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
Amyloidosis
abnormal amyloid proteins deposited in tissues (kidney, heart, liver, brain)
The kidney is the most commonly involved organ in patients with systemic amyloidosis
It commonly presents with nephrotic- range proteinuria
Renal biopsy shows expansion of the mesangial matrix due to deposition of lots of amyloid in the mesangium
Congo red stain shows apple-green birefringence
Urinary casts
Made up of Tamm- Horsfall mucoprotein, secreted by the tubules, accumulates in collecting ducts, and then sloughed off in the urine
Hyaline casts
normal patients with concentrated urine, dehydrated on diuretics
Red cell cast
glomerular bleeding (glomerulonephritis, vasculitis)
White cell cast
tubular interstitial disease, acute pyelonephritis, other glomerular disorders
Epithelial cell cast
acute glomerulonephritis due to desquamation of epithelial cells
Granular casts
non-specific, associated with acute tubular necrosis (ATN), and broken down white or red cell casts. Also described as muddy brown casts
most common nephrotic syndrome in adults
focal segmental glomerular sclerosis
EM: loss of epithelial foot processes
minimal change disease
most common nephrotic syndrome in children
minimal change disease
nephrotic syndrome associated with hep B
membranous
nephrotic syndrome associated with HIV
focal segmental glomerular sclerosis
EM: subendothelial humps and tram-track appearance
membranoproliferative GN
LM: segmental sclerosis and hyalinosis
focal segmental glomerular sclerosis
Spike and dome pattern of the basement membrane
membranous nephropathy
Most common nephrotic syndrome in AA males
FSGS
Apple-green birefringence with Congo red stain under polarized light
Amyloidosis
fever, rash elevated creatinine, eosinophilia
acute interstitial nephritis
acute renal failure
a sudden decrease in renal function (UPO, Chemical excretion)
prerenal
intrarenal
postrenal
H and P: asymptomatic fatigue anorexia nausea oliguria gross hematuria flank pain mental status changes pericardial friction rub HTN fever diffuse rash edema
Labs:
Azotemia: increased BUN, increased Cr
Urinalysis: hematuria, red cell casts, epithelial casts
Radiology may be useful to detect masses:
US, CT, IVP, renal angiography
prerenal acute renal failure
hypovolemia
sepsis
renal artery stenosis
drug toxicity
FeNa20
intrarenal acute renal failure
acute tubular necrosis
glomerular disease
renal vascular disease
FeNA>2%
-intrinsic renal, or postrenal
postrenal acute renal failuer
BILATERAL obstruction of renal calyces, ureters, or bladder
stones
tumors
adhesions
backpressure from the obstruction
FeNA>2%
-intrinsic renal, or postrenal
Fraction of excreted sodium (FENa)
(urine Na/serum Na)/
urine Cr/serum Cr
Chronic kidney disease
at least 75% of the time is due to HTN, DM
with this you will see gradual development of uremic syndrome
H and P: changes in mental status decreased consciousness HTN pericarditis anorexia n/v GI bleeding peripheral neuropathy peripheral edema
Labs: hyperkalemia hyponatremia increased PO43- decreased Ca2+ anemia metabolic acidosis increased BUN and Cr urine osmolality similar to serum osmolality screen diabetic patients by checking urine microalbumin check 24-hr protein
US
hydronephrosis
shrunken kidneys
Treatment for chronic kidney disease stop smoking aggressive BP control -diuretic (loop) -ACEI or ARB -Beta blockers to reduce CAD risk -dihydropyridine CCB
DM- aggressive control to HgbA1C goal of
Treatment for chronic kidney disease
- stop smoking
- aggressive BP control
- diuretic (loop)
- ACEI or ARB
- Beta blockers to reduce CAD risk
- dihydropyridine CCB (nifedipine)
DM- aggressive control to HgbA1C goal of
Complications of CKD
ESRD electrolyte problems renal osteodystrophy encephalopathy severe anemia
Dialysis
hemodialysis peritoneal dialysis (osmotic drive through the peritoneum)
severe hyperkalemia severe metabolic acidosis fluid overload uremic syndrome chronic kidney disease (Cr>12 mg/dL, BUN>100mg/dL) severe overdose or toxin exposure
kidney transplant
Causes of metabolic alkalosis
- vomiting (dump bicarb in urine to compensate)
- diuretics (volume contraction, loss of fluid without losing bicarb causes bicarb to rise)
- Cushing syndrome
- hyperaldosteronism
- adrenal hyperplasia
Causes of respiratory alkalosis
this requires hyperventilation of some sort
high altitude
asthma
aspirin toxicity
pulmonary embolism
Causes of respiratory acidosis
CO2 retention:
COPD
respiratory depression
neuromuscular diseases
What is AG and what causes high AG metabolic acidosis?
