1.

Subjective and objective examination of urinary system a) main complaints and their characteristics - pain in lumbar region, disordered urination, edema headache n dizziness - deranged vision, pain in heart, dyspnoe, absence of appetite, nausea, vomiting n temperature - if ureters are affected the pain is felt at their course - if bladder is involved, pain is suprapubically - radiation of pain is characteristic of an attack on nephrolithiasis - sharp n sudden pain on the side of loin due to renal infarction b) percularities of anamnesis morbid ( present illness ) and anamnesis vitae ( life history ) - establish connection of present disease w previous infection ( tonsillitis, scarlet fever, onitis, acute resp d ) wh is characteristic for acute glomerulonephritis - find out whether he had deranged hearing or vision in his childhood that might sudde congenital renal pathology - special attn to the presence in the ptts past history of d of the kidney n urinary eg acute nephritis, pyelitis, cystitis or sympt that suggest dysuria, hematuria, edema, arterial HT. - drugs wh are consumed by ptt eg aminoglycoside, expired tetracycline, barbiturates - the ptt is asked abt character of d course wh may be gradual ( arteriosclerosis, chronic diffuse glomerulonephritis, amyloidosis of kidney ). Anamnesis vitae. - attn is given to factors wh provoke the present d or have effect on its further course. - spreading of genital infection onto urinary syst can be the cause of pyelonephritis. - necessary to establish the presence or absence of TB of lungs or other organs. - necessary also to establish if the ptt has other d that might cause affection of kidney. - occupations assoc w walking, riding, weight lifting. - some abnormalities of kidney, nephrolithiasis, amyloidosis can be inherited. - thorough info about op done on kidney or urinary tracts in the past. c) gen inspection - give the dr the idea of ptts condition - very grave condition w loss of consciousness may be due to severe affections of kidney attended by renal insufficiency n uremic coma - pay attn to ptts posture in bed eg active in initial stage of many d of kidney, passive in uremic coma, forced in paranephritis, restless in renal colic - convulsion r observed in uremic coma, renal eclamppsia, nephropathy of pregnancy - edema is characteristic of acute n chronic glomerulonephritis, nephritic syndrome, amyloidosis - face is pallid, swollen, edematous eyelids n narrow eye slits ( fascies nephritica ) - pronounced signs of pathology,edema affects the upper n lower extremities n trunks ( ansarca ) - color of ptts skin where edematous skin in chronic nephritis is pallid due to spasms of skin. - scratches on the skin n coated dry tongue n unpleasant odour of ammonia from mouth of ptt. - inspection of abd n loin not reveal any changes but in presence of paranephritis possible notice swelling on the affected side of loin

- especially tumor of kidney may be manifested by protrusion of abd wall. d) exam of other systems ( lung, heart, GI syst ) e) percussion and palpation of the kidney, diagnostic meaning. Palpation - when in lying position, ptts leg should be stretched n head placed on a low pillow where the prelum will be relaxed n the arms are freely placed on the chest. - dr assumes position on the R of ptt w L hand under ptts loin below 12th rib so the finger tips are near SC.During palpation L kidney, drs hand should be moved further beyond SC to reach L part of lumbar region. - the R hand is placed on abd slightly below costal arch perpendicular to it n somewhat outward of rectus m. The drs hand should press deeply w each expiration to reach post and wall while L hand presses the lumbar region to meet the fingers of R hand - the low pole of kidney ( if it is slightly descended or enlarged ) descends still further to reach the fingers of R hand - as dr feels the passing kidney, he presses it slightly toward the post abd wall n makes his finger slide over the ant surf of kidney by passing its lower pole - dr access the shape, size, surf ( sm or tuberous ), tenderness, obility n consistency of kidney - bimanual palpation of kidney can also be done w ptt lying on his side - enlarged kidney can be assessed by ballotment ( guyons sign ). - palpation of kidney in standing position can also be done where the dr sits on a chair facing the ptt. - palpation can be used to diagnose ptosis where a few degrees can be distinguished a) 1st - lower pole of kidney palpated b) 2nd - entire kidney palpated c) 3rd - kidney moves freely in all direction to pass beyond the SC to the side of other kidney n sinks downwards a distance Percussion - impossible to percuss the kidney in healthy subject. - dullness can only be determined in the presence of marked enlargement of kidneys - a much > informative method for examining of kidney is tapping where the dr places his L hand in the ptts loin n using R hand taps w mod force on the hand overlying the kidney region. f) Percussion and palpation of the urinary bladder, their diagnostic meaning Palpation - if contain much urine in ptt w thin abd wall, the bladder can be palpated over the pubic bone as an elastic fluctuate formation. - tenderness in palpation of ureter along its course n sensitive loin over the kidneys ( sensitive to pressure exerted in the angle btwn rib n long thoracic m ) is of certain diagnostic imp - the area overlying the the ureter extends on the ant abd wall btwn supr ureter pt ( at edge of recctus m at the level of umbilicus ) n the infr pt ( at the intersection of bi-liac line n vertical line passing pubic tubercle ) Percussion- a full bladder gives a dull sound on percussion of the supra pubic region

- is carried out fr umbilicus downward along median line where the pleximeter finger is placed parallel to pubic bone 2)Laboratory examinaion of urine a)Normal complication,properties of urine i)Normal daily amount of urine (daily diuresis) excrited by an adult varies frm 10002000ml,ratio of urine evacuated during the day to nocturnal diuresis 3:1 or 4:1.Daily amount of urine below 500ml and over 2000ml are pathological under certain circumstances. ii)Colour-depends on its concentration varies from straw yellow to colour of amber.urobilinoids,uroerythin.Most marked urine colour changes depend on presence of greenish brown bilirubin,large quantities of RBC,reddish brown urobilin medicines.Normal urine is clear.Cloudiness may be due to salts,mucus,fats,bacteria. iii)Smell-smell is specific,not pungent when decomposed by bacteria in urinary bladder,urine smells by ammonia.In presenceof ketone bodies,smell is fruity iv)Specific gravity-varie from 1.001-1.040.It is measured by urometer.It gives information on concentration of substance dissolved in it (urea,uric acid,salts)Specific gravity depends on molecular weight of particles.Osmotic concentration depends on presence of electrolyte and urea.Minimal concentration of urine = 910 mosin/l in healthy person. Clinical PropertiesIn healthy person is about 6.0.Normal urine doesn't containprotein.Small quantity of plasmaproteins present in urine.In healthy person,contains very small amout of glucose (0.030.5g/l),no ketone bodies,free from bilirubin. b)Rules of urine collection for urine analysis. Microscopy of urine sediment-urine specimen is stirred throughly and its 10ml are transferred into a centrifugal test tube. After centrifugation, the supernatant is decanted while the precipitate transferred onto an object glass for microscopy. Precipitate is first examined at small and then at large magnification to study formed elements, cyclinders and salts. Nechpirenko's method is now used to count RBC and WBC in 1ml of urine. Main advantages is that an average sample of urine is taken for analysis and presence of pus from the sex organ is thus excluded. Disadvantages ; it doesnt account for diuresis. Normal count is 1000 RBC, 4000 WBC, 220 Hyaline cast. Zimnitsky's test- Main advantages is that renal function is tested without interfering with normal life. Patient collects his urine at 3 hours intervals(8portions during 24 hours).Volume of day and night urine are compared and a conclusion is derived concerning day and nocturnal diuresis. Volume of each portion and specific gravity of urine are determined. Fluctuation in specific gravity of urine during course of day and its maximum value determined. c)Daily diuresis,ratio between day and night diuresis in norm and pathology. i)Nocturnal diuresis prevails in renal insufficiency ii)Hyposthenuria occurs in pronounced renal insufficiency iii)Polyuria + hyposthenuria is characteristic for renal dysfunction

d)Physical properties of the urine amount, diuresis, colour, odor, conc or specific gravity, transparency. 1. Amount daily amount of urine excreted by men = 1000 2000ml - daily diuresis is <500ml & >2000ml is considered pathological under certain conditions. 2. Colour depends on its conc. & varies from straw yellow colour to amber. - most marked changes of urine colour:i) presence of greenish-brown bilirubin ii)large quantity of RBC iii)reddish-brown urobilin 3. Transparency normal urine is clear - cloudiness may be due to salts, fat, bact. , mucous,etc. 4. Smell in normal it is specific & not pungent - when decomposed by bact. in or out of bladder, urine smells of ammonium. 5. Specific gravity normal = 1.001 1.040 - measured by hydrometer - maximum osmotic conc. = 910 mosm/l - in glucosuria, specific gravity = 1.030 1.040 bcos conc. of 10g/l increases gravity of urine by 0.004. e)Microscopy Microscopy of urine sediment RBC- can be altered or unaltered. Unaltered RBC contain Hb and appear as greenish yellow disc. Altered RBC are free from Hb and are colourless. These RBC occurs in urine of low specific gravity. RBC shrink in urine of specific gravity. Urine of healthy person can have single RBC. RBC liberated by kidneys or from urinary tract. Presence of RBC is hematuria. Hematuria established by microscopy is called microhematuria. Hematuria can be glomerular or nonglomerular origin. If blood originates from urinary tract, highest amount of blood is present in 1st portion of urine. If bleeding is from the urinary bladder. The urine is from the 3rd portion of the urine. If source of hemorrhage is located in other parts of urinary system, all 3 parts of urine will contain same amount of RBC. WBC-found in urine as small granular rounded cells. They swell in urine of low specific gravity.

