GU Flashcards
pyelonephritis what is is and where does it come from? (5 common organisms)
infection of renal parenchyma
UTI, ascending infection common organisms are: e. coli s. saprophyticus klebsiella proteus mirabilis candida
risk factors for pyelonephritis
Urinary obstruction immunocompromised history of previous pyelonephritis diabetes frequent sexual intercourse
pyelonephritis h and p
flank pain chills n/v urinary frequency dysuria urgency fever
these are systemic symptoms
labs will show: increased WBC increased ESR and CRP WBC casts in urine \+ urine cultures
Treat pyelonephritis
A few days of IV abx followed by outp PO abx
fluoroquinolones
aminoglycosides
3rd gen cephalosporins such as ceftriaxone
Complications of pyelonephritis in pregnancy
increased risk of
preterm birthweight
low birthweight
treat with ceftriaxone and avoid fluoroquinolones in pregnancy
Nephrolithiasis: Calcium oxalate stones
most common type
idiopathic
needs to hydrate well and minimize stone formation
Nephrolithiasis: struvite stones
contain ammonium, magnesium, phosphate
Associated with UTIs (esp proteus, klebsiella)
urease splits urea producing ammonium
staghorn stones
radio-opaque
nephrolithiasis: calcium phosphate stones
think of
- hyperparathyroidism
- renal tubular acidosis
nephrolithiasus: uric acid stones
not seen on plain xray
diagnose with constrasted study or CT
associated with gout and chemotherapy
Can be dissolved: alkalinize urine with potassium citrate or bicarbonate
Nephrolithiasis: cystine stones
hereditary form of stone in patients with cystinuria
risk factors for nephrolithiasis
- family history
- personal history (anyone with a stone has a 50% chance of developing another stone within the next 10 years)
- diabetes
- gout
- hypercalcemia
- hyperparathyroidism
- drugs: loop, thiazide, acetazolamide diuretics, and topiramate
nephrolithiasis h and p
acute, colicky, flank pain with radiation to ipsilateral lower quadrant
genital pain
hematuria
n/v
lower UTI symptoms (frequency, discomfort while voiding)
nephrolithiasis diagnosis
Plain film or KUB
non-contrast stone protocol CT abdomen/pelvis is the most sensitive and also picks up uric acid stones
US if pregnant Intravenous pyelography (IVP)
where do stones most commonly get stuck?
ureterovesical junction
renal colic versus peritonitis
patient with renal colic will be writhing around, can’t find a comfortable position
peritonitis patient tends to be rigid to avoid irritation associated with movement
What is the general treatment for calcium nephrolithiasis?
8-9mm stones are about 50% likely to pass
If in the proximal ureter, about 50% likely to pass.
If in the UVJ, about 80% likely to pass
Expectant management:
1. PAIN CONTROL (nsaids, opioids)
2, HYDRATION
3. TAMSULOSIN/NIFEDIPINE
Strain urine with strainer and bring stones to lab for analysis
Tamsulosin (relaxes stone in the distal ureter)
Nifedipine
Pain medications: NSAIDs (diclofenac), hydrocodone/acetaminophen PRN breakthrough pain
A repeat CT can be used to see if the stone has passed
Hospitalization by urology is required if…
- clinical complete obstruction (regardless of hydronephrosis on CT scan)
- unable to tolerate PO intake despite nausea meds
- intractable pain not able to be relieved with PO meds
- acutely elevated BUN or creatinine or anuria
- fever (sepsis), pyelonephritis, or urosepsis
Surgical treatment if…
- 10-20% of all kidney stones require surgical removal
- required if: unable to pass stone after 4-6 weeks, complete urinary obstruction, persistent infection, impairment of renal function
Extracorporeal shock wave lithotripsy (ESWL) for stones in renal pelvis or upper ureter
Ureter stones- ureteroscopy with possible lithotripsy and possible stone placement
staghorn calculi- percutaneous nephrolithotomy (PNL) for gigantor stones
Hematuria in a patient
idiopathic UTI kidney stones exercise trauma endometriosis in the bladder
persistent hematuria in a patient
glomerular disease
persistent hematuria in a patient 20-50yo
APKD
Neoplasm
Glomerular disease
Persistent hematuria in a patient >50yo
APKD
Neoplasm
Glomerular disease
BPH
What are the steps in evaluating hematuria?
