CRAM Flashcards

1
Q

Dietary recommendations: Ca++ stones and high urinary Ca++

A

Limit Na+
Maintain normal Ca++ (1-2g/day)

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2
Q

Dietary recommendations: Ca++Oxalate stones + high urinary oxalate

A

Limit oxalate
Maintain normal Ca++ (1-2g/day)

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3
Q

Dietary recommendations: Ca++ stones + low urinary citrate

A

Limit non-dairy animal protein and increase fruits and veggies

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4
Q

Dietary recommendations: Uric acid or Ca++ stones and high urinary uric acid

A

Limit non-dairy animal protein

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5
Q

Dietary recommendations: Cystine stones

A

Limit Na+ and protein intake

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6
Q

Medical therapy:
Recurrent stones + high urinary Ca++

A

Thiazide diuretic

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7
Q

Medical therapy:
Recurrent Ca++ stones + low urinary citrate

A

Potassium citrate

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8
Q

Medical therapy:
Recurrent CaOx stones + hyperuricosuria + normal urinary Ca++

A

Offer urinary allopurinol

If uric acid stones, DON’T offer allopurinol as first-line therapy

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9
Q

Medical therapy:
Recurrent Ca++ stones without other lab abnormalities

A

Empiric thiazide diuretics and/or K-cit

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10
Q

Medical therapy:
Uric acid and cystine stones

A

K-cit to raise urinary pH (these stones form in acidic urine)

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11
Q

Medical therapy:
Cystine stones refractory to dietary changes (adequate hydration, limit salt to 2-3 g daily) and urinary alkalinization (pH >7) or large recurrent stone burdens

A

Offer cysteine-binding thiol drugs (alpha-mercaptopropionylglycine = Thiola = tiopropin), which is better tolerated than D-Penicillinamine

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12
Q

Medical therapy:
Residual/recurrent struvite stones after surgery exhausted

A

Offer acetohydroxamic acid (AHA = Lithostat; urease inhibitor)

q3month CBC to monitor for hemolytic anemia

This drug decreases stone growth rate, doesn’t change stone recurrence

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13
Q

Renacidin = citric acid glucono-delta-lactone magnesium carbonate

A

Used for dissolution treatment of residual struvite stones/fragments

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14
Q

Urease-producing organisms

A

Proteus, klebsiella, staph aureus, pseudomonas, providentia, ureaplasma

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15
Q

Enteric/acquired hyperoxaluria is a/w:

A

IBD and short-gut syndrome

Unabsorbed fat binds to Ca++ –> oxalate goes unbound until it is reabsorbed in the colon –> high oxalate in the blood and then urine –> treat with Ca++ supplementation to bind oxalate in the gut

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16
Q

Crohn’s stone formation

A

low urine volume (dehydration) + low urine pH and hypocitraturia (metabolic acidosis) + hyperoxaluria (over absorption of intestinal oxalate –> CaOx stones

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17
Q

Isolated hypomagnesemia

A

Suggests IBD –> refer to GI

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18
Q

PO Reloxaliase

A

Recombinant oxalate decarboxylase enzyme derived from B. subtilis and expressed in E. Coli

Degredes oxalate within GI tract –> decreased oxalate absorption and urinary excretion

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19
Q

Lumasiran = Oxlumo

A

siRNA
decreases glycolate oxidase, which decreases glyoxylate’s conversion to oxalate

Approved for Tx of type 1 primary hyperoxaluria

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20
Q

CF is a/w which urinary abnormalities?

