UG I Flashcards
(22 cards)
Name Congenital Diseases of Kidneys
Size - Hypoplastic/Dysplastic; Polycystic
Shape - Horseshoe, fusion of poles
Number - agenesis - failure of ureteral BUD development
Location - displacement; leads to ureter kinking
Brief description of Kidney Embrology
Metanephric Primordium + contacting Ureteral Bud
Metanephros - permanent kidney
Horseshoe Kidney Cx
Drainage impaired - UTI + Calculi
Name Inherited Cystic Diseases [2]
- associations?
Polycystic Renal Disease (AD, PKD1 PKD2 mutations)
- Cysts small @ childhood, enlarge into adulthood + new ones
- non-functioning tubules: CRF
- Kidney large, parenchymal compressed
- associated w aneuryms, cos global gene
- Cx: Subarachnoid hemorrhage along w Aortic Coarctation
Cystic Renal Dysplasia
- abnormal differentiation of metanephros w primitive structures still present
- hence Histo: cartilage, islands of undifferentiated mesenchymal cells
Cystic Kidneys Gross Appearances, Histology
ENLARGED KIDNEY, Irregular, Cystic
Cysts lined by flattened epithelium
- Abdominal Distension
- Simple Cuboidal epithelium!
Urolithiasis causes
[6] secondary causes
Primary - Supersaturation, commonly calcium
Secondary
- Obstruction, foreign bodies
- Functional
- Squamous metaplasia - keratin; from Vit A deficiency
- UTI (nidus of formation)
- Low pH - Uric acid stones
- Infection - Triple stones
Types of Stones
Calcium
Triple Stones - Mg, NH4, PO4 - AKA Struvite AKA Infection stones
Uric Acid
When can calcium stones form
- Idiopathic and Non-idiopathic
When can Triple Stones and Uric Acid stones form
Whats the presentation of Triple Stones
- Hypercalcemia (blood) - 2nd to hyper PTH, Milk-Alkali
- Without hypercalcemia (blood): increased secretion, decreased reabsorption,
Triple: infection Proteus, urea splitting - Ammonia, high pH allowing precipitation
- present as Staghorn Calculi
- magnesium ammonium phosphate (MgNH4PO4 · 6H2O)
Uric Acid stones: Low pH
Categorize Kidney diseases [3]
- based on location + mode of damage
Acute Tubular Necrosis - Ischemia and Toxins
Acute Interstitial Nephritis/ Acute Tubulointerstitial Nephritis
- Toxins, Allergy, Drugs
- Most commonly DRUGS
Infective - Bacteria
- Acute Pyelonephritis
- Xanthogranolomatous Pyelonephritis
- unique w abscess, granulomatous abscess, foam cells
Effects of Stones
Urinary Stasis, Ulcers
- Pain, Infection, Fistula, Bleeding
What’s Acute Tubular Necrosis
Tubular epithelial death ONLY; Common cause of AKI
- independent of damage to glomeruli/cortical tissue
- Simple Cudoial!
AKI Phases
Oliguria - Tubular dead, no pee
Polyuria - Tubular regenerating, cannot concentrate urine, GFR normal - high pee
Recovery - Tubular concentrate urine
What can cause ATN [2]:
Ischemic - note tubules v sensitive to hypoxia like brain
- hypotension, hypoperfusion of kidneys
Toxic
- myoglobin, haemoglobin
- drugs, metals, toxins
Histology of ATN:
Dilated Tubules, Flattened tubular epithelium
Mitosis, necrosis
- regeneration involves the flattened cells
Acute Interstitial Nephritis
Pathophysiology and Key features
Not caused by infections
DRUGS, allergic
- Eosinophilia! Infiltrate of inflammatory cells
- Type 4; AB, NSAIDs, Diuretics
Acute Pyelonephritis
Cause and Cx
Bacteria - retrograde from bladder
- hematogenous spread
Cx: abscess, sepsis, AKI
Chronic Pyelonephritis
Causes [2]
Histology
- impt!
Obstruction
Vesico-uterine reflux
Atropied, Dilated tubules
- thyrodisation of kidney w colloid-like hyaline cast of protein
- this is a pattern of tubule atrophy; w dilated tubule of flattened epithelium, w abundant protein
- chronic pyelonephritis and reflux nephropathy can see Thyrodisation of kidney
Whats Xanthogranulomatous pyelonephritis
Histology
Cause
Presentation
Xantho - golden - yellow
Foam Cells
Granulomatous - w high macrophage; giant cells,
Proteus infection
- Staghorn calculi
Mimics RCC due to enlarged nodules
Obstruction Causes [3 categories]
[3] sites of common stone obstruction
Acquired
- BPH, tumor, stones, clots, slough
Functional, Neurogenic
- functional means muscle cannot work;
Congenital abnormalities
- Urethral valves occur when a boy is born with extra flaps of tissue that have grown in his urethra, the tube through which urine exits the urinary tract.
- Pelvi-Ureteric Junction
- As ureter enters pelvis, crossing common iliac split
- Vesico-ureteric Junction
What is histology of UT
Simple Cuboidal - Kidney
Transitional - PELVIS Ureter, Bladder, 2/3 of Urethra
SSC - Distal 1/3 of urethra
Hydronephrosis Pathology Features
Enlarged kidneys Dilated pelvis, tubular spaces Tubular epithelium flattened Tubular atropy, fibrosis, Parachymal atropy, compressed - Thin rim
Distinct histological feature between
- acute and chronic pyelonephritis
Both have flattened epithelium, atrophied tubules
- chronic nephritis associated w Thyroidisation of tubules w colloid