anion gap= [Na] - [Cl] - [HCO3-]
normal is 8-12
high anion gap due to unmeasured anions in the serum, and these are usually organic acids
Methanol uremia DKA Paraldehyde/propylene glycol (antifreeze) INH Lactic acid Ethylene glycol (antifreeze) Salicylates (initially stimulates resp center in brain leading to alkalosis hyperventilation, then leads to lactic acidosis by uncoupling oxidative phosphorylation)
What is the differential diagnosis for metabolic acidosis with a normal anion gap
diarrhea
renal tubular acidosis
TPN
hypoaldosteronism (Addison disease which is type 4 RTA anyway)
How can serum potassium be useful in narrowing the differential diagnosis?
Low serum potassium: think renal tubular acidosis types I and II, diarrhea, and Fanconi syndrome
If serum potassium is high: think Addison disease, renal tubular acidosis type IV, or hyperalimentation (TPN)
Renal tubular acidosis
abnormalities in proton secretion or bicarb reabsorption
hyponatremia
sodium
What is pseudohyponatremia? How is this different from hyponatremia from hyperosmolality?
When the serum volume is expanded by a substance, such as lipid or protein (MM), the amount of sodium per volume of serum may decrease even though the amount of sodium per unit of water in serum is appropriate.
This is different than hyponatremia due to hyperosmolality from elevated glucose or mannitol administration
hyperosmolality- increased serum osmols pulls water out of cells, thereby diluting serum sodium
Plasma sodium falls 1.6 mEq/L for every increase of 100 mg/dL of plasma glucose (which increases to 2.4 mEq/L decrease per 100 mg/dL glucose after levels exceed 400mg/dL)
Use this calculation to determine how much you expect sodium to rise as the plasma glucose begins to fall with treatment and water is consequently shifted back into cells
Treatment for hyponatremia
treat underlying conditino restrict free water loop diuretics hypertonic saline vasopressin receptor antagonists- conivaptan, tolvaptan
What condition may result from rapid correction of hyponatremia? What are the manifestations?