3. Study of gastric secretion a) technique. Portions NG tube-into stomach.Gastric cont aspirated:1st portion-fr fasting stomach(N= 50 ml) 4 Subsequent 15 min. samples of gastric juice collected by continues aspiration (basal acid output BAO) Subcutaneously pentagastrin - 4 subsequent 15 min. samples (maximal acid output MAO) - samples titrated with NaOH to calculate BAO & MAO secretory rate Normal BAO level ranges from 50-150mg HCL & normal MAO level-fr 200-400mg HCl Level above normal BAO(50-150mg)&normal MAO(200-400mgHCl) hyperchlorhydria Level below normal BAO(50-150mg)&normal MAO(200-400mgHCl) - hypochlorhydria If both BAO & MAO = 0 - achlorhydria Absence of pepsin in gastric juice - achylia Achylia arises suspicion of stomach carcinoma b) physical properties of gastric juice Fasting stomach = 50 ml .Hourly basal secretion = 30 -150 ml (~50 ml) Evacuating function gastric juice vol(aft parenteral stimulants 25 min after meal)=75 ml Hourly secretion after stimulation: ~ 60 ml (intermittent aspiration) ~100 - 120 ml (continuous aspiration) c) clinical properties of gastric juice ( acidity of gastric juice, peptic activity, debit hour ) Debit-hour of HCl - amount of free HCL secreted during 1 hour Formula: D ( HCl ) = A X B X 0.0365 D ( HCl ) - debit-hour of HCl -A - amount of gastric juice secreted in 1 hour B - acidity of gastric juice in titrating units -0.0365 - molecular weight of HCl d) microscopic studies - Gastric juice precipitate of healthy subjects contains mostly cells of the mouth (squamous epithelium & leucocytes).The presence of food remains(mus fibers,fat,fatty acids,SC fat) is dysfunction of stomach. - Acid stagnant juice contains sarcinae.If acidity absent, lactic bacilli are present in juice. - Erythrocytes in small quantities present (due to injury,strain, during vomiting). - Ample erythrocytes suggests ulcer, tumour, erosive gastritis. e) gastric pH-metry Normal pH in esophagus - neutral or slightly alkaline (7,0-7,2) Normal pH in stomach: cardia = 1,3-2,0 -antrum >2,5 0,9-1,3 hyperacidity -2,0-3,0 moderate hypoacidity

 3,0-5,0 significant hypoacidity - > 6,0 veritable achlorhydria - After ingestion of 0.5 mg of NaHCO3, stomach pH increases from about 20 min. & then returns to initial level - Decreased esophagus pH - gastro-esophageal reflux.Neutral gastric pH - achylia - Increase of gastric pH after administration of NaHCO3 >30 min. - duodenogastric reflux suspected. 4)Malabsorption,signs.Causes.Clinical Pic a)Defi of malabsorption.Causes -this symptom complex is due to upset absortion in small intestine.Develope in combination with syndrome of inadequate digestion.Primary and secondary malabsorption are distinguished. -explain by congenital disorder in fine structure of intestinal mucosa and genetically determined intestinal enzymopathy. -onset of secondary is due to acquired structural changes in intestinal mucosa evoked by acute and chronic enteritis,sprue,intestinal lipodystrophy,exudative enteropathy,lesions of small intestine in amyloidosis,systemic scleroderma. b)symptom and sign of GIT affection -gradual wasting, symptoms of metabolic disorders,dystrophic changes in internal organs constant steatorrhea,creatorrhoea. -stool is pale, bulky,offensive. -mouth-glossitis,angular stomatitis, intraoral purpura, hyperkeratotic white patches. c)symptom and signs in the musculoskeletal and nervous system affection -osteoporosis, progressive atrophy -rash -bone pain(vit. D deffiency) d)symptom and signs in genitourinary,haemopoietic system and skin affection -hypoproteinaemic edema,acidosis. -folds of loose skin,pallor,anemia,pigmentation,rashes on limbs,in abdomen include scars from previous surgery dermatitis.Itchy red clumps on extensor surface. -hypoproteinemia, hypochlolesterolaemia, hypocalcemia. e)Lab and instrumental methods of examination -Lab examination determine hypoproteinaemia,hypocholesterolaemia,hypoglycaemia and other diseases due to malabsorption -coprologic studies reveal increased content of undigested food in feces and increase excretion of products of enzymic decomposition of food. -enterobiopsy reveal atropic changes in mucosa of proximal part of small intestine. -test with carotene,folic acid,galactose,D-xylose absorption test -Caseine,albumin,oleic acid,methionine,glycine,vit B12,folic acid labeled with radioactive isotopes -study chemical composition of food and stools

5)syndrome of git bleeding (upper,low and occult GIB) a)upper GIT bleeding.etiology.clinical symptoms and signs. Bleeding of esophagus,stomach and duodenum. Etiology: 1)hematomesis : vomit blood with bright red colour and also ground coffee due to digested by HCL. 2)melena:passage of block stool : 50-150ml of blood loss in upper GIT. Clinical symptom :faintless,nausea,weakness,sweat and restlessness Signs:1)painless bleeding with internal hemorrhoids,diverticulosis and angiodypepsia. 2)bleeding with pain in anal fissure and inflammation bones diseased. 3)bright red blood in rectum b)lower GIT bleeding.etiology.clinical symptoms and signs. Etiology :1)tumor af any site of git 2)peptic ulcer 3)esophagitis 4)angiodydpesia 5)infection :hooked worm clinical symptoms : same as upper GIT c)occult bleeding.etiology.clinical symptoms and sign. is small loss of blood in upper GIT d)instrument and laboratory examination. Sigmoidoscopy,colonoscopy,gastroscopy,angiography and xray e)method of first aids

6. Inadequate digestion syndrome. Gastric dyspepsia. Intestinal dyspepsia. a) Etiology. Pathogenesis. Cause; due to non-compensated secretion of stored exocrine, dysfunction of pancreas/ Upset secretion of bile, disorder passage of chime through GIT tract. - also due to intestinal infection, dysbacteriosis, alimentary disorders. Path: incomplete breakdown of food particles, active propagation of bacterial flora in intestinal with its invasion of proximal part small intestine, dysbacteriosis, abnormally high activity of bacteria in enzymatic decomposition of food with formation of toxins that irritate intestinal mucous, intensify peristalsis cause symptoms of toxaemia due to their penetration into blood. b) Clinical pic of gastric dyspepsia - occur in achlorhydria achylia, long standing decompensated pyloric of stenosis, atrophic gastritis and cancer of stomach. - characterized: feeling of discomfort, pressure and distension in epigastrium after meals, frequent eructation, regurgitation, unpleasant taste in mouth, nausea and poor appetite. c) Clinical pic of intestinal dyspepsia. - Occur in presenceof exocrine funct. of pancreas,ch. infectious disease of small intestine. - If present as inflation rumbling in abdomen (borborygmus), intensive passage of flatus, diarrhea with putrefracture and acid small and constipation. d) Inadequate parietal digestion, Symptoms. - can be seen in congenital secretory insufficiency.of intestine wall and chronic disease of small intestine attended with dystrophic, inflammatory and sclerotic changes in mucous, upset structure of villi and microvilli. The decrease no. deranged intestinal peristalsis. - symptoms : i) gradual wasting. ii) symptom of metabolic disorders of all type iii) dystrophic changes in intestinal organs dysfunction. iv) Hypoproteinaemia develop edema v) polyhypovitamirosis osteoporosis, anemia vi) trophic changes in skin, nails vii) atrophy of muscles viii) weakness ix) acidosis cachexia e) Laboratory and instrumental methods of examination. Intestinal dyspepsia

i) coprologic finding steatorrhoea, amylorrhoea ii) X-ray finding accelerated passage of barium contrast through small intestine. iii) studies of secretory function of pancreas, aspiration biopsy iv) determination of enterokinase and alkaline phosphate in intestinal juice. v) test for hyperglycemia with oral starch load and radionucleid studies with glycerol trioleate, sunflower seed and olive oil. Question 7: subjective examination of the patient with digestive system disorders a)Main complaints in esophageal disorders. Dysphagiadifficult passage of food via the esophagus.Due 2 functional narrowing/organic stenosis. Pain in acute inflammation of esophageal mucosa (esophagitis) and in burns. Patient feels pain in the entire course of the entire esophagus both with and without swallowing. Radiates to interscapular region. Patient with achlasia of the cardio (cardio spasm) will have spontaneous attacks of pain usually during night. In severe radiates to the back, upward by the esophagus, into the neck, jaws and continues for minutes to hours. Esophageal vomiting. in the narrowing of the esophagus.Food is accumulated at the constricted part of the esophagus and is expelled by antiperistalistic contraction of the muscle. contain undigested food with foul odor has it can long time retain in esophageal diverticulums or degrading tumor. Regurgitation-Return of food to the mouth in esophageal obstruction but in neuropathic patient in could be due to habitual symptoms or result of cardio spasm. Hyper salivation-Result of esophagosalivary reflex in esophagitis, cicatrical narrowing, cancerous stenosis. Foul breath-Due to cancer tumor of the esophagus or congestion and decomposition of food in cardio spasm. Heartburn (pyrosis)-Burning sensation behind the sternum associated with regurgitation of gastric content into inferior portion of esophagus (reflux esophagitis). Hemorrhage -Ulcer of esophagus, injury to the esophagus by esophagus, degradation of tumor, bleeding of dilated esophageal vein (in congestion of blood in the portal vein system) Bleeding of mucosa due to small laceration of the vessel in esophagus-gastric function in straining and vomiting (Mallory-Weiss syndrome). b)Main complain in stomach disorder Deranged appetite -Poor appetite or complete absence (anorexia) is characteristic of gastric cancer.Increased appetite in peptic ulcer especially in duodenal ulcer.Perverted appetite in pregnant patient and patient with achlorhydria where desire to eat charcoal,chalk, kerosene. Heartburn -Arises in the gastro-esophageal reflex mostly in presence of gastric hyper acidity in various disease of alimentary tract(peptic ulcer or cholecystitis), hiatus hernia, pregnancy. In healthy person can be due to hyper sensitivity to some food. Nausea -Refectory act associated with irritation of the vagus nerve, indefinite feeling of sickness and sensation of compression in the epigastria. Others: vomiting, pain, gastric hemorrhage, perigastritis. c)Main complains in intestinal disorder.

Pain: boring and spasmodic. Colicky pain is characterized by short repeated attacks which arise and disappear quite of a sudden. Changes in location quickly, the main site being round the navel. Boring pain is sometimes permanent, which intensifies during cough. Meteorism: the patient feels flatulence, inflation and boring distension of the abdomen. Diarrhea: frequent and liquid stools is a common sign of intestinal pathology. Putrid dyspepsia: often in secretory hypofunction of the stomach. Obstipation: this is obstinate constipation during which faeces are long retain in the intestine for more the 48 hours. Intestinal hemorrhage: due to ulcerous affection of the alimentary system. It develops in presence of tumour, protozoal acute infection d)Particularities of anamnesis morbid. -pt should be asked about his nutrition,then it is imp to establish if meals are regular bcoz taking food at random is an imp factor in the etiology of gastric diseases. -food quality is as imp as its amount taken during one meal. -mastication of food matters as well.donditions of rest & work, & possible occupational hazards should be established. e)Particularities of anamnesis vitae. -abbuse of alcohol & smoking are imp factors in the etiology of gastric diseases. -it is very imp to find out if the pts condition has changed during recent times(loss of weight, anemia, blood vomiting or tarry stools. -GIT diseases of the past, surgical intervention of the abdominal organs, long medications with preparations irritating the stomach mucosa(salicylates,steroid hormones,potassium chloride) are also very imp.

