Conditions Flashcards
Developmental Pathologies.
Renal agenesis Pathophysiology?
Horseshoe kidney?
Duplication defects?
Where will it lie?
Ureteric bud fails to interact with intermediate mesoderm
Inferior poles fuse
Splitting of the ureteric bud.
Pelvic region - does not ascend
GFR.
What is the normal GFR?
During pregnancy how much does GFR increase by?
Why is inulin not used to calculate GFR?
Is creatinine an overestimate or underestimate of GFR?
2 draw backs?
Give 3 factors that can increase creatinine?
Why is eGFR less accuracy in mild kidney injury?
90-120ml/min/1.72m^2
(140-180L/day)
~50%
Requires continous I i infusion to maintain a steady stat e
Requires catheter and timed urine collections.
Overestimate
Overestimate
Requires 24 hour uterine collection and Hereford need to carry a bottle around of urine lol
Male
Black
Creatine supplements
Meat
Mild injury - nephron hypertrophy so may not show decline in GFR
Reduced filtration due to low GFR means more secretion due to increased serum creatinine levels.
Diabetes insipidus.
GIve two tests that can be done?
Water deprivation
Vasopressin stimulation test
Central pontine myelinolysis.
Symptoms.
Why does it occur?
Diplopia Dysarthria Dysphagia Acute paralysis Loss of consciousness
Rapid correction of hyponatremia
Hyponatremia.
Give two causes of hypertosmotic hyponatremia?
Once hyponatremia is confirmed what tests should be done?
The final one of these tests should be done to confirm what?
Give some causes of hypovolemic hyponatremia.
Mannitol
Hyperglycaemia
Osmolarity
Fluid status
Urine sodium
Whether the cause of the hyponatremia is due to the kidneys or not.
If urine Na+ is high then - kidney problem
If urine osmolarity is low - means the issue is else where due to osmolarity being low just as it is in blood.
GI losses (V/D, pancreatitis and fistulas)
Excessive sweating
third spacing of fluids
Cerebral salt wasting syndrome
Hyperkalemia.
Give a GI manifestation.
Hypokalemia.
Give a renal manifestation.
Treatment?
Ileus
Nephrogenic DI
Potassium replacement
Urodynamic studies.
What two parts can these studies be divided into?
How do you calculate detrusor pressure?
What does Qmax measure and what shape should it be? Different shape to this would indicate what?
Using urethral closure pressure and physical contraction pressure describe how stress incontinence might occur.
Voiding (voiding pressure flow study)
Filling and storage phase (cystometrogram)
Abdominal pressure - bladder pressure
Voiding rate
Bell shaped curve.
Obstruction to flow.
If the pressure when the spontaneous physical contractions occur is close to closing pressure of the urethra that means small increases in abdominal pressure will lead to leakage. The bladder is classified as unstable.
UI.
Give some risk factors.
Conservative management?
Refractory to this?
Acute cause?
Pregnancy Pelvic floor prolapse Menopause UTI AGe Obesity Intraabdominal pressure increased
Fluid intake modification Stop smoking Lose weight Less caffiene Avoid constipation Timed voiding
Indwelling catheters
Incontinence pads
Sheath device
Delirium
Stool impaction
UTIs
Stress urinary incontinence.
Main cause in men?
Women?
Investigations?
What would be seen on urodynamic testing?
Management?
TURP
Pad test
Cough test
Q tip test (hypermobility of the sphincter)
Urodynamic testing
Low static urethral pressure
PFMT (kegel excercises)
Duloxetine
Urge urinary incontinence.
Causes?
Treatment?
Difference between this and OABS?\
Surgical?
Bladder irritation (cystitis, stones and cancer) Loss of bladder inhibition (Parkinson’s stroke and spinal cord injury)
Bladder training
Anticholinergics (oxybutynin)
Mirabegron
Intravesicle injection of botulinum
You may not actually lose bladder control in OABS.
Sacral nerve augmentation
Augmentation cystoplasty
Minimal change glomerulonephritis.
Syndrome associated?
Age of onset?
What is seen on electron microscopy?
Treatment?
Nephrotic syndrome (due to albumin loss)
Early childhood and adolescence.
Podocyte foot process effacement.
Steroids - responds well to steroids.
Focal segmental glomerulosclerosis.
Syndrome?
Give three causes of secondary FSGS.
What will you see on histology?
More or less responsive than minimal change disease to steroids?
Progression to renal failure?
People affected?
Nephrotic.
Sickle cell disease
Heroin
HIV-associated nephropathy
Segmental sclerosis and hyalanosis
Less responsive
Can progress
Children and adults (Hispanics and afrocarribeans)
Membranous glomerulonephritis.
Two autoantibodies involved?
Typically affects?
What can it occur secondary?
Steroid use?
PLA2-R
Neutral endopeptidase
Caucasian adults.
Lymphoma
Mixed results.
Diabetic nephropathy.
Why does the glomerular pressure increase?
Why does mesangial expansion occur?
What two things need to be tightly controlled?
4 histopath changes.
What are the clinical stages?
Risk factors.
What reversal can tight glucose control lead to?
Hyaline arteriosclerosis drew to glycation of the basement membrane of the efferent arterioles.
Dilation of the afferent arteriole also occurs.
To support the increased pressure the mesangial cells secrete more matrix
Hypertension and hyperglycaemia
Mesangial expansion
GBM thickening
Glomerular sclerosis
Kimmelstierl Wilson nodules.
Hyperfiltration Latent Microalbuminuria Overt proteinuria ESRD
Hyperglycaemia Hypertension Genetic susceptibility (if first degree relative who also has it) Increased age Smoking
Reversal of initial hyperfiltration
Can delay. The microalbumin urea
IgA nephropathy.
Name another condition in which IgA is deposited around the body?
How can you distinguish between this and post-streptococcal GN?
Where is the deposition?
Henoch–Schönlein Purpura (IgA vasculitis)
Symptoms present a few days post URTI.
In the mesangium.
