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1

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

2

risk factors for pyelonephritis

Urinary obstruction
immunocompromised
history of previous pyelonephritis
diabetes
frequent sexual intercourse

3

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

4

Treat pyelonephritis

A few days of IV abx followed by outp PO abx

fluoroquinolones
aminoglycosides
3rd gen cephalosporins such as ceftriaxone

5

Complications of pyelonephritis in pregnancy

increased risk of
preterm birthweight
low birthweight

treat with ceftriaxone and avoid fluoroquinolones in pregnancy

6

Nephrolithiasis: Calcium oxalate stones

most common type
idiopathic
needs to hydrate well and minimize stone formation

7

Nephrolithiasis: struvite stones

contain ammonium, magnesium, phosphate

Associated with UTIs (esp proteus, klebsiella)
urease splits urea producing ammonium

staghorn stones
radio-opaque

8

nephrolithiasis: calcium phosphate stones

think of
1. hyperparathyroidism
2. renal tubular acidosis

9

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

10

Nephrolithiasis: cystine stones

hereditary form of stone in patients with cystinuria

11

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

12

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)

13

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)

14

where do stones most commonly get stuck?

ureterovesical junction

15

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

16

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

17

Hematuria in a patient

idiopathic
UTI
kidney stones
exercise
trauma
endometriosis in the bladder

18

persistent hematuria in a patient

glomerular disease

19

persistent hematuria in a patient 20-50yo

APKD
Neoplasm
Glomerular disease

20

Persistent hematuria in a patient >50yo

APKD
Neoplasm
Glomerular disease
BPH

21

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

22

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

23

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

24

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

25

increased EPO

renal cell carcinoma
hepatocellular carcinoma
pheochromocytoma
hemangiolbastoma
high altitude
lung disease and hypoxia

26

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

27

Cardiac manifestations of APKD

aortic regurgitation
mitral prolapse

28

Biggest risk factor for RCC

smoking

29

PT presents with polycythemia, weightloss, flank pain, hematuria- what should you do?

imaging studies to evaluate kidneys for tumor

30

What is the cut-off between heavy and light proteinuria?

>3.5 g/day is heavy proteinuria= nephrotic syndrome

31

Glomerulonephritis

acute hematuria
proteinuria
casts in the urine
increased BUN and creatinine

32

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"

33

PHAROAH features of strep gn

proteinuria
hematuria
azotemia
RBC casts
Anti-strep titers/Anti-DNAse B
oliguria
hypertension

sub-epithelial IgG deposits

34

Microscopic appearance of post- strep gn

subepithelial humps
neutrophils within the glomeruli

35

general treatment for most glomerulonephritis

steroids
ACE I
statins

36

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

37

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

38

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

39

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

40

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

41

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

42

Definition of nephrotic syndrome

>3.5g/day proteinuria

43

Minimal change disease

bx looks almost normal except for distortion/effacement of foot processes
idiopathic

MCC nephrotic syndrome` in children
Tx: corticosteroids

44

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

45

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

46

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

47

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

48

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

49

Urinary casts

Made up of Tamm- Horsfall mucoprotein, secreted by the tubules, accumulates in collecting ducts, and then sloughed off in the urine

50

Hyaline casts

normal patients with concentrated urine, dehydrated on diuretics

51

Red cell cast

glomerular bleeding (glomerulonephritis, vasculitis)

52

White cell cast

tubular interstitial disease, acute pyelonephritis, other glomerular disorders

53

Epithelial cell cast

acute glomerulonephritis due to desquamation of epithelial cells

54

Granular casts

non-specific, associated with acute tubular necrosis (ATN), and broken down white or red cell casts. Also described as muddy brown casts

