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.
Hereditary nephropathies.
BM appearance in both?
What is Alport syndrome associated with?
Give two that can cause RPGN.
Alport - abnormally split and laminated
Thin in BFM
Leiomyomatosis
Good pastures
ANCA vasculitis
Post-streptococcal
SLE
ANCA vasculitis.
Name three types.
ENT symptoms GPA
Ages affected by GPA
Other symptoms?
Granulomatosis with polyangitit s
Microscopic polyangitis
Churg-Strauss disease (Eosinophillic granulomatosis with polangitis)
Chronic sinusitis
Rhinitis
Nose bleeds.
All ages.
Non-age specific - arthralgia, myalgia, fatigue, weight loss
Eye - conjunctivitis, episcleritis, uveitis.
SLE.
Syndrome?
Can be both.
LUTI.
Give three types.
Give two reasons why UTI risk is higher in women.
Pain where?
Why might nitrites not be seen?
What are we looking for in urine culture?
If Pyuria with negative urine culture then what?
Bacterial and abacterial cystitis
Prostatitis
Shorter urethra
PM - less estrogen -> loss of protective vaginal flora
Suprapubic
If gram positive bacteria is causative organism as they do not convert nitrates to nitrites
Atleast 100,000 CFUs/mL
Sterile pyuria (urethritis)
Upper UTI.
Give two types
Name a risk factor for Upper UTI that isn’t for lower UTI.
Give a cause for this risk factor.
If UTI is suspected in neonate how is urine sample collected?
Treatment pyelonephritis?
Acute pyelonephritis
Chronic interstitial nephritis
Vesicoureteric reflux
Posterior urethral valves.
Suprapubic aspiration.
Co-amoxiclav, ciprofloxacin and gentamicin.
AKI - intra-renal
What two things are investigated to define stage of AKI?
Describe difference in urine biochemistry between ATN and pre-renal AKI.
What would you see on urine?
Give some endogenous nephrotoxins.
Give three investigations that should be carried out.
Give some indications for dialysis.
Urine output
Serum creatinine
Higher gravity - pre-renal
Higher osmolarity pre-renal
Lower urine sodium in pre-renal
Muddy brown casts (ATN Pathognomonic)
Myoglobin
Bilirubin
Urate.
Urine electrolytes
Urinalysis
Urine microscopy
High K+ Fluid overload refractory to diuretics Metabolic acidosis Uraemia Dialysable nephrotoxins presence
Ureteric obstruction.
Give three intramural causes.
Extrinsic?
What is pyonephrosis?
Chronic ureteric obstruction is usually painless except in which case?
In which cases might you see hydronephrosis without obstruction?
What functional test can be done to diagnose upper tract obstruction?
TCC
Strictures
PUJO
Locally advanced prostate cancer
Retroperitoneal mets
Retroperitoneal fibrosis
Direct obstructio
Obstruction (stones) pluses superimposed infection leading to pus building up in the kidneys collecting system.
PUJO
VUR and pregnancy
Diuretic renography
PUJO.
Why intermittent pain?
Surgical Tx?
Pain where?
Sudden fluid intakes - pelvis dilates - blood vessel above the pelvis kinks and this leads to a sudden episode of pain.
Pyeloplasty
Loin pain
Retroperitoneal fibrosis.
Ureteric position?
Treatments?
Causes?
Becomes more medial (pipestem ureters)
Ureteric stunting
Steroids
Azathioprine
Ureterolysis
Idiopathic Peri-aortitis Autoimmune Drug indicted Malignancies (breast, lung lymphoma)
Infravesicle obstruction.
Give differences in the symptoms between Acute and Chronic retention.
Give some causes in women?
What do you need to watch out for after chornic retendtion?
Acute retention treatment? Refractory to this?
Acute painful and cant void
Chornic painless - may still be able to void small amounts.
Urethral stenosis
Fibroids
Ovarian tumour
Postobstructive dieuresis leading to dehydrationand electrolyte imbalance.
Alpha blocker - TWOC if not then TURP.
Renal cell carcinoma.
Give specific signs.
Histology?
Risk factors.
What is removed other than the kidney, adrenal glands and surrounding fat in radical nephrectomy?
Why might it cause a pulmonary embolus?
Varicocele
Hypercalcaemia
+/- mass
Pulmonary embolus
Chicken wired appearance
Clear cytoplasm
Smoking
Obesity
Dialysis
Upper Ureter
Spread to the right atrium via the IVC
Bladder TCC.
Symptoms.
Risk factors.
What stage is it if it has not invaded through BM?
Difference between T2a and b?
T3?
T4?`
Lymphoedema
DVT
Renal colic
Phenacetin abuse
Smoking
Balkan’s nephropathy
Occupational exposure (plastics manufacture - arylamines)
Ta Tis
2a - muscle wall 1/2 way
2b - 2nd half og the muscle
Perivesicle fat
Prostate
Prostate cancer.
Risk factors.
Why should it not be screened for?
If picked up on elevated PSA and DRE?
IF on LUTS?
What grading system?
Why might LHRH be used?
Increasing age
BRCA2
Family history - first degree relatives
Black > white > Adrian
Overdiagnosis
Overtreatment
QoL affected due to co-morbidities of established treatments.
Transurethral US guided biopsy of the prostate
TURP.
Gleason.
Medical castration in met CaP
Alongside chemotherapy and possible surgical castration.
ADPKD.
Genes involved? Which one more involved in earlier disease and ESRD?
ADPKD?
Secondary complications?
What will often be seenrpior to renal function change?
2 things predisposed to?
PKD1-2 (3)?
PKD1
Newborns affected - 30% death rate.
Pain due to bleeding into cysts
Infection
Renal stone due to stasis
Increased diastolic pressure - hypertension
Heart valve abnormalities
Intra-cranial abnormalities.
CKD.
What two things are considered in the staging?
Histology?
Give a cancer associated?
Give some symptoms of uraemia.
How do you treat the acidosis associated?
Give some reasons for anaemia.
Give three please calcium can deposit.
Albuminuria and GFR
Glomerular sclerosis
Fibrotic cortex
Arteriole thickening
Thyroidisation
Myeloma.
n/V loss of appetite Asterixis Encephalopathy - coma Pericarditis Bleeding Uraemic frost Uraemic fetor
NaHCO3 tablets
Decreased EPO Iron deficiency (functional and absolute) Vit B12 and folate deficiency ACEi meds Store RBC lifespan Bone marrow supression due to uraemia
Joints, calciphylaxis and aorta
Haemo dialysis.
Contraindications
Complications.
Peritoneal dialysis.
Contraindications.
Complications.
Failed vascular access
Heart failure
Coagulopathies
Infection
Thrombosis
Steal syndrome
Adhesions
Peritoneal membrane failure
Patient or carer unavle to connect and disconnect
Obese or large muscle mass to relatively small peritoneal size
Peritonitis
Hernia development.
Refeeding Syndrome.
Pathophysiology
Already low magnesium levels