8. Syndrome of gastric juice hypersecretion and hyposecretion a) disease w hypersecretion and hyposecretion. Pathogenesis. Hypersecretion - abnormal increase in gastric juice amount.Gastric hyperacidity or hyperchlorhydria excessive gastric acidity.Hypersecretion: gastric juice > 160 ml extracted in 1 hour. - Hypersecretion manifested by constant effusion of gastric juice containing free HCl:amount content in fasting stomach>70ml(w complaints of heartburn,vomiting&hunger pain) Hyposecretion - Hypochlorhydria - secretory function impairment w reduced free HCl secretion in stomach - Anacidity or achlorhydria - secretory function impairment with totally absent HCL - Gastric achylia - simultaneous absent of pepsin & HCl from gastric juice - HCl & pepsin may disappear as result of functional disturbances (causes differentiated by means of histamine test) - Organic stomach lesions - HCl not secreted even after histamine injections - Functional disorder - free HCl in gastric content - Absence of free HCl - often in diseases accompanied by toxicosis & derangement of CNS function causing inhibition of stomach secretion. - Main signs: gastric & intestine dyspepsia b) clinical picture. Laboratory signs of gastric juice hypersecretion Normal BAO level ranges fr 50-150mg HCL &normal MAO level -from 200-400mg HCl Level above normal BAO(50-150mg)&normal MAO(200-400mgHCl)hyperchlorhydria c) clinical picture. Laboratory signs of gastric juice hyposecretion Level below normal BAO(50-150mg)& normal MAO(200-400mgHCl)- hypochlorhydria If both BAO & MAO = 0 - achlorhydria Absence of pepsin in gastric juiceachylia.Achylia arises suspicion of stomach carcinoma d) exam of gastric juice ( amt, acidity, debit-hour ) Debit-hour of HCl - amount of free HCL secreted during 1 hour Formula: D ( HCl ) = A X B X 0.0365 D ( HCl ) - debit-hour of HCl -A - amount of gastric juice secreted in 1 hour B - acidity of gastric juice in titrating units -0.0365 - molecular weight of HCl e) gastric pH-metry. Meaning in hypo and hypersecretion Normal pH in esophagus - neutral or slightly alkaline (7,0-7,2)

 Normal pH in stomach: cardia = 1,3-2,0 -antrum >2,5 0,9-1,3 hyperacidity -2,0-3,0 moderate hypoacidity 3,0-5,0 significant hypoacidity - > 6,0 veritable achlorhydria - After ingestion of 0.5mg of NaHCO3,stomach pH increases fr about 20 min& then returns to initial level.Decreased esophagus pH - gastro-esophageal reflux.Neutral gastric pH - achylia - Increase of gastric pH after administration of NaHCO3 >30 min. - duodenogastric reflux suspected. 9. Chronic enteritis. Chronic colitis a)etiology and pathogenesis. -chronic enteritis:i)infection:thyphoid fever, dysentery, salmonelosis,etc ii)acute enteritis iii)dysbacteriosis iv)elimentary factor:irregular meals,ingestion of cold food,overeating of poorly digestable foods. v)radioactive exposure vi)alcohol abuse. vii)allergic factors viii)congenital enzymopathy ix)endocrine factors x)diseases of othe elimentary organs(stomach,hepatobiliary system,pancreas) -chronic cholitis:i)infections:dysentery,salmonellosis,TB,shyphylis. ii)parasites iii)toxic effects:poisoning w arsenic, phosphorus, mercury iv)irregular nutrition,overeating & ch. Constipation patho:-in the presenceof motor hyperfunction of the small intestine, the ingested food is not processed sufficiently b4 it enters the large intestine, thus irritates mucosa.Then mucosa of large intestine has the excretory function.It releases microbes & their toxins. B)Complains of local & general disorders. -chronic enteritis - pain in the umbilical region -distention of the abdomen -constipation alternating w diarhoe. -chronic cholitis - pain in the lower abdomen /the iliac region,distention of abdomen, tenesmus,constipation & diarhoe. -irritability, deranged sleep, headache & low moods. -appetite is dec,nausea & vomiting. c)General & local objective examination -chronic enteritis:general inspection-pale skin,dry skin,brittle and laminated nails. Auscultation-splashing & rumbling sounds are heard in the R iliac region. -chronic cholitis:auscultation-rumbling sounds along the course of large intestine. d)clinical & laboratory character of the stool.

-chronic enteritis:-stool contain mucous,microscopy of feces reveal the presence of drops ofneutral fat & muscle fibers. -chronic cholitis:-protozoa can be found in feces.stools may also contain trases of blood & mucous. e)complication -involvement of the pancreas,the liver,large intestine,by development of hypochromic anemia & polyhypovitaminosis. -hemorrhage. -perforation. 10.Coprological examination a)Macroscopic analysis Features Small bowel diarrhea Large bowel diarrhea Stool vol Large Small Stool colour Light Dark Stool smell Very foul Foul Stool nature Soapy n greasy Mucinous n jelly like Stool type Watery Mucoid Blood in stool / melena Rare ( if present it is Common ( usually fresh altered ) blood, if fr cecum is maroon ) WBC in stool Rare Common Abd pain, location Periumbilical region, Lower abd mid abd - gripping n continous - crampy n intermittent - maybe colicky Tenesmus Absent Present but maybe normalized Undigested material ( in May be seen Invisible feaces ) Steatorrhea / fat in stool May be seen Not seen Frequency Less More b)Microscopic analysis -prepared from fecal emulsion in small quantity of water. -food residues -muscle fibers- yellow cyclinders with transverse located pattern. -connective tissue-semi translucent fibers. -starch vegetables. -Neutral fat -Cells-leukocytes,erythrocytes,macrophages,cells of intestinal epithelium and malignant tumors. -Pigments -Parasites c)Chemical analysis.Clinical meaning. -Medium using litmus paper. -Fermentative and Putrefactive- determine organic acids and ammonia. -Test for stercobilin

-Gregensen test -Weber's Gnaic test -Triboulet Vishayakov test d)Determination of occult bleeding -Gregerien test -Weber's gnoic test e)Difference between fermentative and putrid dyspepsia. -If carbohydrate assimilation is insufficient the fermentative fibers is activated and feces becomes acid--> fermentative dyspepsia.If protein are poorly assimilated (gastric or pancreatic acholia) and also in presence of inflammation in large intestine with exudation of protein, putrid flora becomes more active-->Putrid ammonia due to formation of ammonia. 11.SYNDROME OF INTESTINAL DYSPEPSIA a)etiology. -occurs in the presence of the exocrine dysfunction of the pancreas, chronic inflammatory disease of the small intestine and other condition.Mainly in the disturbance of the carbohydrate cause by the ingestion of the ferment food ,sustained and overloading. b)pathogenesis -acid product in the intestine cos intensified peristalsis c)peculiarity of fermentive dyspepsia.Coprological examination -occurs in the upset of equilibrium between fermentative and the putrefactive flora of the intestine .If the fermentative flora prevails ,fermentative dyspepsia occurs.It is characterize by the flatulence of the abdomen and semi liquid acid feces(2-3 stools per day),the feces contains numerous gas bubble numerous starch grains, vegetable cellular tissue, and iodophilic microbes d)peculiarity of putrid dyspepsia.coprological examination --putrid dyspepsia more often occurs in secretory hypo function of the stomach. The absence bactericidal action of the gas juice is connected with the absence of the hydrochloric acid ,rapid passage of the insufficiently digested food from the stomach to the intestine has negative effect in the first instance on digestion of proteins. this provokes putrid dyspepsia. -it is characterize by liquid dark excrement containing clots of undigested food. -fecal react alkaline ,with dark color and offensive odor -microscopy reveals of feces reveals much fats,muscular fibers with vivid tranverse and longitudinal striation even ends(creatorrhoea). -the iodophilic flora is absent. e)peculiarity of fatty dyspepsia.coprological examination -rapid passage of the food from stomach with inadequate lipase and disturbance in bile supply. -a fecal loss of more 6g for 24hours is abnormal

12)Syndrome of intestinal colic a)etiology.Pathogenesis -obstruction due to mechanical block occurring after abdominal operations w peritonitis obstruction of bowel distention above the block,w increase secretion of fluid into distended bowel. -in strangulation, blood supply is impeded, leading to gangrene, perforation & peritonitis. b)Pain character.Diffentiation from gastric one i)by the absence of periodicity;it is long standing & gradually lessensin prolonged inflation. ii)by exact localization;in intestinal obstruction,colicky pain is combined w almost permanent pain in the abdomen & the pain intensifies w intestinal peristalsis. c)Clinical pic of pain due to intestinal distention by gases.Differentiation from gastric one i)nausea,vomiting,pronounced meteorism,constipation & passage of flatus. ii)severe abdominal pain. iii)visible wave like peristaltic protrusions & retraction in the abdomen(wahls symptom) iv)percussion of the abdomen over the inflated zone reveals typany. v)x-ray examination reveals multiple fluid levels(Kloibers symptom). d)Clinical pic of pain due to intestinal obstruction. -dull constant pain. e)Clinical pic of pain appendicula and rectal colic pain -appendicula colici)1st localizes around the navel & the epigastrium but in several hours (or even on the next day) it decents to the R iliac region where it intensifies gradually.Smt, the pain arises straight in the R iliac region. -rectal colici)occurs in frequent & painful tenesmus to defecate & is associated w spasmodic contractions of the intestine & the sphinter ani.Only clots of mucous are smt expresses instead of actual defecation.Occurs in dysentery and other inflammatory or ulcerous disease,& in cancer of the rectum.Pain preceding defecation is associated w the disease of the decending colon or sigmoid colon.Pain during defecation is characteristic of hemorrhoids, anal fissures & cancer.