A

Hyperoxaluria, hypocitraturia (prone to stones)

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21
Q

Prevent stones: Roux-En-Y

A

Dietary Ca++ at mealtime
Decrease high oxalate foods
Metabolic acidosis –>decreased urinary citrate –> K-Cit

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22
Q

Stones: Colon resection and end ileostomy

A

Fluid and bicarbonate loss
Concentrated urine with low pH
Increased risk of uric acid stone formation

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23
Q

Lesch-Nyhan Syndrome

A

Absence of HGPRT
Neuro dysfunction, behavioral disturbances, uric acid overproduction with hyperuricosuria and hyperuricemia

A/w uric acid stones

Patients can get xanthine oxidase stones while on allopurinol –> decrease (don’t stop) allopurinol and start K-cit

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24
Q

Pregnancy and stones

A

Placental production of VitD –> increases calcium absorption and decreases serum PTH –> physiologic hypercalciuria

BUT

Urine citrate and GAG also increased so stone formation risk is unchanged

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25
Ammonium acid urate stones
Rare, a/w chronic diarrhea and heavy laxative use/abuse, decreased urinary Na+ excretion, pH >6.3, and ileal or large volume colon resection Radiolucent stones, can be mistaken for uric acid stones AAU stones no NOT dissolve with alkalinization Idiopathic (endemic) bladder stones are also AAU (kids with cereal based diets)
26
Keto(genic) diet affect on stones
Excess meat (purine) consumption Hyperuricosuria, increased urinary sulfate + urea nitrogen Hypercalciuria Hypocitraturia Decreased urine pH Uric acid + calcium nephrolithiasis Treat with dietary changes +/- allopurinol
27
Topiramate and stones
Topiramate creates a chronic intracellular acidosis Urinary milieu similar to distal RTA with hyperchloremic acidosis, HIGH urine pH, SEVERE hypocitraturia and hypercalciuria Treat with cessation of topiramate or K-cit
28
Vitamin C effect on urine
10-20% is metabolized into oxalic acid and excreted into urine
29
Most common risk factor for Ca++ stones
Hypercalciuria
30
Absorptive hypercalciuria pathophysiology
Increased GI Ca++ absorption Normal or increased serum Ca++ Decreased serum PTH and decreased vitamin D
31
Absorptive hypercalciuria management options
Avoid excess dietary Calcium Decrease salt and animal protein in diet Thiazides +/- K-Cit
32
Renal calcium leak hypercalciuria pathophysiology and management
Increased calcium loss into urine Normal or decreased serum Calcium Increased serum PTH Management: Thiazides +/- K-Cit
33
Renal phosphate leak hypercalciuria pathophys and management
Increased phosphate loss in urine, decreased serum phos Increases vitamin D, which increased GI calcium absorption treat with PO orthophosphates
34
Resorptive hypercalciuria pathophys and management
HyperPTH leads to increased Ca++ resorption from bone + increased GI Ca++ absorption --> increased serum Ca++ Tx with parathyroidectomy
35
Drug-induced renal calculi: TIME
Triamterene: K sparing diuretic for edema and HTN Indinavir: protease inhibitor for HIV (non-dense stone on CT) Magnesium trisilicate: antacid for GERD Ephedrine +/- guaifenesin: stimulant/expectorant
36
Stones form due to metabolic effect of the drug
Furosemide: increases urinae Ca++ excretion, causes stones in low birth weight infants Acetazolamide and other carbonic anhydrase inhibitors Topiramate: severe hypocitraturia and high urinary pH --> 2% of chronic users get CaPhos stones Zonisamide: sulfonamide anticonvulsant --> 4% of long term users get CaPhos stones Laxative abuse: ammonium acid urate stones Vitamin C supplements - metabolized into oxalate Vitamin D supplements: increase Ca++ absorption
37
Type 1 RTA
Distal tubule can't excrete H+ (in the form of ammonium) Leads to systemic acidosis (decreased serum CO2) and alkaline urine (pH >5.5) Increased urinary calcium Decreased urinary citrate 3/4 of these patients get CaPhos stones Treat with K-Cit + bicarb to address systemic acidosis - Type I RTA can be drug-induced (ifosfamide for NSGCT pr penile cancer) Anion gap is not elevated in RTA Type 1 distal RTA is a/w nephrocalcinosis
