc to a disorders of the mie, in severe cases of malaria tropica (seldom insite © Cerebral malaria -» consciousness, gop ° vulsion up to persisting coma opisthotonos @ Cerebellar syndrome (common in Ind; intention tremor, hypotonia, dysarthria mus © Pulmonary’ ocdema—spossible at any sta, Neraliy, (oj Perey ia), and hy, BE dys crepitations ARDS (adult respiratory qj drome) ies © Cardiovascular shock—>collapse, skin, extre, temp nly @ Renal dysfunciton—combined with Jaundice longed coma, hypoglycaemia and hypovol,." Chronic malaria : large spleen and anaemia, ir Malaria in infants appear with’ anaemia and pater, within a day or tow children being breast fed are less to get malaria. Diagnosis : History and examination, blood examination : Thick film ; taken from the side of the fingerball, should be able to read through the patch. If possible | Field’s stain. Thin film : smaller drop than needed in thick film. S| with Giemsa. In doubtful cases repeat blood exam eve four hours. One negative slide does not mean no infect Every doctor should be able to carry out this two examinations. Fluorescent stain : (a) quantified Buffy coat tech (QBC), (b) RNA-specific fluorochrome-benzothiocarbox: (BPC) Serological tests (a) indirect fluorescent antibaody (IFAT). Positive 6-10 days after beginning of disease ( used).GENERAL EXAMINATION a py indirect HAemaggtitination teq, (IA); only simple ‘pment nessecary, but legs qv Sensitive ) enzyme-linked immunogor « antity Of Antigen require Pe MAY (ELISA) smal 0 (a) radioimmunoassay (RIA). fp reseeioh tions Other tests : (a) PI, falciparum-histidin-rich Protein 2 pFIHRP-2) Paper-strip est prepared w \" bodies to detect malaria tropica, but Ie. ar yoscopic examination, we) polymerase chain rea «ification: system (TAS) eae immediatly after di known or you face a mix, malaira. Generally keep in ming 3 1, Select falciparum drug tratement according to your local resistant Pattern! 2. There are chloroquine-resis, regions, so be aware of if 3. Do not treat with chloroqu: ith Monoclonal SS Sensitive than ction (PCR) and transcript to detect DNA and RNA, ‘agnosis if g the species is not ed infection treat as falciparum tant species in some success stays away! ‘ine when used as pro- phylaxis! 4, Reexam patient after some weeks for signs of recrudescence! Drug groups Effectivity Side effect Arylaminoalcohols _| blood schizontocides © Quinine/Qinidine |severe m.tropica and | hypoglycaemia, (iv.,p.0.) in pregnancy allergy | 5 ‘© Mefloquine (p.o.) | prophylaxis bradycardia aus !not in pregnancy! 5 oe © Halofantrine (p.o.} multiresistent malaria | Prolongation ot ECG tropica (MPF) QT interval !o PSSENTIALS OF CLINICAL Digg NON, 19 pee ero Fffectivity St = benogn malaria un, = Sed complicated m, tro. hy, jee (not everywhere) | 10% parent ne MRP fe Pyronandine Fg aminoguinolines —_.—fredical cure of P.vi] He Pamaquine Sev | sexual cycle in hypnozoites, gameto. cyotcides blood schizonticides “ePyrimethamine fin ‘combination with sulfonamides for Rot in; arute treateent and prophylaxis of falciparum malaria blood schizonticides in combination with pyrimethamine and proguanil Sulfadoxine © Cotrimoxazole Peroxides ¢ blood schizontocides @ Artemisinin severe complicated experimen falciparum;. cerebral new drugs} jee malaria erytrot @ Anemether severe falciparum row, +—_—— @ Artesunate uncomplicated Feticide falcuparum; better combined wil mafloquine Naphthoquinones = all growing stages @ Atavaquone experimental drugs in research stage @ BW566C80a ONE: RAI, "XAMINATIOg 1097 the WHO {NNOUNCEg joplem iN the future, ppt At ma * lary : eC Ke) 1 he, e rich cot A Kciey MCC py Caaaneden eee (USA i ke esearch yy Malor wer malaria, ane ney eltectiyg ) have te na gainst 1 I. » 0 fy He but hot Nere are some j vaceh net ment, D yet in esearch 4 8 about future tm matter in malaria jg (he fast Fins: ino 7 ficult espicially plasmodium falc 0 a of tropica. Parum, which