Year2 Sem1 PPP2 renal patho Flashcards
Diagnostic Tools for renal system (Urine)
Dipstick (Rapid Urine Test), Urinalysis, Urine culture and sensitivity (C/ST), 24-hour-urine for Creatinine Clearance (CrCl), 24-hour-urine for Protein, Urine Cytology Test, Residual urine
Substances can be checked by urine dipstick test
Normal range:
pH value (5-7)
Negative:
Protein, Sugar, Nitrate, Ketone, Bilirubin, Urobilinogen, Red blood cells
(erythrocytes), White blood cells
(Leukocytes)
3 steps of urinalysis:
- Assessment of color, cloudiness and
concentration of the urine - Chemical composition examination using a test strip
- Examination under a microscope to look for bacteria, cells and parts of cells
24-hour-urine for Creatinine Clearance
(CrCl)
◦ Collecting urine over 24 hours
◦ Creatinine (Cr) is a waste product of protein
breakdown
◦ Clearance of Cr by kidneys approximates the Glomerular Filtration Rate (GFR)
Procedure
First urine sample after waking up is NOT used, but the time of urination is noted and documented
From then on, EVERY SINGLE DROP of urine is collected and saved in a container for the next 24 hours
Blood test for assessing renal system
Blood urea nitrogen (BUN)
Creatinine (Cr)
BUN/ Creatinine ratio
Uric Acid
Sodium (Na)
Potassium (K)
Calcium (Ca)
Phosphorus
Bicarbonate (HCO3)
Radiology tools in renal system
Kidneys, Ureters, Bladder (KUB) X-ray
Intravenous Pyelogram (IVP)
Renal arteriogram
Renal Ultrasound
Computed Tomography Scan (CT Urogram)
Magnetic Resonance Imaging (MRI)
Key Differences in uses
KUB X-ray: Quick assessment, best for stones and calcifications.
IVP: Focused on urinary tract function and obstructions, using contrast.
Renal Arteriogram: Detailed vascular imaging for blood supply issues.
Renal Ultrasound: Non-invasive, assesses structure and blood flow, no radiation.
CT Urogram: Detailed anatomical imaging, excellent for stones and tumors.
MRI: Superior soft tissue detail, useful for masses and vascular evaluation without radiation.
Signs and Symptoms (S/S) of Polycystic Kidney Disease
◦ Haematuria
◦ Polyuria
◦ Flank & Abdominal pain
◦ High blood pressure
Pathophysiology of Polycystic Kidney Disease
◦ Genetic Disorder: Mutations in one of two genes, PKD1 or PKD2, account for most cases of autosomal dominant PKD
◦ Renal tubules become structurally abnormal, resulting in the development and growth of multiple cysts within the kidney
Diagnosis of Polycystic Kidney Disease
◦ S/S
◦ History (Hx)– Family Hx, Medical Hx
◦ Urinalysis
◦ USG/ CT/ MRI
Treatment of Polycystic Kidney Disease
- Supportive
✓ Dietary restriction
➢ Low salt diet – reduce hypertension
➢ Diet with Vit B3 to slow down rate of creatinine production - Antibiotics (if infection)
- Surgical Nephrectomy
- Percutaneous or surgical drainage of the cyst
✓ Not frequently necessary and hard to perform, as difficult to ascertain radiologically which of the many cysts is infected
✓ +/- Drainage: for a perinephric abscess (diagnosed by ultrasonography or computed tomography (CT) scan) - Renal replacement therapy (RRT)
✓ Refers to therapies to replace kidney function temporarily
e.g. Peritoneal Dialysis, Haemodialysis
✓ Treat end-stage kidney disease/ ESRF
Pathophysiology of nephritic syndrome
Mostly autoimmune
➢ A number of biological processes (e.g. Complement activation, Leukocyte recruitment, Release of growth factors and cytokines) → Result in glomerular inflammation and injury
➢ Capillaries swelling → ↑ permeability → inappropriate contents (e.g. blood and proteins, etc.) begin to spill into the urine
➢ ↓ GFR → Uremic symptoms, retention of sodium and water in the body → Edema and hypertension
S/s of nephritic syndrome
➢ Proteinuria
➢ Hematuria
➢ Oliguria (<400mL/ day)
➢ Severe: Uremic symptoms
Diagnosis of nephritis syndrome
Physical examination
Lab test: GFR, BUN, Urinalysis
Renal biopsy
Treatment goal and treatment for nephritic syndrome
◦ Goal
1. Control hypertension
2. ↓ Active inflammation of kidneys
3. Prevent recurrence and CKD
Treatment:
◦ Bed rest
◦ Fluid restriction - ↓ edema
◦ Diet control - ↓ Na, K
◦ Drugs – diuretics, anti-HT, anti-inflammatory (e.g. steroids, NSAIDs)
◦ Dialysis – AKI/ end-organ damage
Pathophysiology of glomerulonephritis
◦ Inflammation of the glomerular capillary membrane
◦ The damaged glomeruli cannot effectively filter waste
products and excess water from the bloodstream to make urine
◦ The kidneys appear enlarged, fatty, and congested