Central pontine myelinolysis (osmotic demyelination)
occurs when sodium is corrected by more than 12-20 mEq/L over 24 hours, or is overcorrected to above 140
Symptoms are irreversible and typically are delayed 2-6 days after correction of hyponatremia
Loss of myelin in the central pons: dysarthria dysphagia paraparesis or quadriparesis behavioral disturbances lethargy or coma shows up on MRI or head CT 4 weeks after event
SIADH etiologies
nonphysiologic release of ADH
etiologies:
1. CNS disease
head trauma, brain tumor, stroke, CNS infection, pituitary surgery
2. pulmonary disease
PNA, tumor (small cell)
3. Drugs
NSAIDs, antidepressants, antipsychotics, antineoplastic agents, carbamazepine, ecstasy, vasopressin, DDAVP
4. Other:
HIV/AIDS, major abdominal or thoracic surgery
Labs:
chronic hyponatremia
serum hypoosmolarity
high urine osmolarity
Treat SIADH
same as for other hyponatremia
fluid restriction
vasopressin receptor antagonists (conivaptan, tolvaptan)
loop diuretics
hypertonic saline
Hypernatremia- causes
dehydration
loss of fluid from skin, GI tract, DI, iatrogenic infusion
(hyperaldosteronism- hypernatremia, HTN, metabolic alkalosis)
See 6 D’s (SU 102)
symptoms associated with hypernatremia
oliguria thirst weakness lethargy mental status changes seizures
Diabetes insipidus
disorders of ADH- directed water reabsorption leading to dehydration and hypernatremia
Central (trauma, tumor, anorexia, idiopathic)- not making ADH
Nephrogenic (kidneys not responsive to ADH)- hereditary renal disease, lithium toxicity, hypercalcemia, hypokalemia
presents with polyuria
Labs: high serum sodium
low urine osmolality
high serum osmolality
dilute urine causes concentrated serum
- Confirm diagnosis of DI with water deprivation test
normal: urine osmolality rises
DI: urine osmolality stays low
- Give ADH (desmopressin)
if central DI: urine osmolality increases
if nephrogenic DI: no change in urine osmolality, urine stays dilute
Treatment:
central DI: desmopressin
nephrogenic DI:
-salt restriction
-increase water intake
-thiazides (mild hypovolemia at DCT induces increased absorption upstream at PCT)
-indomethacin (reduced renal bloodflow, reduces UOP)
Treat lithium- induced nephrogenic DI with amiloride
Lithium- induced nephrogenic DI
principal cells of collecting tubules
ADH in sodium channel induces cell to insert aquaporin water channels into the lumen of the principal cell so that water can be reabsorbed
Lithium enters sodium channels and then binds the aquaporin water channels and keeps water out
Amiloride blocks the sodium channels so that lithium can’t enter the cell
Hyperkalemia due to things that shift potassium out of cells
Causes: metabolic acidosis aldosterone deficiency tissue breakdown insulin deficiency renal failure potassium- sparing diuretics beta blockers digoxin
things that shift things into cells - hypokalemia
insulin
beta agonists
alkalosis
hyperkalemia ekg changes
tall spiked t waves you wouldn’t want to sit on
treating hyperkalemia
IV calcium gluconate or calcium chloride to stabilize myocardium
drive potassium into cells with
- insulin + glucose
- beta- agonists like albuterol
- sodium bicarbonate
remove potassium from the body
- hemodialysis
- polystyrene (kayexelate PO or enema)
- loop diuretics
C BIG K Drop calcium gluconate beta agonist insulin glucose kayexalate dialysis
Hypokalemia
Causes: poor dietary intake of K alkalosis hypothermia vomiting diarrhea hyperaldosteronism insulin excess diuretics RTA types I and II
Clinical presentation fatigue weakness hyporeflexia paralysis, paresthesias arrhythmias
EKG changes show
T wave flattening
ST depression
U waves
Treatment:
Treat underlying disorder
oral or IV potassium (either one, central line is best)
give po potassium over several hours so as not to agitate the heart
Hypercalcemia
hyperparathyroidism
neoplasms
PTHrP
local osteolytic factors
Causes:
- thiazide diuretics
- milk-alkali syndrome
- sarcoidosis (by way of macrophages, which generate excess vitamin D)
- hypervitaminosis A
bones, stones, groans, psychiatric overtones
- bone pain
- fractures
- nephrolithiasis
- n/v
- PUD
- constipation
- weakness
- mental status changes
- polyuria
- acute pancreatitis
labs:
-calcium
-increase PTH
EKG- shortened QT interval
Treatment: hydration calcitonin bisphosphonates glucocorticoids surgery if resectable neoplasm or hyperparathyroidism
familial hypocalciuric hypercalcemia
family history
low urine calcium
absence of: osteopenia, nephrolithiasis, mental status changes
hypocalcemia
Ca
Drugs that cause hyperkalemia
ACE I ARBs K-sparing diuretics beta blockers digoxin
Drugs that cause hypokalemia
albuterol insulin loop diuretics thiazides carbonic anhydrase inhibitors
which electrolyte abnormality causes QT prolongation
hypocalcemia
which electrolyte abnormality causes QT shortening?