13)study of duodenal content a)technique -obtain by probing the duodenum by an elastic rubber tube 3-5mm in diameter. The oval bulb at the end of the tube opens into its lumen. Overall length is about 150cm. -The procedure is carries out on a fasting stomach.patients sit with mouth slightly open, the tube is placed on mouth so that the bulb is at the root of tongue and the patients is asked to make a swallowing movement. -If patients vomits he is recomemded to breath deeply though nose. When condition is marked,tube reach stomach,its position is erified by aspiring the stomach condition of a slightly turbid acid fluid show that tube is inside the stomach. -Patient now placed on right side so that the tuibe is would be directly toward the pylorus. Patient continued 2 swallowing the tube marked of 70cm.breathing should be though the mouth. -The outer end of the tube is lowered into a test tube in the stand placed on the low stool at the head-end of the bed.sometime the tube pass the pylorus in a shorter timeif patient walk slowly. b)phases 1st phase(normal duodenal content discharged from the tube) :is golden-yello,slightly viscous,clear and opalescing. If it contain gastric juice,it become turbid from precipating from bile acid and cholesterol. Its designed by letter A.this mixture contain bile,pancreatic and intestinal secretion. 2nd phase(the Oddi sphincter contracts and excretion of bile is discontinued) :continues for 46min. the phase is prolongated if the tone of the Oddi sphincter is increased and shorten in its hypotonia. 3rd phase : is the excretion of golden-yellow content of bile ducts and the neck of gallbladder. 4th phase(is evacuation of the gallbladder) : is attended by thicker dark yellow,brown or olive bile. Then the portion B(bile of gallbladder) whose secretion is associated with positive Meltzer-Lyon reflex. Bladder bile (B bile) is a kind of concentrated liver bile. The wall of the gallbladder has selectively absorbalitily:the Na ions and water was absorbed especially active. 5th phase(examination) :five minute portion are collected separately during entire examination. c)portions.clinical character portion A(is mixture of bile,pancreatic and intestinal secretion) :collected 10-20min. portion A1 is the excretion of golden-yellow contents of a bile duct and the neck of bladder. Portion B is a bile of gallbladder whose secretion is associated with positive Meltzer-Lyon reflexes.it is a kind of concentrated bile of the gallbladder. d)microscopy of duodenal content.

-Presence of leucocytes in bile was given great diagnostic. Their present in B bile was considered as diagnostic sign on cholecystitis and in bile C of cholangitis.if the leucocytes is impregnated with bile, this was considered a proof of their genesis from the gallbladder. -Diagnostic importance can be given to the presence of leucocyes in bile after their identification(by peroxidase staining). Epithelium can be quite informative provided it well preserved and its properties can be indicative of the site of its origin. -The presence of tumor cell in bile.microscopy of native preparation only in rare case can reveal them.Histological study of consolidated duodenal precipitate is more informative. -cholesterol crystals and brown grains of calcium bilirubinate are importance. They can be found in small quantity in healty subjects but large amount suggest cholelithiasis. e)diagnostic meaning -diagnostic importance can therefore only be given to the presence of leucocytes in bile after the indentification. -epithelium can be quite informative provided it is well preserved its properties can be indicative of the site of its origine:fine prisms originate from the bile duct, elongated columnar cells with oblong nuclei originate from bile passages, large cells w large round nucleus & vaculi cytoplasm are attributed to the mucosa of the gallbladder,large epithelial cells w round nucleus accounting for the expanded lower third of the cell & w a thickened cuticle belong to the duodenum. -the presence of tumour cells in bile is of great diagnostic importants. -discovery of cholesterol crystals & brown grains of calcium bilirubinate are of importants. -discovery of parasites in bile, is of great significance.Lamblia intestinalis occur frequently,eggs of liver fluke or Chinese fluke, eggs of duodenal wry head & also larva of intestinal strongiloides stercorilis are found less frequently.

Question 14: objective examination of the patient with digestive system disorder. a)General inspection. general condition- satisfactory with chronic disease. -grave : tumor of stomach, obst of intestine, bleeding in git conformity mal abs syndrome in insufficiency production of enzyme, protein deficiency, vitamin or mineral deficiency. Patient will seem older. consciousness - clear posture active. -forced: supine patient with flexed knee gen. peritonitis, appenditis w raised kneeabdominal pain; to reduce pressure at abd and reduce pain. lying on anterior surface of the stomach: peptic ulcer. Prone patient with peptic ulcer on the posterior wall. - knee elbow posture: acute pancreatitis - restlessness posture: intestinal n interperitoneal hemorrhage. Hippocratic face-acute peritonitis, pancreatitis, Dolly face- pale edematous transparent skin in vitamin b12 anemia Constitution asenthenic peptic ulcer. Nutrition poor in patient with advanced in mal absorption syndrome; cachexia in tumor Pale skin and mucous in git bleeding or anemia( pernicious, B12, Fe deficiency ) Lymph node at the neck between the SCM Large joints in inflammation bowel disease astralgia Fever in patient with inflammatory bowel disease b)Inspection of the oral cavity Bad breath Teeth- carries Affection of gums inflammation. Coated tongue Inflammation of tonsil glands with plugs of pus. Laryngitis Chronic esophagitis- diverticulums in esophagus with h2s rotten egg odor Fistula between colon and transverse, faecal odor Extragastrointestinal problem purulent bronchitis, purulent sputum] Liver problem methyl metcarpton odor: dead mice Acetone rotten apple odor in DM

c)Abdominal inspection Skin notting scars, venous pattern, lesions, stria. Deep irregular scar may indicate burns, kelloids, dense overgrowth of fibrous tissue Distended venous pattern: caput medusa anastomoses of vena cavae inf and v.portal. Lateral side in v.portal hypertension. Strias result from stretching of tissue by obesity, pregnancy, overload of the product of glucocorticoids. Atrophic lines seen on skin of abdomen following rapid or prolonged stretching. Cushing disease gives pink purple stria Abd fistula in patient with cohns disease and ulcerative colitis Hernia protrusion of organ thru abd wall muscles. Shape is abnormal in presence of any masses - Flat,scaphoid,round. Liver or spleen enlargement enlargement in left right hypochondrium. Over low half of abd in varying tumor, early pregnancy, urinary retention. Distention over upper half of abd suggest stomach delation, carcinoma, pancreatic cyst. Diataxis separation of rectus abd and hernia linea alba - abd wall movement examination -has severe abd pain. - Resp movement of abd musculature dec. -Limited abd respiration. d)Aims of abdominal palpation Superficial determine local tenderness - density of abd wall. - Pain in area by tapping method. Deep- to determine each part of intestine separately; place, size, mobility, tenderness, sound. Palpate sigmoid, caecum, ileum, colon ascendens, descendens and transverse. e)Percussion and auscultation of the abdomen. Clinical meaning Ausc best done before palpation and percussion and before meal. -diaphragm of stethoscope placed at 4 quadrant:listening 2 bowel sound & systolic murmurs. - Normally 5-20 seconds to hear bowel sound and it last for half second. - Absent sound: cessation of intestinal motility in peritonitis and paralytic ileus. - Hyperactive sound: loud, increased intestinal motility due to hunger, inflammation of bowel, excess injection of laxatives, reaction of intestine to sustain food, upper git bleeding, stenosis from intestinal lumen. - Loud bruiting: vascular sound, detected over aorta suggesting aortic aneurysm. - Narrowing of abdominal aorta cause soft blowing systolic murmur around umbilicus. Perc in epigasric area: tenderness in acute gastric usually in midline, often midway btw umbilicus and xiphoidus and sometimes to the right. -slightly lateral from umbilicus to left: projection of solar plexus and tail of pancreas, present in acute pancreatitis. - slightly lateral, downwards from umbilicus from both sides: mesenteric plexus

-mc burney point: projection of appendix,located at first one third part from distance of iliacumbilical line, projection of appendix - region of gall bladder: tender in cholecystitis.

15.Portal Hypertension and hepatorenal Syndrome a)Etiology i)obstruction of the blood flow from portal vein like tumor, enlarged lymph node of the portal hepatitis in cancer metastasis ii)obliteration of part of its intrahepatic breaching and chronic affection of the liver parenchyma(cirrhosis) iii)thrombus of the portal vein-Hepatorenal Syndrome-characterized by the concurrent enlargement of the liver and spleen in primary affection of either these agents.(abscess of the liver, blood, certain infections, poisoning, thrombosis of the hepatic veins) b)pathogenesis portal hypertension characterized by the growth and cicatrisation of the connective tissue at site of degraged hepatic cells of the cirrhotic cells liver. It cause stenous or complete obstruction of part of hepatic sinusoids and intra hepatic vessels so the blood flow increases the portal hypertension and interferes with blood outflow from abdominal visera. Hepatorenal Syndrome-involves both organ in pathlogical process.(disease of the liver,blood,certain infectons,poisoning)HS is explained by the rich developed reticuohistocytic tissue..In case of thrombus of the hepatic veins,simultaneous enlargement of liver and sleen is determined by venous congestion in them. c)symptoms and signs PH-dilation of the portocaval anastomoses -ascitis develops -spleen saiz increase -rectal hemorrhage -haematemesis -caput medusa HS-enlargement of the liver -enlargement of the spleen -anemia -leucopenia -thrombocytopenia hemorrhage d)laboratory examination,charafcteristic of changes PH-special needle and pressure gauge -pressure in the spleen(splenomegaly)is measured in varicose vein of the esophagus

-needle is introduced thru esophogscope,pressure in the spleen is the same as in portal vein. -normally it is 70-150mmH2O PH value is 400-600 mmH2O e)methods of the instrumental examination in diagnosis process PH-splenopotography-transumbilical portohepatography HS-scannig and palpation

16. Cholecystitis. Gallbladder colic a) etiology. Pathogenesis - etiology : cholesterol secretion ( elderly, female, pregnancy, rapid weight loss, obesity ) impaired gallbladder emptying ( pregnancy, severe fasting, parenteral nutrition, SC injury, gallbladder stasis ) gallbladder salts secretion ( pregnancy ) b) complaints - pain - digestive distress ( nausea, vomiting, loss of appetite, anorexia, metallic taste in mouth ) c) obj exam anxious and restless patient jaundice and pruritus tachycardia tongue dry and white coated distended abdomen with limited ant wall mvm local tenderness and guarding inflammatory mass around gallbladder palpable enlarged, painful gallbladder +ve Murphy, Boar, Ortner, Ionas, De Mussy, Schotkin-Blumberg sign d) lab studies leukocytosis, ESR clay coloured stool beer colour urine high alkaline phosphatase and small rise in AST serum bilirubin high e) prophylaxis - Abc eg cefotaxime - bile duct drainage ( ballon or basket catheter ) - endoscopic bile duct clearance

17. Renal colic syndrome a)etiology -obstruction of the ureter by a calculus or its bending(moveble kidney). b)pathogenesis spasmodic contraction of the ureter leads to retention of the urine in the pelvis & hence its distention.The spasmodic contractions & distention of the pelvis account for the pain. c)clinical picture i)pain:it could be dull, sharp, constant or intermittent. ii)anuria:due to complete bilateral obstruction or polyuria in partial obstruction. iii)malaise,fever,septisemia. iv)retention w overflow. v)local tenderness,palpable enlarged hydonephrotic syndrome. d)methods of laboratory & instrumental diagnostics. Laboratory: i)UA-presence of free hemoglobin & RBC, increase of creatine level. ii)blood analysis-increase of creatine level. Instrumental: i)ultrasonography to access upper urinary tract dilation. ii)radionuclide studies. iii)excretion urography. iv)spiral CT scanning. v)entegradepyelography & ureterography. vi)retrogradeureterography. vii)cystoscopy urethroscopy. e)first aid. -involves relieving of obstruction. -temporary external drainage of urine by nephrotomy.

