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Clinical syndrome with gross proteinuria and hypoalbuminaemia.
Oedema and hyperlipaemia is severe.
Hypertension might be developed.
Children disease – ‘idiopathic’

Pathology
4 different types depend on appearance.
Some with minimal changes, some with grater changes.
80% cases are minimal change – response to treatment.

Clinical features
Preschool chid
Oedema – swelling in face, leg and abdomen.
Ascites
Protein urea – heavy.
Hypertension might develop later.

Biochemical features
Reduction of total serum protein
Main reduction is albumin.
Reduction of gamma globulin.
High serum cholesterol.

Progress
Most recover completely.
Some might get relapses.
Might develop to renal failure.
Infection - due to low gamma globulin.

Treatment
Steroids – prednisolone for long duration.
At the beginning fluid intake can be reduced with low sodium intake.
Increase protein intake.
Relapses are common.
Careful about side effect of steroids.
Immunosuppressive drugs.

Pathogenesis
Bacterial – from own bowel flora.
Mainly transurethral passage.
Some associate factor help to UTI
Poor personal hygiene, local infection (vaginitis).
Facilitated by catheterization, sexual intercourse.
Short female urethra compare to male. (Prostatic fluid has defensive bactericidal properties).
Bladder defence mechanism is main protection - Low flow rate and poor bladder emptying predispose to infection.
After bacteria establish in the bladder – spread to ureters and kidney is easy.
Bacteria can come – blood, lymphatics, vesicocolic fistula.
Clinical
At least 50% woman experience an episode of cystitis at some time in the life.
Most are single or isolated attacks.
Depend on functionally normal urinary tract or abnormal – recurrent rare in normal tract.
Stones, obstruction, polycystic kidney, vasico-ureteric reflux, diseases like DM – make complicated UTI.

Symptom and signs
Mainly with lower UTI (bladder & urethral infection)
Increase frequency of micturition.
Painful voiding – dysuria
Suprapubic pain and tenderness.
Haematuria
Smelly urine.
Loin pain and tenderness, fever, systemic symptom – suggest upper UTI.
Symptom and signs
Childers – possibility of UTI with all fever, fails to thrive.
Urethral syndrome –
Frequency, dysuria,
50% symptomatic woman with no bacteriuria.
Can be – postcoital bladder trauma, vaginitis, atrophic vaginitis, interstitial cystitis (Inflammatory ulcer in the bladder), irritable bladder.
Diagnosis
Culture of clean catch, mid stream urine. How to collect sample ??
Need refrigerated to prevent organism growth.
Excretion urography – Female if two or more attack, but male and child in first attack.

Treatment
Single isolated attack
If symptoms are sever - antibiotic before culture report.
Increase fluid intake.
If severely ill and suspect acute pyelonephritis – IV antibiotics.
Repeat culture after treatment – exclude relapse and reinfection.
Chronic pyelonephritis
Chronic nfection in kidney.
Results of vesicoureteric reflux, infection in infancy or early childhood.
Normally urine in the bladder don’t go up – value mechanism.
If value not work – reflux urine with bladder empting.
Infection damage – papillary damage, interstitial nephritis, cortical scarring.

Chronic pyelonephritis
If started in childhood – can be progressive renal fibrosis even no further infection.
Doesn’t begin with adult life.
Doesn’t occur if there is not reflux.
Diagnosis – excretion urography – clubbed calyces, irregular renal outline.
Can lead to hypertension and renal failure in later life.
How to collect urine sample
Female
Bladder should full
Labia separate using left hand
Vulva clean front to back with sterile swab (not antiseptics, no soap)
Start urination, when half done, without stopping container hold to stream.
How to collect urine sample
Male
Bladder should full
Foreskin retract
Gland penis clean front to back with sterile swab (not antiseptics, no soap)
Start urination, when half done, without stopping container hold to stream.

Acute cholecystits – Clinical
Severe pain
Vomiting
Mild jaundice in some case.
Investigation – AP, serum bilirubin, ultrasound, Xray,
Treatment
Conservative management
Nil by mouth, IV fluid, antibiotic,
Liver abscess
Pyogenic abscess
Cause not know
Can be single or several abscess
Common in elderly.
Can be with fever, abdominal pain..etc
May be not ill and last for days.
Management – aspiration with under ultrasound and antibiotics.
Liver abscess
Amoebic abscess
Entamoeba histolytica
Gradual onset – fever, anorexia, weight loss.
Treatment – aspiration, metronidazole.

Acute pancreatitis
Chronic pancreatitis – absence of continuing inflammation with irreversible changes.

Acute Pancreatitis
Acute abdominal pain with raised pancreatic enzyme.
Pathogenesis
Pancreatic necrosis
Associate with gall stone.
Autodigestion of pancreas.
Can be haemorrhage.
Oedema and exudates.
Acute Pancreatitis –clinical features
Abdominal pain – epigastrium or upper abdomen.
Severe pain with abdominal rigidity.
Nausea and vomiting.
Severe case – multisystem failure.

Acute Pancreatitis –Investigation
Increase serum amylase – 5 times than normal.
Abdominal xray.
Ultrasound.
Exploratory laparotomy might need.
Acute Pancreatitis – Treatment
Nasogastric suction might need
No feeding, only IV nutrition.
Analgesia.
No special treatment.
Acute Pancreatitis – Complication
Pancreatic abscesses – secondary infection.
Pseudocysts – usually not required treatment.