38
Type II Proximal RTA
Proximal tubule can't reabsorb HCO3 Increased urine calcium but stable citrate, so not increased stone formation risk
39
What is a thiazide challenge?
Give two weeks of a thiazide Recheck serum Ca++, PTH, urine calcium Used to differentiate renal hypercalciuria (thiazide corrects primary problem of renal calcium leak so urinary Ca++ goes to normal) and true hyperparathyroidism (thiazide blocks appropriate renal response of Ca++ excretion leading to worsening hypercalcemia --> tx with parathyroidectomy)
40
Medullary sponge kidney + hypercalciuria treatment
Thiazide to arrect stone development They still need metabolic evaluation
41
Radiolucent Stones
Ammonium acid urate Indinavir Uric acid Xanthine Triamterene
42
Citrate mechanism
Binds Ca++ in urine and intestines Raises urine pH Decreases spontaneous nucleation of CaOX
43
Medical treatment of nonobstructing uric acid stones (HU 300-500) with acidic urine (pH <5.5)
Try to dissolve stones by raising pH with K-Cit
44
Uric acid or cysteine stone formers whose urine remains pH <6.5 despite K-Cit...
Can try adding acetazolamide (CAI) to further raise pH
45
Recurrent CaOx stone former sand high urinary oxalate refractory to diet changes
Treat with pyridoxine (vit B6) Increases conversion of glyoxylate to glycine and decreases conversion to oxalate by LDH
46
What should Cr level be in an adequately collected 24 hr urine study?
About 1 gram
47
Improved dusting efficiency
Longer pulse width/duration Lower peak power (lower energy and higher frequency)
48
Improved fragmentation efficiency
Shorter pulse width/duration Higher peak power (low frequency, higer energy)
49
Physiologic changes with ureteral stent placement
Hyperplasia and inflammation of urothelium Smooth muscle hypertrophy Decreased ureteral contractility Increased VUR Increased intrapelvic pressure
50
Physiology of complete ureteral obstruction
Increased glomerular perfusion pressure via preglomerular vasodilation (BL and UL) Efferent arteriolar constriction (BL only)
51
Pathophysiology of unilateral renal obstruction
Acute phase (1-2 hours): Increased renal blood flow (decreased afferent arteriolar resistance) Little change in GFR - Mediated by increased NO and PGE2 Mid phase (2-5 hours): Renal blood flow decreases (increased afferent arteriolar resistance) GFR decreases (increased proximal tubular hydraulic pressure, increased afferent arteriolar resistance) Late Phase (24 hours): Renal blood flow decreased (increased afferent arteriolar resistance) GFR still decreased (now decreased proximal tubular hydraulic pressure, increased afferent arteriolar resistance) - Mediated by decreased NO In solitary kidney, GFR immediately goes down. Late phase mediated by ANP.
52
Physiology: PCT
2/3 of glomerular ultrafiltrate is reabsorbed in PCT (all AAs and glucose) in isosmotic fashion coupled to Na+ active transport PCT is responsible for ammoniagenesis (formation of ammonia from glutamine)
53
Physiology: Descending Thin Loop of Henle
Descending = downhill = 'easy' for water to exit through the wall of the loop --> filtrate becomes hypertonic
54
Physiology: Ascending Thick Loop of Henle
Thick LoH = ascending = water impermeable Reabsorption of Na+ via 2Cl-K-Na triporter is blocked by loop diuretics here The medullary thick ascending loop of Henle is most ischemia-sensitive part of kidney and may be damaged with prolonged ischemia during partial nephrectomy
55
Physiology: Distal Convoluted Tubule
Thiazides block Na-Cl cotransporter in early distal tubule - Promotes net calcium reabsorption Directly in Distal tubule and indirectly by way of extracellular volume depletion in proximal tubule --> decreased urine Ca++ PTH and Vitamin D stimulate calcium reabsorption in distal tubule Renin promoters: Decreased BP (JG cells in glomerular afferent arteriole), Decreased Na+ delivery (Macula densa in DCT -- abuts JG cells), increased sympathetic tone (Beta1 receptors)
56
Physiology: Collecting Duct