18)Nephrotic syndrome a) Definition Diseases with nephrotic syndrome are chronic glomerulonephritis, amyloidosis, malaria, sepsis, TB, Diabetes Mellitus, Collagenosis. b)Pathogenesis Metabolic disorders, derangement or trophic and capillary permeability in capillary. Protein or lipid large quantity in primary urine or these pathogens infiltrate the tubular to cause drastic dystrophy in epithelial cells. Auto immune mechanism for development of chronic nephrotic syndrome. c)Mechanism of edema development Diffuse increase in permeability of capillary wall. Colloid osmotic mechanism : Hypernaturemic edema occurs in acute anaemia. -Auto immune process and increase hyaluronidase activity and decrease calcium in blood serum. -Decreased plasma oncotic pressure and decrease of blood protein. -Retention of highly hydrophillic Sodium in blood tissue. -In acute poisoning and glomerular filtration. d)Methods of instrumental and laboratory diagnostic Laboratory levels of 3 signs including protein urea, hypoproteinaemia, hypocholesterolaemia. Functional renal test and decrease of tubular secretion. Valuable information connecting the nature of nephrotic syndrome. Palpation reveals edema. Mc-Clvre- Alderton test-0.2 ml isotonic Nacl injected in to skin on median surface of forearm. Time taken for it to dissappear is noted. In normal adults it dissappears within an hour. Heightening and daily diuresis and h20 balance of body causes fluid to accumulate in plural and body cavities. e)Clinical features -Protein edema especially in the face and eyes normally eye in the morning.Leg, skin of abdomen and hand also. Mobile.Fluid accumulation in internal organs serrous cavities. Diuresis (250-400ml) containing much protein(10-20). Hyaline granular and cell or renal epithelium found in urinary sediment. Decreased albumin in blood. Proteinuria and hypoproteinaemia, hyperlipidaemia.

No. 19 Gastrointestinal system. Complains A) Abdominal pain. Clinical features of visceral, parietal, superficial, referred pain Esophagus pain in acute inflammation of esophageal mucosa and in burns at the entire course of esophagus both with or without swallowing ptt w achalasia of cardia may have spontaneous attacks of pain,usually at night,quite severe Stomach - pain is the leading symptoms in diseases in stomach - seasonal character of pain is characteristic of peptic ulcer during spring and autumn - perigastritis also manifested by pain developing right after food intake Intestine - boring&spasmodic(intestine colic).may change quickly in location,main site round navel - pain sometimes may rise to other areas of abdomen. - intestinal pain caused by obstruction of intestinal patency and upset motor function, mostly caused by spasm or distension of intestine by gases B) Nausea, vomiting. Etiology. Pathogenesis. Clinical types and features the reflectory act associated with irritation of vagus nerve is an indefinite feeling of sickness and sensation of compression in the epigastrium often attended by pallidness of skin, general weakness, giddiness, sweating, salivation, fall in arterial pressure, cold in limbs and sometimes semisyncopal state often preceed vomiting.Leading role is disturbance in nervous system & the tone of stomach C) Regurgitation. Causes . Clinical features is the return of swallowed food into the mouth.Maybe due to esophageal obstruction occurs in neuropathic pt whom it becomes habitual symptom or as a result of cardiospasm in stomach might implies sudden loud uprise of wind from stomach or esophagus ( eructation ) and return of swallowed food into the mouth ( sometimes with air )

acid regurgitation usually associated with hypersecretion of gastric juice and occurs mostly during pain attacks in ulcer bitter regurgitation occurs in cases with belching up of bile into stomach fr duodenum D) Constipation and abstipation. Definition, causes and clinical features the long retained of feaces in large intestine and rectum caused by worry or by a diet which does not contain enough roughage or by lack of exercise, as well as more serious diseases of the intestine limited mobility of subject, hunger and irregular defecation may prolonged pauses btw defecation.Organic and functional constipation is differentiated organic due to mechanical obstruction, eg. narrowing of intestine lumen functional constipation maybe divided into alimentary constipation, neurogenic constipation, constipation associated with inflammation, toxic constipation, constipation associated with endocrine, constipation due to lack of exercise, constipation caused by flaccidity of the prelum. E) Diarrhea. Etiology. Pathogenesis. Clinical character is the frequent and liquid stools, a common sign of intestine pathology occurs in acute and chronic intestinal infection, various exo and endogenous intoxication, endocrine disorder and hypersensitivity to food accelerated mvm of liquefied food in intestine due to peristalsis is one of the pathogenesis others maybe disordered absorptive function of intestine. inflammation of intestine and organic affection also caused diarrhea

20)Diffuse lomerulonephritis.Clinical pic a)etiology.pathogenesis -diffuse glomerulonephritis is general infectious allergic disease with predominat affection of glomerular vessels.Divided to acute and chronic -etio for acute:dev after acute infectious disease,eg tonsillitis,scarlet fever,acute resp disease,pneumonia,otitis.GroupA haemolytic streptococcus,type XII.Overcooling,damp weather,after vaccination -pathogenesis for acute:Attempts to isolate streptococcus from kidney end in failure.onset is the period when antibodies to streptococcus are produced.it is a infectious allergic disease.Bacterial antigens get into blood during infection,injured kidney tissue,affect protein act as antigen to stimulate production in reticuloendothelial system. -aetio and pathogenesis of chronic:secondary to acute form is patient not timely and properly treated.Secondary to nephropathy of pregnancy,chronic glomerulonephritis is one of the 3 classical forms of Brights disease. b)Cli pic of acute.Main syndrome -oedema,arterial hypertension,changes in urine(haematuria and proteinuria) -oedema on face,under eyes,entired body and extremities -headache,heaviness in head,deranged vision,general fatigue,reduced work capacity -severe dyspnoea,attacks of asphyxia,dull lumbar pain,frequent tenesmus,complete anuria c)Cli pic of chronic.Main syndrome -1st stage:stage of renal compensation -weakness,headace,vertigo,oedema,asymptomatic,increase arterial pressure,proteinuria,clindruria,present waxycasts,urine contain little leached erythrocytes.blood serum cholesterol ncrease.hypoproteinaemia -2nd stage:stage of renal decompensation

-decrease quantity fuctioning kiney tissue.concetration capacity of kidney decrease along with decrease in specific gravity of urine.Nocturnal diuresis increase.increase nitrogenous slag.weakness,lassitude,headach,nausea,skin itching,unpleasant ammonium breath,impair vision,uraemic coma then death d)methods of instrumental and lab examination -X-ray:chest confirm presence of pleural effusion and congestion in lung roots.Dilatation and hypertrophy of LV.heart apex is rounded. -sphygmomanometry hypertension,systolic Pa increase to 200-220,diastolic100-160 -ECG:amplitude of ECG waves decrease in pronounced oedema of trunk. -Urine:diuresis decrease to oliguria.contain much protein and erythrocytes due to increase permeability of renal arteries.urine reddish brown.microscopy reveal present of casts. -clearance test reveal reduction of glomerular filtration -immunological shift:content of alpha2 globulins in blood increase during acute period e)current and prognosis i)palpation ii)mc Clure-aldrich test:0.2ml of isotonic NaCl solution is injected into the skin on the median surface of the forearm & the time of disappearance of the resulting weal is noted. In a healthy subject, the weal is resolve within 1 hour. iii)In the presence of a marked adematous syndrome, the dynamics of edema can be assest w measurement of girths of the extremities & the abdomen at the same level. iv)by determining the fluid level in the plural & abdominal cavities. v)by weighing the patient. vi)by determining daily diuresis & water balance of the body(the ratio of the taken & eliminated liquid during 24 hour period).

21. Diffuse glomerulonephritis. Clinical picture. -there are 2 types- acute & chronic etiology of acute:-streptococcal infection, viral infection, mononucleosis vaccinasion,alcohol. Pathogenesis of acute: -arise not during infectious diseases but only following a period of time(2-3week). -if not simple infectious disease but an infectious allergic disease. -both kidney are involve, all glomerular are equally affected. -both glomerular capillaries & vessels or other organs & tissue affected. Etiology of chronic:-acute glomerunephritis,rheumatoid arthritis,systemic lupus erythematous, nodular arteritis. Pathogenesis of chronic:-often secondary to acute form this disease. -autoimmune mechanism. b)Clinical picture of acute diffuse glomerulonephritis. Main syndromes. -pain in lumbar region over both side,fever,oliguria,hematuria,proteinuria,leukocytosis,increase ESR, increase globulin. -sympathomatic hypertention, syndrome of edema, cerebral syndrome. c)Clinical picture of chronic diffuse glomerulonephritis.Main syndrome. i) Latent form protein urea,increase casts, no clinical symptom. ii)Nephrotic form symptom of nephritic form. iii)Hypertension form renal hypertension. iv)form of hematuria macrohematuria. v)mixed form. vi)symptom of uremia headache, nausea, impaired vision. d)Methods of laboratory & instrumental examination. -in acute form:i) X-ray studies.