causes ane? S malaria Treatment Table Falciparum malaira D i re 5 Dosage | Quinine salt 600 ] (not bisulphate type) it me/8h po for 7 days yn SeVere ill patients: Next U files Over 4th iv (max. 1.4 p), | Re by lO merkg iv over 4h] after 8-12h interval (max, 07g) this repeated untill Pat can swal- ete complete 7 days treat- Pyrimethamine plus 3 tablets as a single dose Sulfadoxine or in Fansidar-resistant 250 mg/6h for 7 days areas ‘Tetracycline Mefloquine 20 mg/kg (base) divided in two} doses with 6-8h interval po ] i 3x500 mg 6h in between and| | Heloeniiag repeaed afer one week (on ery stomach) be ly Benign malaria Drug Dosage Chloroquine base 150 mg initially 600 mg ca bore by = psp (go) 20 me 20 og ange supa next wo days 300 me single dese aac aati total amount of 3 days should g/kg. chloroquine base poe thy) oe46 FSSENTIALS OF CLINICAL DIAGNOsig Drug Dosage ~ in P vivax and ovale —— radiation therapy is to be added after above course with Primaquine 11. PULSE (i) Definition—Pulse is the leteral ex, arterial wall imparted by the column blood due to contraction of the jer, Pa (ii) Rate—Beats per minute, normal 69 is Ntrig minute, average 72 beats per minute i, 130 per minute at birth. adult ans Bradycardia —Rate less than 60 per minute. Causes : (1) Physiological—in trained at} - sleep ete. (2) Pathological Vasovagal attacks. Myxoedema. Obstructive jaundice. Raised intracranial tension, Drug eg digitalis propranolol, Different types of heart block ; the Tate 20 to 40 beats per minute in complete hea block. Sick sinus syndrome. Other causes include hypothermia, acute nephritis, phaeochromocytoma, stenosis corotid sinus syncope etc. Tachycardia—Rate more than 100 per minute, found normally in infants and in anxiety state. Relative bradycardia—When with per degree rise o temperature [F] the pulse rate increase is less 10 beats per minute, the condition is called relati bradycardia. For example, when temperature ris to 100°F pulse rate should be about 82 per mim normally, but less than this if there is relati 15 me/d for 14.21 day, Sion hletes, dur aorticmatic carditis, mitral hypertensive heart disease defect, Wolff Parkinson characterised by Paroxysmal atrial ‘tachycardia short P-R. a slur y the QRs complex—the delta ah a _ ctional eg anxiety state etc. . cardiomyopathy Exertion, emotion, coffee, alcohol etc are the aggravat- ing factors. PAT with block is sometimes encountered in digitalis intoxication with hypokalaemia. ii) Rhythm—Spacing of successive pulse waves time. The rhythm may be regular or irregular. tbe Talkt may be completely irregular Garegularty Ricco dts rhythm is occasionally inerrant a cope ae 2 recurring pattern of iregulaiy (oe ies, il the pulse in atrial fibrillation.i 48 RSSENTIALS OF CLINICAL DIAGNOSIS heart block with dropped beats, atrial flutter with varyin, degrees of A-V block are irregularly irregular whereas Ml premature beats, sinus arthythmia and atrial flutter wig, 2: 1 block it is regularly irregular. Sinus rhythms ; Impulse originates in the SA node Types—(a) sinus bradycardia, (b) sinus tachycardia, (c) sinus, arthythmia in which the heart rate increases with inspiration and slows down in expiration. It is increased by deep breathing and abolished by exercise. This variety is normally encountered in children and young people om usually absent in elderly individuals large ASD, hear, failure, sick sinus syndrome etc. Ectopic rhythms : Here the impulse arises from a site other than the SA node eg in the atria, A-V node or ventricles. The rhythm may be regular or irregular. Premature (Ectopic) beat or Extrasystole—It arises from some abnormal focus in the heart, occurs prematurely, is small and followed by a compensatory pause. It may be caused by overindulgence in cofee, tobacco and alcohol: dyspepsia, anxiety or organic heart disease like rheumatic carditis, ischaemic heart disease, hypertension or cardiomyopathy etc. When