Thorough physical exam, UA, CBC, chem 8, PSA (men over 40)
UA in women with hematuria should be via straight cath, or after perineum is cleansed and a tampon is placed in the vagina
CT scan abd/pelvis stone protocol (no contrast) to rule out renal stone
If CT stone protocol reveals no stones, then CT abd/pelvis with contrast and post- CT plain film KUB (equivalent to IVP) to view any radiopaque stones
If low suspicion of disease, consider treatment for UTI and f/u UA in 3-5 days
If smoker, over age 50, cyclophosphamide use, FHx or urinary tract cancer, or suspicious for cancer, then send urine for cytology and perform cystoscopy
If workup reveals no pathology, consider igA nephrology or thin basement membrane disease. Routinely (q6m) repeat UA and urine cytology, and consider f/u with renal sonogram and cystoscopy in 1 year
Hydronephrosis
dilation of renal calices as a result of increased pressure in the distal urinary tract
generally caused by urinary tract obstruction- kidney stones (Unilateral hydronephrosis)
BPH
Cancer
posterior urethral valves
H and P asymptomatic dull or intermittent flank pain history of UTI anuria
Radiology dilation of renal calyces -US -IVP -CT
Treatment
Drainage
Treat the underlying issue
leave a stent in the ureter
complications:
renal failure
adult (audosomal dominan) polycystic kidney disease h and p
hereditary
AD
large multi-cystic kidneys, prone to develop SAH (15%)
presents like RCC:
flank pain chronic UTIs gross hematuria large palpable kidneys HTN
Labs:
increased BUN and increased creatinine
anemia (low EPO)
urinalysis- hematuria, proteinuria
Radiology: US or CT
- large multicystic kidneys
- stones
Treatment:
- vasopressin receptor antagonists
- amiloride
- treatment of UTIs and HTN
- drainage of large cysts
- dialysis or transplant
Complications:
- ESRD
- Hepatic cysts
- Intracranial aneurysms
- SAH
- mitral valve prolapse
RCC
MC primary neoplasm of the renal parenchyma
risk factors:
smoking
exposure to cadmium or asbestos
age
H and P: flank pain weight loss abdominal mass HTN fever hematuria scrotal varicocele (11%)
labs:
polycythemia due to increased EPO
DO NOT BIOPSY, because you can seed the tract causing metastasis
Treatment:
nephrectomy or renal- sparing resection with lymph node dissection
immunotherapy
radiation
chemotherapy
early recognition significantly improves prognosis
increased EPO
renal cell carcinoma hepatocellular carcinoma pheochromocytoma hemangiolbastoma high altitude lung disease and hypoxia
Acute interstitial nephritis
aka allergic interstitial nephritis
or drug-induced interstitial nephritis
damage of interstitial tissue, caused by drugs and toxins
less often, caused by autoimmune processes or infections
meds: beta-lactams sulfonamides aminoglycosides NSAIDS Allopurinol PPIs Diuretics Cadmium (can cause RCC and interstitial nephropathy) Lead Copper Mercury Poisonous mushrooms Infections Sarcoidosis Amyloidosis Myoglobinuria
H and P: rash fever increased creatinine eosinophilia
Labs:
granular or epithelial casts
urine eosinophils
Treatment:
stop the offending agent
supportive care
corticosteroids, may be beneficial in refractory cases as well
Complications: ATN Renal failure Renal papillary necrosis ESRD
Cardiac manifestations of APKD
aortic regurgitation
mitral prolapse
Biggest risk factor for RCC
smoking
PT presents with polycythemia, weightloss, flank pain, hematuria- what should you do?
imaging studies to evaluate kidneys for tumor
What is the cut-off between heavy and light proteinuria?