ii)Sphygmomanometry arterial hypertention, systolic pressure increase 200-220 mmHg, diastolic 100 160mmHg. iii)ECG- hypertrophy LV myocardium. iv)urine volume-development edema,oliguria. - increase protein &WBC. v)blood increase alpha2 & globulins. -in chronic form:i)urine-proteinuria,cilinduria. - presence of waxy casts. - decrease RBC. ii)blood-increase cholesterol,hyperproteinemia. iii)increase arterial pressure & hypertrophy of LV. iv)insulin & clearance test- decrease functioning kidney disease. e)current & prognosis. -in chronic, leads to kidney failure &pt can live with disease for 3-5 years. 22. functional study of the liver. a) carbohydrate metabolism liver cells synthesize glycogen and deposits it. glycogenolysis and glyconeogenesis occur here. Blood sugar content in the fasting stomach changes only in severe liver affection, therefore functional test can only reveal carb hypofunction of the liver. Glycogen stored in liver, muscle in condition of vegetative nervous system. Galactose tolerance test Galactose is assimilated by liver. Patient given to drink a solution of 40g of galatose in 200ml of water. Galactose excretion in urine is determined. Norm max 3g galactose excreted in 4 hours. Renal function and absorption power of intestine may affect its excretion. Max rise of blood sugar in 30 60 min in normal liver function. If the liver function is inadequate, sugar level is higher, decrease of galactose level in blood is lower. Adrenaline test Glycogenolysis function determined. Patient given subcutaneously 1ml of 0.1% adrenaline solution. In norm, this injection increases blood sugar lever by at least 50%. If liver is affected no rise of blood sugar. b) protein metabolism liver synthesizes and retains protein. Amino acid, polypeptide (food), breaks down product of the tissue protein delivered to liver to be catabolized, detoxicated, removed. paper electrophoresis depends on size, shape, charge, other factors. protein molecules move with diff velocity to positive electrode

protein of blood plasma separates to albumin, alpha 1 globulin, alpha 2 globulin, beta- and gamma- globulin. Albumin to globulin ratio decrease in liver disease - acute inflammation of liver :decreased alpha 2 globulin - chronic hepatitis : increased gamma globulin - liver cirrhosis : decreased total protein content, increased gamma globulin protein fraction ratio immunoelectrophoresis and ultracentrifuging protein decomposition product : 1. amino acid increase in severe liver affection with deaminating and urea forming function impairment. 2. residual nitrogen increase in renal insufficiency and hepatorenal dysfunction. 3. ammonia increase when liver not detoxify ammonia from intestine

c) study of liver enzyme 1. determination of isoenzyme by electrophoresis: - LDH 1 - 5 ( LDH 5 increase in chronic hepatitis, LDH 1 increase in MI ) - aldolase - aspartate 2. changes of organospecific enzyme activity - ornithine carbomyl transferase and arginase - sorbitol dehydrogenase - guanine deaminase - quinine oxidase 3. transaminase - ast - alt 4. alkaline phosphatase hydrolyzes phosphoric acid ester 5. serum cholinesterase - acetyl choline d) detoxication function of liver blood of portal vein from GIT contain various toxin to liver. Liver detoxifies toxin through oxidation, reduction, deamination, hydrolysis, methylation. Substance excreted through bile and urine. Ammonia changes to urea, free bilirubin binds with glucoronic acid. Sodium benzoate binds with glycine.

e) excretory function of liver 1. water soluble compound from kidney 2. water insoluble compound from liver bromsulphtalein test 1. bromsulphtalein given IV 5 mg/kg body weight 2. first blood specimen taken in 3 mins. Another specimen taken in 45 mins. 3. bromsulphtalein concentration determined calorimetrically. 4. red-violet when alkali added - if liver function normal, concentration at 45 mins less than 5% of initial concentration - stain detected 15 mins after injection in bile. Indocyanine test (more sensitive than bromsulphtalein) 1. same method as above but use IV 0.5mg/kg IV dose 2. less than 4% of injection stain remain in blood in 20 mins

23.CANCER OF THE STOMACH a)pathological anatomy, Location. Metastasis -gastric carcinoma remains the as the leading causew of the death in world wide.Gastric carcinoma is comman in the male compared to the female and rises sharply after the age of 65. -H.pyloric is associated with chronic atrophic gastritis and gastic cancer.This bacteria may be responsible for 60-70% cases &acquisition of infection at an early age is an important factor. -Altough majority of the H.pylori infected individual may have normal or increased secretion or few with hypo or achlorhydric and these people are tought to be at the greatest risk. -predisposing factors low socioeconomic factora dietary factors pernicious anaemia partial gastrectomy &gastrojejunostomy due to intestinal metaplasia in the resected stomach.Increases the risk of gastic cancer. Blood group A Chronic /benign gastritis -sites of stomach cancer-pylorus antrum,body of stomach,fundus. -type of stomach cancer a)Adenocarcinoma-85% b)lymphoma &leiomyosarcoma-15% metastasis to:-extension tru stomach wall -lymphatics -embolism via portal vein then to systemic blood . -left supraclavicle node-Virchows Node -Umbilical nodule-Sister Mary Joseph Nodule -ovarian metastasis-Krubenbergs tumor

-rigid rectal shelf-Blumers shelf -pararectal metastasis-Schnitzlers metastasis b)complaints -usually it is asymptomatic,patient usually comes at the advanced stage. epigastric pain(not relieved by antacid, not periodic,not relieved by eating or vomiting) -lose appetite -cachexia -dysphagia c)Objective examination -cachexia -pallor-(due to iron decreasd )yellowish and grey due to liver metastasis -epigastric tenderness -palpable epigastric mass -peritonealmetastasis-ascites -apathetic look -palpable left supra clavicle lymph node-Virchows Node (Troisiers ) -Paraneoplastic sign -peripheral edema -migratory thrombophlebitis -Acanthosis nigricans d)laboratory examination(blood,gastric juice,feces) -gastroscopy &biopsy -blood test reveals iron deficiency anaemia -occult blood in stool-guaiac positive result e)clinical forms i)fibrile form ii)anemic form iii)adematous form iv)dyspeptic form v)hemorrhagic form vi)latent form

24. Renal hypertension syndrome. Renal eclampsia syndrome a) disease w renal hypertension and eclampsia syndrome Renal HT - is a symptomatic HT caused by affection of the kidneys or renal vessels and upset renal mech of arterial pressure regulation - among all cases of arterial HT, renal HT makes about 10-15% - many diseases of kidney in the first instance, acute and chronic glomerulonephritis, pyelonephritis, nephrosclerosis and various affection of the renal BV are attended by elevated arterial pressure - disorders in cerebral circulation w paralysis, deranged sensitivity, dysfunction of pelvis organs n also MI can develop as result of arterial HT atherosclerosis Eclampsia - usually develops in acute diffuse glomerulonephritis and can also arise in aggravated chronic glomerulonephritis and nephropathy of pregnancy b) etiology. Pathogenesis Pathogenesis Obstruction in the presinusoidal venous compartment may be anatomically outside the liver (portal vein thrombosis) or within the liver itself but at a functional level proximal to the hepatic sinusoids so that the liver parenchyma is not exposed to the elevated venous pressure (schistosomiasis) Post sinusoidal obstruction also may occur outside the liver at the level of the hepatic veins (e.g., Budd-Chiari syndrome), the inferior vena cava, or, less commonly, within the liver (venoocclusive disease in which the central hepatic venules are the primary site of injury).

 Portal hypertension also may arise from increased blood flow (e.g., massive splenomegaly or arteriovenous fistulas), but the low outflow resistance of the normal liver makes this a rare clinical problem. Cirrhosis is the most common cause of portal hypertension in the United States. Portal vein obstruction is the second most common cause; it may be idiopathic or occur in association with cirrhosis, infection, pancreatitis, or abdominal trauma. Portal vein occlusion may result in massive hematemesis from gastro esophageal varices, but ascites is usually found only with cirrhosis. Noncirrhotic portal fibrosis accounts for only a few patients with portal hypertension. c) clinical syndromes The major clinical manifestations of portal hypertension: hemorrhage from gastroesophageal varices, splenomegaly with hypersplenism, ascites, & acute & chronic hepatic encephalopathy. Development of portal-systemic collateral channels. The absence of valves in the portal venous system facilitates retrograde (hepatofugal) blood flow from the high-pressure portal venous system to the lower-pressure systemic venous circulation. hemorrhoids, esophagogastric varices,periumbilical or abdominal wall collaterals. Abdominal wall collaterals appear as tortuous epigastric vessels that radiate from the umbilicus toward the xiphoid and rib margins (caput medusae). Worsening azotemia, hyponatremia. d) methods of lab exam -biochemical test- increase level of creatine & uria. -UA- proteinuria,leucocytouria. e) methods of instrumental exam ( changes on ECG, X-ray, opthalmoscopy ) i)ECG-signs of LV hypertrophy ii)X-ray-signs of LV hypertrophy. ii)opthalmoscopy-rectinopathy.

25. Cirrhosis of the liver a) etiology n pathogenesis - etiology viral hepatitis B, C, B+D alcoholic cryptogenic biliary cardiac eg congestion of b in liver, biV affection - pathogenesis : irreversible chronic injury of hepatic parenchyma extensive fibrosis with regenerative nodules formation loss of function hepatocellular mass b) subjective exam - weakness, fatigue, weight loss, m atrophy, cramps, anorexia, nausea c) obj exam - jaundice, hippocrates nail, finger clubbing, ascites, gyneacomastia, biliary cirrhosis, spider nevi, distended abdomen, stria, caput medusa d) lab blood test mitochondria Ab r present in titre >1:60 high serum alkaline phosphatase serum cholesterol serum Ig M

 low Na e) main clinical syndromes - portal HT ( splenomegaly, hypersplenism, collateral circulation, encephalopathy ) - hepatic insufficiency ( jaundice, palamar erythema, spider nevi, endocrine disorders ) - ascites

26)Gastric outlet obstruction(Pyloric stenosis) a)Etiology -occurs when there is a narrowing of the pylorus canal & this causes difficulty in evacuation of food mass fr the stomach to duodenum.Causes include complication of peptic ulcer, congenital hypertrophic pyloric stenosis,adult pyloric stenosis,polyps,cancer,hypertrophy of pylorus. b)Subjective examination -Vommiting of food mass that has brownish appearance and have foul odour. -Profuse morning vomiting with food that was ingested days ago. -Permanent pain which intensifies by night. Eructation with rotten egg wind. -Constipation alternated with diarrhoea. -Irritation of the small intestine by fermented food discharge into it from the pylorus which by intensified peristalsis. Poor appetite, dehydrated. c)Objective examination. General inspection. -tongue slightly coated.There's a rotten eg adour coming from the mouth. Patient is cacchetic. -Abdomen reveals distention in some cases peristaltic and anti peristaltic waves are visible. Palpation :-there is distention of the stomach, displacement of the lower borders of the stomach and in some cases hypertrophied pylorus. Percussion : -may reveal displacement of lower border of the stomach. Succussion may reveal fluid in the stomach. Auscultation :-late splashing sound can be heard.

d)Examination of diagnostic system. -Fibrogastroduodenoscopy shows gastric ulcers&cicatrization due 2complication of peptic ulcer. -Barium meal(contrast X-ray) shows a distended stomach and may show the stenosis. Pyloric sphincter is narrowed. e)Investigation( X-ray, stomach lavage) -Barium X-Ray- shows stomach distended, displacement of lower borders of stomach and narrowed pylorus canal. -Stomach lavage- to evacuate the contents of the stomach to observe if undigested food suggesting obstruction of the gastric outlet. May show undigested food mass ingested days before. -Fibrogastroduodenoscopy- may reveal cause of the stenosis, show fermented food if done without lavage. May see fermented food discharged into the duodenum from the pylorus.