a premature beat follows each normal beat, the pulse is said to be coupled and designated as pulsus bigeminus. Atrial fibrillation, atrial flutter and atrial tachycardia may be regarded as similar ectopic rhythms which differ only in the rate of the ectopic atrial focus. A rate of 140 per minute result in atrial tachycardia; a rate of 250 50 per minute is atrial flutter and rates above 350 per ite is atrial fibrillation. xysmal tachycardia may be supraventricular (atrial, “tachycardia with AV block nodal) or ventricular. lar tachycardia (VT)-is commonly encountered in heart disease, digitalis toxicity, electrolyte and imbalance etc. er—Rapid regular generation of impulse ‘of 250-350 per minute in the atria, all of erse the AV node and so usually thereGENERAL BXAMINATION CL 03! 1 or ; tid pressure is applied, (due to ine east cnieatl Sie fe so the ventricular rate aiminis hes sisti6i re a rare rhythm is not restored. vee! stim (SVT) ite paroxysmal supraventricular racy eae tg t. Rh will siher terminate the paroxysm of ave o effect. amas heart disease, ischaemic heart ease ‘and thyrotoxicosis are the common causes of atrial flutter Atrial {fibrillation—Rapid fibrillary waves (f waves in ECG) take the place of normal atrial contractions and ventricles respond at random. The atrial rate is between 350 and 600 per minute. The A-V node cannot conduct jo many impulses and varying degrees of heart block always exist in an untreated patient as a result of concealed conduction. The ventricular rate is usually 100—150 per minute. It is recognised clinically by complete irregularity of the pulse both in rate and volume and the varying intensities of the irregular heart sounds. Rheumatic, ischaemic, hypertensive and thyrotoxic heart diseases are the common causes of atrial fibrillation. Heart block—It is either SA or AV block. In SA block a complete cardiac cycle is missed so that a gap appears in the pulse and is due to incresed vagal tone or intrinsic SA nodal disease. Conduction between the atria and the ventricles is impaired in AV block which may be of three types : (a) First degree bloc! the ECG which reveals P Ri (b) Second degree or partial es from the atria do not reach the three types :— (1) Mobitz Type I or Wenckebach type Gradual prolongation of PR interval followed by a dropped beat—the cycle is repeated; better prognosis. (2) Mobitz Type IL (periodic block)—The P-R or P- P intervals remain unaltered and any one P-wave is not followed by QRS complex eg. 6 : 5 AV block. k : —detected most commonly by interval more than 0.2 second. 1 heart block—Some impuls- e ventrical. It may be of» FSSENTIALS OF CLINICAL DIAGHOSIS (3) Second degree constant block eg, 2: 5,3: 4 om 4-1 AY blocks (©) Third degree or complete heart block—In this type #0 impulse from the atria reaches the ventricles and hence the atria and ventricles contract independent of each Other and the ventricular rate is usually between 20 to 40 per minute. Ischaemic heart disease, calcific aortic stenosis rheumat. ic cardiovascular diseases, syphilitic heart disease, congen. ital cardiac Sesions, digitalis, infectious diseases like diph. theria etc are the common causes of heart block. Ventricular fibrillation (VF)—This arrhythmia js characterised by rapid, irregular, uncoordinated and inef. fective contractions of the ventricles. It may occur in acute myocardial infarction as a complication of general anaesthesic by chloroform of cyclopropane, after toxic doses of digitalis or quinidine etc. Clinical presentation May be as Stokes A dams syndrome with syncope and convulsion. (iv) Volume—It is defined as amplitude of pulse wave, It signifies left ventricular outpur per beat. Causes of high volume pulse—Hyperkinetic circulatory States eg, fever severe anaemia, thyrotoxicosis, aortic incompetence and corpulmonale, atheros clerosis of acrta, complete heart block or gross bradycardia from any cause