Principal cells facilitate NaCl reabsorption and Intercalated cells facilitate acid secretion ADH increases the water permeability of distal tubule and collecting duct - Blocked in kidney by lithium and release blocked in brain by alcohol DDAVP works in collecting duct to absorb water Aldosterone increases open Na+ channels and regulates Na+-K+ exchange in the collecting duct - Amiloride blocks epithelial sodium channels in DCT and collecting duct --> reduces Na+ reabsorption and K+ secretion (K-sparing)
57
Parathyroid hormone
Secreted by chief cells in parathyroid in response to hypocalcemia or ectopically by peripheral malignancies (SCC of lung) Primary role is in kidney: decreases phos reabsorption in proximal tubule and increases calcium reabsorption in ALoH, DCT and collecting duct PTH activates enzyme 1 hydroxylase in proximal tubule --> increases vitamin D metabolism --> Increases gut absorption of Calcium
58
Primary hyperparathyroidism
Most common type Inappropriate PTH secretion by parathyroid gland = absorptive hypercalcemia
59
Secondary hyperparathyroidism
Appropriate PTH secretion Occurs in response to hypocalcemia Most commonly due to vitamin D deficiency
60
Angiotensin II maintains GFR during hypovolemia by...
Causing vasoconstriction of the efferent arteriole
61
ATN effects on urine
Renal tubular cells can no longer resorb sodium or water or excrete urea Urine will have increased Na, decreased urea, decreased Osm
62
Urinary concentration is primarily the result of...
...hypertonic medullary interstitial fluid
63
Cisplatin is nephrotoxic because of...
...a direct toxic effect on renal tubular cells
64
IgA nephropathy vs. post-strep glomerulonephritis
In IgA, will have URI with renal/UA abnormalities simultaneously --> get renal biopsy In post-strep, the renal/UA changes will be a few weeks after URI. Path from biopsy: IgA = crescent shaped glomeruli + mesangial proliferation Post-strep GN = cellular proliferation
65
Sensitivity, specificity, PPV, NPV
66
Spot Urine Na+ meaning
Prerenal failure: UNa+ is <25 mEq/L because the nephron can still reabsorb Na+ and does so to increase intravascular volume Intrinsic renal failure: UNa+ is >40 mEq/L because the nephron is no longer reabsorbing Na+ effectively
67
Sacral neuromodulation is FDA approved for:
Non-obstructive retention UUI Urgency/frequency syndrome Chronic fecal incontinence Interstitial cystitis
68
Botox mechanism of action
Decreased acetylcholine release from postsynaptic efferent nerves at presynaptic junction at bladder (by cleaving SNARE proteins (SNAP25) that otherwise allow ACh to be released into the synapse
69
On clinical evaluation, a patient has global polyuria as defined as >40 ml/kg urine in 24 hours. Testing and ddx?
Overnight water deprivation test If >800 mOsm/kg --> primary polydipsia, tx with behavioral modifications If <800 mOsm/kg --> Diabetes Insipidus, do renal concentrating capacity test
70
NLUTD: Unknown Risk - Stratification - Further workup - Goal
Lesion in suprasacral SC (SCI, MS, transverse myelitis, spinal dysraphism) or any lesion with any GU complications or change in LUTS Further workup: upper tract imaging + renal fxn + UDS - Don't perform cystoscopy Goal: Determine medium vs. high risk
71
NLUTD: Medium Risk - Stratification - Surveillance
Imaging and renal function are normal, BUT PVR is elevated and/or UDS demonstrated retention, BOO, or DO with incomplete emptying Surveillance: Annual H+P, renal function, annual vs. biannual upper tract imaging - Don't perform surveillance cysto UDS: Repeat PRN if new symptoms/abnormalities arise
72
NLUTD: High Risk - Stratification - Surveillance
Abnormal/unstable imaging (hydro, scarring, parenchymal loss, staghorn, large/increased stone) and/or renal function and/or UDS demonstrates poor compliance, increasing storage Pdet with DO, DSD, or VUR Surveillance: Annual H+P, renal function, annual upper tract imaging - Don't perform surveillance cysto UDS: Repeat when clinically indicated and PRN if new symptoms/abnormalities arise
73
How is normal micturition initiated?