27. Gastric outlet obstruction a) Etiology i) peptic ulcer in the region of pyloric due to edema, spasm and fibrosis struc. ii) duodenal ulcer : calcinoma of atrium b) subjective examination i) permanent pain erectation ii) vomiting iii) constipation alternated with diarrhea iv) achylia increase ferment ability of HCL c) Objective examination. General inspection. -cachexia -dehydration -epigastrium peristaltic -antiperistalic contractions of stomach - splashing sound 4 hours after eating General inspection : -tongue clear moist - dry skin

d) Examination of digestive sys. -peristalsis anti peristalsis movement -enlargment of stomach e) investigation (x-ray, stomach lavage) -stomach lavage -aspiration of stomach content, increase volume of contents -x-ray with barium shoiows the dilation of stomach (barium will stay in stomach for 6 hours)

29. Renal insufficiency.Coma a)etiology.pathogenesis. -def+rapd deranged in renal fx due to resulting action of nitrogen waste,rapid increasing of nitrogen accumulation n change in renal fx -causes: 1.prerenal -inadequate renal perfusion,hypovolumia,skin,gastrointestinal,renal volume loss -in sequestration of ECF in pancreatitis n peritonitis -in cardiac failure,M.I,vascular pulling in anaphylaxis,sepsis,hemorrhage -normal kidney but cannot fx properly due to hyperperfusion 2.intrinsic renal acute failure -implies disease process win kidney itself -causes: Acute tubular injury in ischemia toxin,haemoglobinurea Glomerulonephritis Disseminated IV coagulation Acute tubular interstitial nephritis due to drug rxt of pyelonephritis Intrarenal precipitation due to hypercalcemia,urates 3.obstruction of renal flow -obstruction mei b due to occlusion blood,prostatic,retroperitoneal neoplasm,prostatic hypertrophy,carcinoma,calculi,pus,blood clot.

-pathogenesis: -renal failure develop due maily to shock n the accompaniying circulatory disorder mostly in kidneys. -anoxia develops to cause dystrophic changes in the renal glomeruli n tubules -when renal failure due to poisoning or grave infectious disease,direct action of poisons n toxins on renal parenchyma -in both cases glomerular filtration is deranged,diuresis decreases n oligria develops b) acute renal failure -4 stages of acute renal failure: Initial stage lasting frm several hours to 6-7 days,its characterized by main symstoms of the disease(traumatic or transfusion shock,severe infectious disease,poisoning) Oligoanuric stage is characterized by changes in diuresis(to complete anurea),uraemia toxicosis n water-electrolyte disorders -proteinuria,cylindruria n erythrocyuria r revealed. -can end with death or recovery Polyuric stage -diuresis suddenly or gradually increase -the specific gravity of the urine is low,the concentration of residual products of protein metabolis in blood decrease,water-electrolyte balance is restored n pathological changes in urine disappear Recovery -begins with normalization of diuresis,lasts frm 3-12 months. c) chronic renal failure -development of chronic renal failure is determined by progressive affection of kidney parenchyma -the latent period of chronic renal failure,when renal dysfx has no clinical symptoms can be only revealed by special lab methods -the manifested period characterized bymarked clinical picture of uraemia D) clinical picture Acute -Vomiting -Mental confusion - deranged respiration -upset heart activity - oedema in anuria. Chronic polyuria -Hypostenouria -Slight azotemia -hypokalemia -skin: pale, puluritus, dry skin. E) laboratory examination. i)acute-blood test(anemia, leukocytosis,hypercalcemia,hyponatremia,increase creatine & urase

in metabolic asidosis). - urine test (proteinuria. Erythrocytouria,increase cast in urine) ii)chronic_moderate increase in conc of nitrogen decomposition

30. Syndrome of the Intestinal Obstruction a) Etiology. Pathogenesis. Types of Obstruction. i) dynamic intestinal obstruction. - peristalsis, working against obstruction agent, which may be in intestinal lumen and in wall of intestinal outside the intestinal. ii) strangulated from intestinal obstruction. - peristalsis arise but no progressive wave lead to paralysis and mesenteric vascular occlusion. iii) abdominal dysfunction. b) Subjective examination. Charac. of pain and complaints. - absence of periodicity : it is longostanding and gradually lessens in prolonged inflation. - exact localization permanent pain. - pain intensifies with peristalsis. c) Objective examination. Inspection. Palpation. - increase of liver size. - hemorrhagic syndrome - arterial hypotension

Inspection - profusion of abdominal. - peristalsis and antiperistalsis movement. - derangement of conciousness and loss of orientation in time. - partial loss of memory. - disordered speech. - hallucination. - specific tremor (slow and fast) of upper and lower limbs. Palpation Pain, not mobile, hard, firm and enlargement in size of obstruction area of intestine gangling sound. e) Lab. Blood tests. - anemia - leukocytes - increase ESR - thrombocytopenia - dysproteinemia - increase bilirubin - increase AST - increase ALT 31.HEPATIC INSUFFICIENCY.COMA a)etiology and pathogenesis -despite considerable compensatory capacity of the liver ,its numerous and and very important functions can be disturbed due to disorder in hepatocytes. -hepatic insufficiency is explained by various complicated metabolic disorder in the liver,upset bile secretory & excretory function and impaired detoxicating function of the liver. -substance like chemical (phosphorus compound,arsenic)large doses of alcohol,viruses,tumor,mushroom poisons,non detoxicted product of intestinal bacteria protein, -acute hepatic insufficiency arises in form of virus hepatitis and poising with hepatotropic -chronic hepatic insufficiency develops in many chronic disease of the liver. -pathogenesis of the hepatic come is manifested by grave self-poisoning of the body due to complete dysfunction of the liver b)clinical stages -the are 3 stages distinguished 1.early compensated stage-the clinical symptom are absent during early stages of the hepatic insufficiency but bodys tolerance to alcohol and other toxic substance is also decreased 2.pronounced decompensate-signs are mild,poor appetite,increased weakness in usual physical exertionfrequent dyspepsia(poor tolerance of the fat food)meteorism,rumbling and painin the abdomen and changed stool.

3.terminal dystrophic stage that end in hepatic come and death. c)subjective examination -posture-restless posture in right hypochondria there is hyper pigmentation tiger skin -abdominal swelling-accumulation of the fluid in the abdominal @ascites factors contributing-high liver venous Pressure @portal hypertension, liver cirrhosis. -low serum oncotic pressure,hypoalbuninemia,secondary to hepatic failure -changes in the feces-pale /dark -pale:due to lack of stercobilin &urobilinogen in intestinal lumen in i)decrease in liver disorder associated with cholestasis,bile out flow decreased/not stopped (partial obstruction of the bile) ii)stopped:in complete bile tract obstruction -dark color of the feces due: hemolytic anemia-fecal stercobilin excursion -urine changes:beer like brownish (conjugated bilirubin in cholestasis/bile duct obstruction --pruritus, itching (cholestasis ,intensive at night) -hemorrhagic (nasal bleeding ,ecchymosed), hematuria,coagulation disturbance,impa -jaudice.Presence of flapping tremor.Dead mice odor d)objective examination -inspection ascites with dilated periumbilical veins @ caput medusa (distended collateral veins due to anastomoses of the superior and inferior vena cava. -frog belly abdomen due to fluid collection -palpation-in normal liver has soft and smooth edges . -In pathology 1.soft sharp & smooth of enlarged liver in acute hepatitis, fatty infiltration, liver congestion(right ventricle failure),early biliary obstruction. 2.cirrhotic edge is firm, blunt & irregular(individual cirrhotic nodules palpable in late fibrotic stages of cirrhosis percussion -in normal the size (9 + -normally in the 5th intercostals(upper border in mid clavicular line) -increased of the size due to the (lung atelectasis ,in ascites,flatulence,pnemosclerosis ,hepatitis,fatty infiltration and tumor) -decreased size (hepatitis,necrosis,hepatic cirrhosis) auscultation -friction rub over right costal arch(friction rub in neoplastic disease/abscess,friction fub in left costal arch at left ant.axi.line,splenic friction rub in spleen infarction. e)laboratory blood tests -decreased substance produced by the liver albumin,cholesterol,fibrinogen,blood platlet count, -endocrine disorders-disturbances in hormone secretion(gynaemastia)

-accumulation of bilirubin glucuronide in the blood. -moderate anaemia -leucocytosis increased ESR -increased bilirubin increased nitrogen and ammonia hyponatremia and hypokaliaemia

32. Peptic ulcer a) definition. Etiology. Pathogenesis Definition = grp of ulcerative disorder of upper GIT involving principally the most prox portion of duodenum and the stomach which have in common the participation of acid-pepsin in pathogenesis - risk factor and provoking factors -male -1 relative with duodenal ulcer -Helicobacter pylori -genetic markers -stress, smokers -Alcohol liver cirrhosis -Zollinger-Ellison syndrome -Chronic renal failure -COPD -Drugs eg NSAIDs, aspirin - pathogenesis : an imbalance btwn aggressive and defensive forceinitial damage to defensive mucousal barrier fr H.pylori infection,NSAIDsfacilitation acid&pepsin damaging factor aggressive factor break defensive mucousal barrieracid-pepsin cause destruction & ulceration b) classification - acc sites of peptic ulcer 1 duodenum 90-95% 2 stomach mostly in lesser curvature 3 esophagus fr reflux esophagitis 4 jejunum Zollinger-Ellison syndrome 5 Meckels diverticulum ectopic gastric mucosa

