GU Flashcards

1
Q

pyelonephritis what is is and where does it come from? (5 common organisms)

A

infection of renal parenchyma

UTI, ascending infection
common organisms are:
e. coli
s. saprophyticus
klebsiella
proteus mirabilis
candida
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2
Q

risk factors for pyelonephritis

A
Urinary obstruction
immunocompromised
history of previous pyelonephritis
diabetes
frequent sexual intercourse
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3
Q

pyelonephritis h and p

A
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
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4
Q

Treat pyelonephritis

A

A few days of IV abx followed by outp PO abx

fluoroquinolones
aminoglycosides
3rd gen cephalosporins such as ceftriaxone

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5
Q

Complications of pyelonephritis in pregnancy

A

increased risk of
preterm birthweight
low birthweight

treat with ceftriaxone and avoid fluoroquinolones in pregnancy

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6
Q

Nephrolithiasis: Calcium oxalate stones

A

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

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7
Q

Nephrolithiasis: struvite stones

A

contain ammonium, magnesium, phosphate

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

staghorn stones
radio-opaque

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8
Q

nephrolithiasis: calcium phosphate stones

A

think of

  1. hyperparathyroidism
  2. renal tubular acidosis
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9
Q

nephrolithiasus: uric acid stones

A

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

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10
Q

Nephrolithiasis: cystine stones

A

hereditary form of stone in patients with cystinuria

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11
Q

risk factors for nephrolithiasis

A
  • 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
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12
Q

nephrolithiasis h and p

A

acute, colicky, flank pain with radiation to ipsilateral lower quadrant

genital pain

hematuria
n/v
lower UTI symptoms (frequency, discomfort while voiding)

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13
Q

nephrolithiasis diagnosis

A

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)
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14
Q

where do stones most commonly get stuck?

A

ureterovesical junction

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15
Q

renal colic versus peritonitis

A

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

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16
Q

What is the general treatment for calcium nephrolithiasis?

A

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

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17
Q

Hematuria in a patient

A
idiopathic
UTI
kidney stones
exercise
trauma
endometriosis in the bladder
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18
Q

persistent hematuria in a patient

A

glomerular disease

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19
Q

persistent hematuria in a patient 20-50yo

A

APKD
Neoplasm
Glomerular disease

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20
Q

Persistent hematuria in a patient >50yo

A

APKD
Neoplasm
Glomerular disease
BPH

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21
Q

What are the steps in evaluating hematuria?

A

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

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22
Q

Hydronephrosis

A

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

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23
Q

adult (audosomal dominan) polycystic kidney disease h and p

A

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
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24
Q

RCC

A

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

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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