ete, Causes of low volume pulse—aortic stenosis, tight mitral stenosis, pulmonary stenosis, severe pulmonary hyperten- ion, obstructive cardiomyopathy, pericardial effusion, shock to any cause etc. ) Tension : Pressure required to obliterate the pulse Mm as systolic tension. Optimum pressure exerted by imal finger to have the maximum thrust felt by finger is said to be diastolic tension. Sphyg- being such a simple, easy, and accurate imation of tension has become obsolete. of arterial wall : It should be noted for ial thickening or undue mobility. UsingGENERAL EXAMINATION sN fingers, exsanguinate the artery and then roll over the y Surface, Sufficient pressure is applied on the brachial ty to abolish pulsation in the radial artery which should be rolled over the bony surface. Normally the arterial Il is not palpable. It may be palpable in old age due arteriosclerosis (tortuosity and cord like thickening). (vii) Equality : Comparison of volume of pulse of two er and lower extremities. Causes of inequality between radial pulses are— a. (i) Anatomical variations. (ii) Thoracic inlet. syndrome. (iii) Pre-subclavian coarctation (iv) Pressure over axillary artery. (vy) | Volkmann’s ischaemic contracture. (vi) Aortic arch syndrome. (vii) Supravalvular aortic stenosis etc. N. B. —Radial artery and femoral artery should be palpated simultaneously to detect coarctation of aorta. Delayed pulsation of femoral artery compared to that of radial artery, ie/radio femoral delay suggests coarctation of aorta. Difference of timing of radial and dorsalis pedis pulse is 0-02 to 0-03 ‘second: Inequality of brachial pulse may be due to thrombosis, embolism or atherosclerosis of aorta. Bounding pulse—A large pulse wave signifying a high pulse pressure, associated with increased blood flow, seen in hyperkinetic circulartory states. 12. RESPIRATION The rate, rhythm and type of breathing are determined by placing the hand over the epigastrium and noting the features of respiration without the patient's knowledge. (@ Rate : 18-20 per minute in adults. Increased rate (tachypnoea) @ Fever Gi) Exertion (iii) Excitement and emotion (iv) Pulmonary diseases eg. pneumonia pulmonary embolish etc.oe 52 ESSENTIALS OF CLINICAL DIAGNOSIS (v) Hypoxaemia from cardiac or pulmonary causes as in interference with reflex control of respi- ration by structural changes in lung ¢g, fibrosin alveoli ‘ (vi) Shallow and frequent breathing in pleurisy and peritonitis. (b) Rhythm : Varies considerably even among normal individuals. | Biot's breathing : This is a type of periodic breathing where periods of apnoea are interrupted by a phase of hyperpnoea consisting of four or five breaths only all of | which are of the same amplitude and the beginning and the end of the phases are abrupt but no waxing and waning of respiration is seen. This is commonly found in children suffering from meningitis, but may occur in primary sions and in increased intracranial tensions, y be unduly prolonged in laryngeal or whereas expiration may be prolonged in brainstem le: Inspiration ma; tracheal diseases, bronchial or pulmonary disease. Cheyne-Stoke breathing : This is the commonest variety of periodic breathing jependently described by John Cheyne in 1818 and William Stokes in 1846) in which the respiration becomes gradually deeper until a peak is reached and this is followed by a complete pause of breathing or apnoea. The pause lasts for 10 to 30 seconds “white the hyperpnoeic phase of 30 or more breaths lasts for 1 to 3 minutes. The patient may remain asymptomatic; it is usually prominent at night. Causes of Cheyne Stokes respiration + (i) Left ventricular failure ; —Commonest cause, particularly in those with degenerative arterial diseases. (ii) Renal failure. (iii) Morphine poisoning (iv) Bronchopneumonia or other tions in the elderly Occasionally during recovery attacks. respiratory infec- () from Stokes-AdamsGENERAL EXAMINATION 53 (vi) Increased intracranial tension, cerebral haemorrhage, thrombosis cerebral tumours, and severe head injuries. (vii) In sleep in apparently healthy elderly subjects. (viii) In normal subjects at high altitudes and after hyper ventilation. (C) Types : (i) Thoracic, eg. (ii) Abdominal eg. (iii) Abdominc-thoracic ‘Women * eg In men. Anxiety states young children Hysteria, Pneumothorax, Pleurisy (restriction Diphragmatic chest movement due of severe pain). palsy. Acute to losing spondylitis. Anky-Intercostal peritonitis. paralysis. Huge ascites. 