- acc penetration of mucosa 1 acute / erosive gastritis Cushings ulcer 2 chronic c) subjective exam Pain Vomiting d) obj exam -Wasting -Pallid skin and mucosa ( after hemorrhage ) -Clean or white coated tongue -Normal abdomen configuration -Possible brown pigmentation of abd skin -Pyloric stenosis -Local strained m ( Mendels sign ) -Late splashing sound e) complications. Investigations - complication Hemorrhage, occult bleeding Perforation Penetration beyond the duodenal wall into other struc eg pancreas Pyloric obstruction - investigation Endoscopy with biopsy for presence of H.pylori or malignancy Ba meal Provement of H.pylori Invasive test ( rapid urease test, microb test, histology ) Non-invasive test ( urea breath test, serological test ) 33. Acute & chronic gastritis a)classification. i)chronic gastritis- there is no universally accepted classification of gastritis. S.Ryss proposed a classification based on 4 principles: a)etiological(exogenous & endogenous) b)morphological c)functional(chronic gastritis w preserve secretion & w secretory insuff. of various degree, up to achlorhydria. d)clinical(compensated chronic gastritis / remission phase, decompensated gastritis/exarcerbation phase). ii)acute gastritis a)catarral b)corrosive c)acute phegmonous. b)etio. And patho. -acute gastritis:i)ingestion of fatty course, poorly decomposed food of very cold or hot meals/alcoholic drinks. ii)prolonge taking of some medicines(salicylates,sulpha preparation, steroid hormones, iodine preparations).

iii)allergic reaction to some foods (fish/eggs). iv)various infectious diseases such as influenza, measles/scarlet fever. -chronic gastritis:i)all exogenous etiological factors responsible for acute gastritis. ii)reflex effects on the stomach fr pathologically changed organs(gallbladder,intestine, pancreas) iii)upset of hormone sys(affection of thyroid,pituitary adrenal glands) iv)chronic infections(TB, malaria, syphilis) v)chronic septic foci(tonsillitis,caries) vi)disordered metabolism(DM, obesity, gaut, renal failure) vii)secondary to diseases acconting for hypoxia of tissues(chronic circulatory insufficiency, cor pulmonale & uremia) patho:-disorders in the nervous, humoral, &hormonal mech.regulating the digesting function but the direct action of irritants on the gastric mucosa cannot be disregarded either. -autoallergic processes are important for maintaining the disease. c)subjective examination. -acute gastritis:i)lost of appetite, unpleasant taste in the mouth, nausea, &vomiting(1st w food remains & later w bile) ii)pressure, bulging & pain in epigastrium. iii)rise of tempterature w chills. -chronic gastritis:i)meteorism, rumbling sounds in the abdomen, constipation &diarrhoe. ii)pressure, pain & distension in the epigastrium(pain is dull & boring but smt becomes severe) d)objective examination general inspection. i)acute gastritis-pt is pale,pulse is accelerated,tongue coated & breath is faul. ii)chronic gastritis-some pt dont loss weight, while others loss weight, bcom flaccid & slow.Examination of abdomen, smt reveal inflation. Palpation. i)acute gastritis-palpation of the epigastria region is painful & stimulates nausea. ii)chronic gastritis-palpation of the epigastrium is in most cases painless. e)investigations. Laboratory i)acute gastritis-amount of excreted urine decreases,in persistant vomiting hemoglobin & erythrocyte count increase while the level of chlorides decrease. ii)chronic gastritis-acid secretion may remain normal or it may decrease, free hydrochloric acids may be absent fr the gastri juice.in neglected cases, secretion of pepsin is upset.

Instrumental i)acute gastritis-gastroscopy(reveals hyperemic mucousa coated by a thick layer of glassy mucous, hemorrhage & erosion may occur,morphological reconstruction of gastric mucosa complete by the end 2nd week). -X-ray (fails to reveal any changes in the relieve of gastric mucosa) ii)chronic gastritis-gastroscopy -X-ray.

34. Jaundice. a)Classification & reason. - Hemolytic jaundice-excessive distruction of erythrocyte in cells of reticulohisticocyte system(spleen,liver,bone). -Parenchymatous(hepatocellular)jaundice-damage of parenchymal cells by infections,toxic effections of liver &liver cirrhosis. -Obstructive jaundice- partial or complete bile duct distruction.Its due to obstruction by stone, compression of duct from outside as a cancer of stomach,cancer of major duodenal pupula. b)Subjective &objective examination. -Hemolytic jaundice- skin is lemon yellow & skin is itchy absent. - during objective examination, sometime enlargement of liver and spleen. - amount of unbound bilirubin in blood increase. - if absent in urine, urine is coloured due to increase stercobilin & increase in urobilinogen. -Parenchymatous jaundice- skin yellow & reddish,itching. - free bound bilirubin is increase in serum, free bilirubin increase, bound bilirubin increase, bound bilirubin increase in urine & bile

acids are found in urine &feces stercobilin decrease. -Obstructive jaundice- Skin & mucousa is yello colour. - later appear greenish-brown. - rapid fatigue, general weakness, adenoma, irritability,headache. c)Changes in the blood stream. - in hemolytic jaundice it is lemon colour skin, free bilirubin increase in blood. - in parenchymatous jaundice skin yellow, free bilirubin increase in blood. - in obstructive jaundice converted bilirubin increase. d)Changes in urine. - In hemolytic jaundice, dark urine & increase urobilin, bilirubin absent in urine. - In parenchymatous jaundice,dark urine,conjested bilirubin, bile acids. - In obstructive jaundice, dark urine, due to conjugated bilirubin not urobilin. e)Changes in the feces. - In hemolytic jaundice dark feces & urobilin increase. - In parenchymatous jaundice pale colour of feces & cercobilin decrease. - In obstructive jaundice pale colour faces, cercobilinogen decrease.

35)Endocrine system disease. a)Inquiry -Complains are increased excitability, interrupted and superficial breathing, impaired memory, hyperhidrosis, chills, blood rush to lack, increased thirst and considerable wasting. Doctor can notice foreigness, rapid movement, nasty speech, apathy, anaemnesis showing strong emotions, fear and psychic traumas. b)Physical examination. Inspection. -Face may be normal. -Examination of the thyroid gland may show enlargement of the thyroid gland. Height may be gigantism if > 195cm or dwarfism is less than 135. -Skin may be moist in hyperthyroidism, thickened in acromegaly, edema in hypothyroidism, atrophy of skin on femur and abdomen may be noticed, cholesterol deposition may also be found on the skin indicating increased chances of dm. -Hair growth of female pattern in men indicates eunochism. Male pattern of hair growth in female may show Cushing syndrome. Losing of hair may indicate myxedema. Subcutaneous fat may be uniformly distributed in thyrogenic obesity. If only on pelvic region it is pituitary

obesity. Excess fat on face and trunk indicates Henko-Cassing syndrome. Excess wasting leads to diabetes mellitus. Muscle-tonic convulsions if affection of parathyroid. Palpation -Palpation assesses the density of the organ, the character of its surface,presence of nodes. -pt make swallowing movement:-tyroid w larynx move btw examiners thumb. -reveal presence or absence of pulsation,tenderness. -thyroid isthmus palpated by sliding movements of examining fingers in the direction of the sternal manubrium. Percussion - can reveal a retrosternal struma (goiter). Auscultation -Sounds are murmurs can be heard over the enlarged thyroid in patients with thyrotoxicosis. -These are explained by accelerated flow of blood & its intensified supply to the thyroid gland. c)Expression of faces. Hyperthyroidsm- exopthalmos, scarry expression on face. Hypothyroidism- eyes round and wrinkles present. Acromegalic face- abnormal nose, tongue, eyes, lower jaws and teeth. Pituitary hypofunction-is attended by obesity wh gives women,the expression of a males face. d)Diabetic coma. Symptoms. -toxic symptoms develop gradually and onset is preceeded by precursors. -General signs are excessive thirst,epigastric pain, headache, loss of appetite. 1st stage of diabetic coma develops nervous excitation, insomnia,convulsions, Kussmaul's breathing.2nd stage followed by marked inhibition of nervous system. Signs are dizziness, dry skin, face pink, or pale, decreased reflexes, eyeball tone decrease, pulse is low and fast and arterial pressure falls. Hypoglycemic coma. -Usually due to treatment by insulin in diabetes mellitus. -In the diet lack of carbohydrate. Or it is result of insulin overdosage. -Normally preceeded by sudden tremor of hands, weakness, sweating, tremor affecting the body too, pallor and moist skin,muscular tone and tendon reflexes, convulsions, pupils are dilated and eyeball reflexes form. e)Laboratory test Blood test shows decreased blood sugar. In urine sugar and acetone absent- Hypoglycemia In Hyperglycemia- high blood sugar, acetone and sugar may be present in urine.

28.chronic hepatitis. a) Etiology. - any hepatitis lasting for 6 months or longer is called chronic hepatitis. - infectious- hepatitis B virus, Hepatitis C, Brucellosis, TB, Siphylis. - toxic facious- caused by medicomental, domestic & food poisoning by toxic substances such as parasitamol, antituberculous drug, methyl dopamine, erythromycin. -autoimmune factors - hereditary factors - metabolic disorders like fat, vitamin, protein difficiency. b)pathogenesis. - 3 types of hepatitis: i) Chronic non active characterized by inflammation in peripheral zone, preservation or lobular structure &moderate dystrophic changes in hepatocytes. ii)active hepatitis inflammation extends from periportal zones inside or liver lobules called parenchymal hepatitis, hepatocyte are extensively necrotized&fibrosis is formed in liver. iii)Cholestatic hepatitis characterized by marked affection of bile duct, cholangitis & signs of cholesteris. c)subjective examination.

- Chronic non active hepatitis- upper abdominal discomfort, fatigue, anorexia, bitter taste in mouth, eructation. - Chronic active hepatitis weakness, loss of weight, fever, lost of appetite due to dyspepsia, meturism. - Cholestatic sign jaundice, nasal bleeding, pain in hyperchondrium radiates in back & scapula region, feeling of heaviness in right hyperchondrium. d)objective examination. -Chronic non active hepatitis liver enlargement, slight tenderness. - enlargement of spleen. - jaundice is usually absent - maybe asymptomatic recognized by biochemical test. -Chronic active hepatitis recurrent jaundice, liver enlargement, spleen enlargement, bradycardia & hypotension due to vagus nerve stimulation. - Cholestatic hepatitis subfibrile temperature, anemia. e)Laboratory test. - Chronic non active hepatitis plasma bilirubin is normal, plasma aminotransterase moderately rise, alkaline prophate, albumin, globulin is normal. - Chronic active hepatitis anemia, thrombocytopenia due to increase activity of spleen.ESR level increase, hyperbilirubinemia, aminotransferase increase.Plasma globulin increase, alkaline phosphate increase, prothrombin time is low. - Cholinesterase hepatitis anemia due to malabsorption or vit. B12/ folic acid & iron.Anemia is partially due to hemolysis caused by hyperspleenolism.ESR increase, leucopenia, thrombocytopenia,syndrome or hepatocyte insufficiency.Liver inflammatory syndrome,syndrome of chlolestasis.iron increase significantly.