hypercalcemia
pathogens commonly implicated in UTI
e. coli
s. saprophyticus
enterobacter
enterococcus
proteus mirabilis (urease)
klebsiella pneumoniae (urease)
pseudomonas (indwelling catheter)
urease yields struvite stone
Risk factors for UTI
female bladder outlet obstruction foley catheter immunocompromised diabetes sexual intercouse vesicoureteral reflux pregnancy
UTI in elderly patient
may be asymptomatic
AMS
check for distended bladder
check UA
urethritis will present similarly in young men
UTI labs
UA dipstick: nitrite (bacteria), leukocyte esterase (inflammation)
UA microscopy:
numerous WBCs, variable RBCs
Urine culture:
colony-forming units >10^5
Blood culture appropriate if you suspect pyelonephritis
clean catch, mid stread
or catheter sample
Treat UTI
in pregnancy?
3-5 days of nitrofurantoin amoxicillin TMP-SMX fluoroquinolones
in pregnant women, avoid:
TMP-SMX
fluoroquinolones
if pregnant use: amoxicillin ampicillin cephalosporin nitrofurantoin (7 days)
Urinary incontinence
involuntary loss of urinary control
r/o incontinence as a symptom of another disease, poor urinary control due to impacted stool, delirium, vaginitis, etc.
urge incontinence
leaky urine a/w strong urge to void
clinical diagnosis
Treatment: Anticholinergic medications: oxybutynin tolteridine fesoterodine trospium solifenacin darifenacin
Imipramine (anticholinergic and alpha agonist)
Duloxetine (off- label in the US, approved in Europe)
Treatment side effects: anticholinergic constipation dry mouth CNS cognitive deficits
Stress urinary incontinence
involuntary leakage of urine during any maneuver that increases abdominal pressure
- cough
- sneeze
- exercise
- heavy lifting
due to decreased anatomic support and function of the urinary sphincter
Do you have to wear pads regularly? how many pads throughout the day?
Risk factors: obesity multiparity female male (urethral or prostate surgery)
clinical diagnostic
treatment: Kegel exercise weightloss imipramine midurethral sling surgery
Overflow urinary incontinence
overflow of urine from overly distended full bladder/ incomplete emptying
H and P: constant urinary dribbling feeling of incomplete bladder emptying bladder fullness distended bladder
Diagnosis:
Automated US bladder scanner (checking for postvoid residual)
Catheterized postvoid residual
Serum creatinine and electrolytes
Causes:
bladder outlet obstruction
atonic neurogenic bladder
Treatment:
- decompression of bladder with Foley catheter
- address the underlying cause
MC Bladder cancer in the US
transitional cell carcinoma
RFs associated with squamous cell carcinoma
schistosoma haematobium
(chronic infection, hematuria)
tb
chronic irritation of bladder (indwelling foley)
Bladder adenocarcinoma RF
urachal remnant
Bladder transitional cell cancer risk factors
tobacco use schistosomiasis aniline dyes petroleum byproducts recurrent UTIs males>females (3:1)
Bladder cancer- labs to get
urinalysis- RBCs
urine cytology- malignant cells
but cytology may be falsely negative early on
cystoscopy to directly visualize the tumor
upper tract imaging to rule out tumor in the renal pelvis
classic presentation of bladder cancer (painless)
gross hematuria
late in the course, palpable suprapubic mass
Bladder cancer treatment
- transurethral cystoscopic resection
- radical cystectomy and urinary diversion
- radiation and chemotherapy
- surveillance cystoscopies and intravesical chemotherapy or immunotherapy to decrease recurrence