13. BLOOD PRESSURE Blood pressure is measured by the sphygmomanometer. The width of the cuff is 12 cm for an adult, 3 inches for young children. 1 inch for infants and the length should be no less than 25 cm. To avoid a falsely high blood pressure in the leg a wider (8 inch) cuff should be used as this compresses the thigh more effectively than the narrower one which is used for the arm. Casual recording of the blood pressure may not give the true figure due to exercise, fear or emotion and thus it varies from time to time. So the blood pressure should be recorded with the patient at rest in a comfortable position. To measure blood pressure in the arm the patient should lie flat, on his back, whereas for that of the leg the patient should lie prone (as the systolic pressure will be much the patient sits or stands up). Before commencing ing of blood pressure the patient should remain at rest in supine (or prone) positions for 5 minutes. In recording the blood pressure, particular care should last trimen on of pregnency aesa ESSENTIALS OF CLINICAL DIAGNOgyg be taken to weap the cut firmly and eyeny base of the arm about 2.5 6M Above the eth ny the middle of the rubber bag over the brachyyr !i arm should not be hyperextended as it may ign!" in recording the diastolic pressure, The cusp wee 4 be inflated till the radial pulse disappears ang i! slowly. ‘The point at which radial pulse fig” ‘ey indicates the systolic pressure—As the cur "pe deflated, pulsation of radial artery gradully assume, fu hammer character and then all on a sudden ret normal character, the reading corresponding to mes i change repreasent the diastolic pressure, Sud, In auscultatory method the diaphragm ofthe sty, should be placed over the brachial artery close ¢g the edge of the sphygmomanometer cuff. Care en taken that the diaphragm is not pressed heavily guld artery as it may give wrong) diastolic pressure, tye is then inflated quickly to 20 mm above the aaa pressure recorded by palpation’ and slowly deft?! The highest level at which successive clear, Capp sounds (Korotkoff’s phase 1) are heard is the. git pressure. As the pressure is further lowered in the ¢ the point at which louder and sharper sounds sug, become muffled (Korotkoff's phase IV) or inaugiy (Korotkoff's phase V) indicate the diastolic press Norinally sounds disapper few mm below the change ov but in aortic incompetence sounds may be audible ¢ at zero pressure. Experimentally it has been shown direct recording of intraarterial diastolic pressure m closely correlates with muffing than when the sou completely disappear. To measure the blood pressure in the thigh the sphyg- momanometer cuff should be adjusted around the lower part of the bare thigh with the patient in prone position. The diaphragm of the stethoscope is to be placed over Popliteal artery. N. B.