> 3.5 g/day is heavy proteinuria= nephrotic syndrome
Glomerulonephritis
acute hematuria
proteinuria
casts in the urine
increased BUN and creatinine
Postinfectious glomerulonephritis
GAS
-strep throat 1-3 weeks prior to presentation
Treating with abx prevents rheumatic fever and heart disease but NOT gn
-oliguria
-edema
-brown urine (coca cola)
-more common in children
-high anti-streptolysin O titer (ASO) blood test
-Anti-DNAse B (impetigo, non gn strep)
sub-epithelial IgG deposits, “humps”
PHAROAH features of strep gn
proteinuria hematuria azotemia RBC casts Anti-strep titers/Anti-DNAse B oliguria hypertension
sub-epithelial IgG deposits
Microscopic appearance of post- strep gn
subepithelial humps
neutrophils within the glomeruli
general treatment for most glomerulonephritis
steroids
ACE I
statins
IgA nephropathy
Berger disease
increased serum IgA
on electron microscopy there will be immune complexes in the mesangium, with proliferation of mesangial cells
associated with HSP
Goodpasture syndrome
kidneys AND pulm infiltrates seen on CXR
unlike Wegener, Goodpasture doesn’t affect the upper airway
IgG abs against GBM
you will see linear deposits of IgG all along the GBM
Treatment:
plasmapheresis
steroids
Alport syndrome
nephritis
high-frequency hearing loss
cataracts
“can’t pee, can’t see, can’t hear high C”
split basement membrane due to defective type 4 collagen
Rapidly progressive glomerulonephritis, aka crescentic GN
described based on its course (rapidly progressing to renal failure)
Type 1- antiGBM
Type 2- immune complexes
Type 3- pauci-immune pANCA+
Type 4- pauci-immune, pANCA-/idiopathic
Lupus nephritis
Mesangial
Membranous
Focal proliferative
Diffuse proliferative
kidney disease is common in lupus patients, and it can come in various histologies
confirm with +ANA and
+anti-dsDNA
Treat: steroids, ACEI, statin
Granulomatosis with polyangiitis (Wegener)
nephritis
pulmonary involvement
upper airway disease
similar to pauci-immune RPGN
but this is going to be associated with c-ANCA
Tx: corticosteroids
cyclophosphamide
Definition of nephrotic syndrome
> 3.5g/day proteinuria
Minimal change disease
bx looks almost normal except for distortion/effacement of foot processes
idiopathic
MCC nephrotic syndrome` in children
Tx: corticosteroids
Focal segmental glomerular sclerosis (FSGS)
MCC nephrotic syndrome in adults in the US
RF:
AAs and Latinos
HIV patients
Focal and segmental sclerosis
(less than half of glomeruli affected
certain segments of kidney are more likely to be affected with deeper segments being affected first and segments nearer the cortex spared at first)
On IH, some parts look normal and other parts look pink and scleroised
Membranous nephropathy
thickening of the basement membrane
Spike and dome appearance due to immune deposits under the epithelial layer
membranous associated with hepatitis B
Treatment: ACEI, steroids, statins
Membranoproliferative glomerulonephritis
nephritis, hematuria, nephrosis, proteinuria
“tram track” appearance
you now have 2 basement membranes due to subENDOTHELIAL humps
The mesangium proliferates and invades space between the two layers
Causes: lupus subacute bacterial endocarditis hepatitis B hepatitis C
Diabetic nephropathy
proteinuria
nephrosis
check the urine microalbumin
look for
thickened GBM
nodular thickening of the mesangium (Kimmelstiel Wilson nodule- round pink, dense acellular, and mesangial expansion)
The capillaries aren’t nearly as prominent as they would be in a healthy glomerulus