55

most common nephrotic syndrome in adults

focal segmental glomerular sclerosis

56

EM: loss of epithelial foot processes

minimal change disease

57

most common nephrotic syndrome in children

minimal change disease

58

nephrotic syndrome associated with hep B

membranous

59

nephrotic syndrome associated with HIV

focal segmental glomerular sclerosis

60

EM: subendothelial humps and tram-track appearance

membranoproliferative GN

61

LM: segmental sclerosis and hyalinosis

focal segmental glomerular sclerosis

62

Spike and dome pattern of the basement membrane

membranous nephropathy

63

Most common nephrotic syndrome in AA males

FSGS

64

Apple-green birefringence with Congo red stain under polarized light

Amyloidosis

65

fever, rash elevated creatinine, eosinophilia

acute interstitial nephritis

66

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

67

prerenal acute renal failure

hypovolemia
sepsis
renal artery stenosis
drug toxicity

FeNa20

68

intrarenal acute renal failure

acute tubular necrosis
glomerular disease
renal vascular disease

FeNA>2%
-intrinsic renal, or postrenal

69

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

70

Fraction of excreted sodium (FENa)

(urine Na/serum Na)/
(urine Cr/serum Cr)

71

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

72

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

73

Complications of CKD

ESRD
electrolyte problems
renal osteodystrophy
encephalopathy
severe anemia

74

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

75

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

76

Causes of respiratory alkalosis



this requires hyperventilation of some sort

high altitude
asthma
aspirin toxicity
pulmonary embolism

77

Causes of respiratory acidosis



CO2 retention:
COPD
respiratory depression
neuromuscular diseases

78

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)

79

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)

80



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

81

hyponatremia

sodium

82

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

83

Treatment for hyponatremia

treat underlying conditino
restrict free water
loop diuretics
hypertonic saline
vasopressin receptor antagonists- conivaptan, tolvaptan

84

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

85

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

86

Treat SIADH

same as for other hyponatremia

fluid restriction
vasopressin receptor antagonists (conivaptan, tolvaptan)
loop diuretics
hypertonic saline

87

Hypernatremia- causes

dehydration
loss of fluid from skin, GI tract, DI, iatrogenic infusion

(hyperaldosteronism- hypernatremia, HTN, metabolic alkalosis)

See 6 D's (SU 102)

88

symptoms associated with hypernatremia

oliguria
thirst
weakness
lethargy
mental status changes
seizures

89

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

1. Confirm diagnosis of DI with water deprivation test

normal: urine osmolality rises
DI: urine osmolality stays low

2. 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

90

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

91

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

92

things that shift things into cells - hypokalemia

insulin
beta agonists
alkalosis

93

hyperkalemia ekg changes

tall spiked t waves you wouldn't want to sit on

94

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

95

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

96

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

97

familial hypocalciuric hypercalcemia

family history
low urine calcium
absence of: osteopenia, nephrolithiasis, mental status changes

98

hypocalcemia

Ca

99

Drugs that cause hyperkalemia

ACE I
ARBs
K-sparing diuretics
beta blockers
digoxin

100

Drugs that cause hypokalemia

albuterol
insulin
loop diuretics
thiazides
carbonic anhydrase inhibitors

101

which electrolyte abnormality causes QT prolongation

hypocalcemia

102

which electrolyte abnormality causes QT shortening?

hypercalcemia

103

pathogens commonly implicated in UTI

e. coli
s. saprophyticus
enterobacter
enterococcus
proteus mirabilis (urease)
klebsiella pneumoniae (urease)
pseudomonas (indwelling catheter)

urease yields struvite stone

104

Risk factors for UTI

female
bladder outlet obstruction
foley catheter
immunocompromised
diabetes
sexual intercouse
vesicoureteral reflux
pregnancy

105

UTI in elderly patient

may be asymptomatic
AMS

check for distended bladder
check UA

urethritis will present similarly in young men

106

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

107

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)

108

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.

109

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

110

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

111

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

112

MC Bladder cancer in the US

transitional cell carcinoma

113

RFs associated with squamous cell carcinoma

schistosoma haematobium
(chronic infection, hematuria)

tb
chronic irritation of bladder (indwelling foley)

114

Bladder adenocarcinoma RF

urachal remnant

115

Bladder transitional cell cancer risk factors

tobacco use
schistosomiasis
aniline dyes
petroleum byproducts
recurrent UTIs
males>females (3:1)

116

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

117

classic presentation of bladder cancer (painless)

gross hematuria

late in the course, palpable suprapubic mass

118

Bladder cancer treatment

-transurethral cystoscopic resection

-radical cystectomy and urinary diversion

-radiation and chemotherapy

-surveillance cystoscopies and intravesical chemotherapy or immunotherapy to decrease recurrence