—If anaeroid gauges are used, they must be calibrated every 6 months against a mercury manometer. ungORNERAL BXAMINATION Ausculatory (silent) gap Sometimes a phase of 4 appearance of Korotkoft's 46) ance at a lower pressure al The phenomenon tends to unds from their second appear- ind this the auscultatory gap. occur in—(i) venous distension, ‘clocity into the arms as in severe auscultatory gap is of systemic hypertension. In an arrhythmia, the higher . pressui following an ectopic sete nneae beat should be ignored. In atrial fibrillation the systolic pressure should be taken at the point where the Majority of beats come through and the diastolic pressure where the majority of beats become muffled. When there is a difference of pulse volumes between the two arms as in presubclavian coarctation, aortic arch syndrome, supraclavicular aortic stenosis, Pressure over the brachial artery by enlarged lymph gland etc.) blood pres- sure in both the arms should be recorded. Slight disparity (less than 5 mm Hg) between reading from each arm is common in atherosclerotic and hypertensive patients and is not of much clinical significance. Blood pressure should also be recorded in both arms and legs when there is feeble or delayed pulsation in femoral, popliteal, posterior tibial or dorsalis pedis arteries as may occur in saddle shaped embolism at the bifurcation of the abdominal aorta and more significantly in coarctation aorta. Normal Blood. pressure : In infancy the systolic pressure is 75 to. 90 mm Hg; in childhood 90 to 110 mm Hg ; and in puberty 100 to 120 mm Hg. The diastolic pressure varies from 50 to 70 mm Hg. till Puberty. Blood pressure varies widely in healthy adult subjects. Systolic pressure varies from 100 to 145 mm Hgss ESSENTIALS OF CLINICAL DIAGNOSIg and diastolic from 60 to 90 mm He. The 4, normal blood pressure for adults below 44? Pe lim mm Hg. for adults above 45 years 140/99 Cars ig t systolic pressure in legs is upto 20 mm Hy, abou Hg arms in a normal individual in the horizontal the diastolic ones are almost identical, Posig, Pulse pressure is the difference between diastolic pressures. Normally it is 30 to 60 80g In chlidren below 15 years, systolic Pressure" mm Hg and diastolic pressure over 80 mm Hg is tl hypertension. ‘Onsik In adult individuals, if the blood pressures of the above mentioned values after ea hypertension should be diagnosed. __ Divergent blood Pressures (eg 160/20 mm He) are in arteriosclerosis, aortic incompetence, Pheochromog, etc. Systolic hypertension is encountered in atherosc}, aotric incompetence, complete heart block with bradycardia etc. Diastolic hypertension is encount essential hypertension, renal disease, eclampsia, syndrome, pheochromocytoma etc. N. B.—Very recently a simple method has been dey that records only the systolic blood pressure. The in ments is known as finger sphygmomanometer and ie used on any of the four fingers. Compared to the cont tional device, it is claimed to be a more reliable indic for making diagnostic and therapeutic decisions and in recent study in had a specificity of 08-5% during Screening compared to the conventional mercury colur device that had a specificity of 97% (BMJ, 1986, 293, To sum up a few recent recommendations of the Hypertension Society (BMJ, 1986, 293, 611) are 01 here with some modifications. (i) An anaeroid type loses accuracy over time and’ it should be checked at different pressure levels ae in ¢ Veral , *(>160/100 mm Hg)GENERAL connecting with a Y pie, ei rercury Manometer, he tub m (ii) Bladder lengths shout 4, ference + 35 cm for 4 Norma % em a muscular and obese arm, ian i . c years. ; m (iii) Sitting and sy, Pine pres in BP and arm must be at Sure, heart teyey tke measurement otherwise the ps ind suppo, ted durin, high. ading win ye outing (iv) The Mercury m; falsely ‘anometer level, and not more than 3 feet te be Vertical, at eye Ce bias ig deg m the Observer, to the nearest 2mm He. Woided by Tecording (vi) The auscultatory (silent) Bay " 'P sounds disappear between the oyStolie ang " Korotkoft sures and may lead to tnderestimation of yes, Pe pressure unless first recorded by palpation and ieee gap is present, It must be Clearly recorded. a children below 5 i ear measured easily by the usual BP j Years cannot be i ‘trument and in them different Occasions varies Consider- able. Thus only when Clinically indicated Measurement of BP in them should be undertaken and moderate deviations