Chronic pancreatitis
Continuing inflammatory disease, irreversible morphological changes, permanent impairment of function.
Cause – alcohol >85% cases.
Fibrosis and calcification of pancreatic acinar.
Not reversible but will arrest.
Risk factors – smoking, low protein and high fat diet.
Chronic pancreatitis - clinical features
Pain – continuing episodes
Episodes might precipitated by heavy alcohol drink.
Steatorrhoea – reduced lipase.

Chronic pancreatitis - Investigation
Ultrasound
CT
Xray – calcification can be seen

Chronic pancreatitis - Treatment
Stop drinking
Analgesics
Surgery – case with severe pain.
Diabetes might need to treat.
Steatorrhoea – low fat diet.
Acute cholecystits
Inflammation of gallbladder.
Associated with gallstone.
Inflammation is sterile, but soon gut organisms cultured.
Can be mild
Can be severe with localized peritonitis.

Obstructive jaundice (extrahepatic cholestasis)
Stones, tumour in the biliary tract, pancreatic head tumour.
Increase conjugated bilirubin.
No/less urobilinogen
Stool became clay colour.
Significant amount of conjugated bilirubin in urine.

Clinical features
Other features help to diagnosis
Hepatomegaly –hepatitis, malignancy,
Splenomegaly – portal hypertension
Ascites – cirrhosis, carcinoma.
Palpable gallbladder – carcinoma obstructing bile duct.

Investigation
Jaundice is not a diagnosis, but sign so need investigation.
Viral markers -
Ultrasound – extrahepatic obstructions.
Liver biochemistry – AST (aspartate amino transferase, AP (alkaline phosphatase)
Haematological test – Haemolytic jaundice.
Other test – alpha fetoprotein in hepatocellular carcinoma.

Red blood cells normally live for 120 days.
Some diseases cause premature breakdown of red blood cells.
At the end, cell is too fragile.
Cell membrane rupture.
Destroyed by macrophages in the spleen and bone marrow – Reticuloendothelial system.

What is haemolysis?
Haemoglobin splits and globin and heme release.
Heme consists of four pyrrole rings.
Heme ring open and release pyrrole rings.
Pyrrole will under go several reaction and bilirubin form.
Conjugated bilirubin turn to urobilinogen by bacteria in the intestine.
Excrete via stool.
Urobilinogen can be reabsorbed to blood.
5% excrete via urine.

Urobilinogen turn to urobilin by oxidization when expose to air.
Stercobilinogen turn to stercobilin by oxidization when expose to air.
Jaundice
Excess bilirubin in the extracellular fluid.
Detectable when the serum bilirubin >30-60 µmol/letter.

Haemolysis
increase unconjugated bilirubin in plasma.
Urobilinogen increase

Intrahepatic cholestasis
acute and chronic liver diseases including cirrhosis, hepatitis, drugs,
increase in both type bilirubins

Congenital hyperbilirubinaemias
Glibert’s syndrome
common type
2-5% of population with mild increase unconjugated bilirubin.
Asymptomatic
Crigler-Najjar syndrome
rare
Problem of conjugation
Increase unconjugated bilirubin.
Dubin-johnson syndrome
Defect in bilirubin handling.
Increase conjugated bilirubin.

Fluid & electrolyte loss to lumen.
Severe vomiting
Can lead to toxaemia

Intestinal Obstruction - clinical features.
Abdominal pain – colicky pain, around umbilical (s. intestinal), below umbilical (l. intestinal).
Vomiting – early in high obstruction, can be brown.
Constipation
Abdominal distension.
Increase bowel sound.
Might be features of dehydration.
Intestinal Obstruction- investigation
Xray – might see distended bowel loops.

Intestinal Obstruction- Treatment
Primary
Nasogastric aspiration
IV fluid
Surgical
Depend on cause.
Conservative treatment
Simple obstruction with adhesions will response.

Peritonitis
Acute infection of peritoneum.
Cause
Perforation of intestinal tract (common cause)
appendicitis
peptic ulcer.
Malignance.
Salphingitis eg. Gonorrhoea
Ruptured ectopic gestation can infect.
After abdominal surgery.

Peritonitis
Can be localized with pockets of pus or abscesses.
Generalized involved whole peritoneum.
Can lead to
paralytic ileus.
Toxaemia.
Dehydration – move fluid and electrolytes into the paralyed bowel.
In later stages – adhesion formation and intestinal obstructions.
Peritonitis – Clinical features
Abdominal pain.
Vomiting with brown intestinal fluid.
Fever.
Tender abdomen with diminish bowel sounds.
Slight abdominal distension.
If sever paralytic illus – no bowel sounds.
Peritonitis - Treatments
Remove the cause of infection.
Preoperative treatment – antibiotics, gastric suction, IV fluid.
Surgical treatment depend on cause.
Paralytic ileus – withhold fluid, aspiration of stomach content, fluid and electrolytes.
Paralytic ileus - few days to recover.
Intestinal Obstruction
Small or large intestine.
Mechanical or functional.
Obstruction - foreign body, gallstone, malignant growth, neck of a hernial sac.
Several types
Simple
Strangulation
Close loop