from normal should be ignored. REGIONAL EXAMINATION HEAD AND NECK (a) Inspection and palpation. Look for any abnormalities ‘in or for position, size, shape, any asymmetry, deformity, irregularity and depression or elevation. In Kippel-Feil syndrome, the neck is short mobility restricted, a characteristic posture of the neck is seen and there may be mirror movements of the limbs. Slight bending may be noticed in a defect of a (an attempt by the patient to COOESADG 8, en ne in head tilting to the opposite side with supe:58 () ESSENTIALS OF CLINICAL BHAGNey NONI oblique paralysis of one side) op ; i" , localised infections of the neck to a”, void my me We ce Hypertrophic changes in bones a fit lying meningioma without ANY defecy Han tial may occasionally be found. Bossing oy", the "ee, and a square shape may be found in ih nt frontal eminences are very much tae hh n bridge of the nose is depressed ang sf"*ed, it is vertical in congenital syphilis. The 44°" rae a globular form in hydrocephalus. The sun ay opened up and imperfectly ossified are > @ in craniotabes. The skull is bigger Pattion® the transverse diameter in Pager’, disegn ig appears large in contrast to short stature is droplasia. Skull apears small compared tg nent supraorbital ridges and lower Pm. acromegaly. Long headed skull is y on in dolicocephaly where as a bulletheaded ska called brachycephaly. In oxycephaly or a is head” the skull is conical or tower shaped weole the coronal and Saggital sutures undergo synostosis and is seen in gargoylism, Apert’s sy, drome etc. Oxycephaly is also known as acroce and shows overgrowth of the vertex, exophthalmos, optic atrophy and a divergent squint. Localised swelling of the skull may be Present due to sebaceous cyst, tumours like osteoma, fibroma, secondary deposit, acute leukaemias, dermoid cyst, encephalocele etc. Leontiasis ossea is a progressive irregular enlargement of the cranial and facial bones resulting in asymmetry and the superior maxilla is especially prominent. In Parry-Romberg disease there is facial hemiatrophy Occasionally a bruit may be audible on auscultation over the temporal parietal and frontal regions, may be due to— : (i) Carotido-cavernous’ fistula (thrills and bruis over the eyes).ee GENERAL EXAMINATION 9 (ii) Intracranial aneurysms. (iii) Intracranial angiomas eg Sturge Weber Syn- drome (haemangiomas of leptomeninges with mucocutaneous haemangiomas along the distri- bution of trigeminal nerve and facial naevus one on side). (iv) Angiomas of scalp. (v) Brain tumours. (vi) Paget's disease. (©) Neck rigidity (must be seen as a routine). (a) Any evidence of exophthalmos should be looked for. (c) Involuntary moyements of the head in diseases eg—(i) Park-insonism—constant tremor. (ii) Habit spasms—sudden jerky movement with facial gri- mace, (iii) de Musset’s sign—jerky head movemetns with each heart beat seen in severe |aortic regurgi- tation (iv) Chorea—sudden, jerky movements. (f) Neck Veins ; The patient should be propped up by a back rest to any angle that best and maximally demonstrates the jugular venous pulsation (the angle is that between the trunk and the level of the bed at the hip joint). The top to the oscillating venous blood column should be identified and the different waves determined. Normally the pulsations of the neck veins should not be above the root of the neck at an angle of 45%. If it is significantly above that level most ‘possibly the patient is in congestive cardiac failure. If the vein is engorged but not pulsatile superior mediastinal syndrome is suspected where there is obstruction to venous return in the svc. The internal jugular vein is ideally examined in prefe- rence to the external jugular and venous pulsations both sides of neck should be seen as a routine,—but that of the right side is a better indicator of the activities of the right heart. Hepato Jugular reflex : Increased jugular venous pulsa-