Relaxation of the striated (external) sphincter Onuf's nucleus (anterior horn S2-S4) contains the pudendal motor neurons that innervate the EUS Onuf is the gatekeeper of micturition and needs to be inhibited in order to allow for micturition to proceed (Sympa-gastrics, Para-pelvic, Soma-dendal)
74
Detrusor Leak Point Pressure Numbers
Note: This metric is only used for patients with neurogenic lower urinary tract dysfunction DLPP is most reliable predictor of upper tract deterioration in NLUTD DLPP >40 is predictive of future upper tract deterioration DLPP >15 indicates impaired compliance
75
DLPP and VLPP are determined by the resistance of EUS to fluid leak
Interventions that don't affect the resistance of EUS will not affect either LPP
76
Open bladder neck at rest without prior prostatectomy
Multiple System Atrophy Progressive degeneration of neurons in multiple areas of the brain Incomplete emptying, ED, "hot crossed buns sign" on MRI
77
Primary Bladder Neck Obstruction
Level of obstruction on VUDS is clearly the bladder neck itself Reduce bladder neck with TUIP vs. TURP
78
Uroflow curve without pressure data: flattened bell
A/w adequate detrusor function with fixed obstruction
79
Uroflow curve without pressure data: saw tooth
A/w DU or DESD
80
"Poor compliance" on UDS
<10-15 cc/cm H2O is a reasonable rough definition Practically, absolute storage pressure > 40 cm H2O is more relevant as this has been a/w deterioration of upper tracts
81
Spina Bifida and NGLUTD
Highly a/w NGB in children and highly a/w upper tract damage (especially with DESD on initial UDS) if not managed appropriately Unlike SCI, in lumbosacral SB, neural function and UDS findings cannot be predicted by the level of the lesion If SB patient develops new hydro, perform UDS If findings concerning, get spinal MRI to rule out tethered cord or other changes prior to bladder augmentation
82
Higher chance of paternity with SB at which lesion level?
L5 or sacral level
83
Spinal shock
Bladder acontractility, areflexia, synergic internal and external sphincters, absent guarding reflex, absent somatic control of the external sphincter Resolution: return of bulbocavernosus reflex or return of DTRs below the SCI
84
Guarding reflex
Ability of the striated sphincter (EUS) to contract during bladder filling - External sphincter activity at the time of DO is part of the normal guarding reflex
85
Lesions above the pons (brainstem still functioning, CVA or Parkinson's): bladder/ sphincter
Detrusor Overactivity: Yes (Parkinson's with impaired contractility) DESD: No DISD: No Autonomic Dysreflexia: No Intact Bladder Sensation: Yes Detrusor Areflexia: No
86
Neurologic Insult Pons to T6-8: bladder/sphincter
Detrusor Overactivity: Yes DESD: Yes DISD: Yes Autonomic Dysreflexia: Yes Intact Bladder Sensation: Yes Detrusor Areflexia: No
87
Neurologic Insult T6-8 to S2: bladder/sphincter
Detrusor Overactivity: Yes DESD: Yes DISD: No Autonomic Dysreflexia: No Intact Bladder Sensation: No Detrusor Areflexia: No
88
Neurologic Insult Injury below S2: bladder/sphincter
Detrusor Overactivity: No DESD: No (may have fixed EUS tone at rest) DISD: No (may have open or contracted IS) Autonomic Dysreflexia: No Intact Bladder Sensation: No Detrusor Areflexia: Yes
89
Neurologic Insult MS: bladder/sphincter
Detrusor Overactivity: Yes DESD: Maybe DISD: No Autonomic Dysreflexia: No Intact Bladder Sensation: Yes Detrusor Areflexia: No
90
Neurologic Insult Multiple System Atrophy: bladder/sphincter
Detrusor Overactivity: Yes DESD: No (may have EUS denervation) DISD: No (may have open bladder neck at rest) Autonomic Dysreflexia: No Intact Bladder Sensation: Yes Detrusor Areflexia: No
91
Lesions above the pons (brainstem still functioning like CVA or Parkinson's)
DO with synergistic/coordinated activity of internal and external sphincters The sphincters will relax appropriately during involuntary bladder contractions Supra-pontine insults should NOT cause detrusor sphincter dyssynergia Sphincter bradykinesia can occur with Parkinson's --> slow relaxation of EUS at start of void
92
Lesions involving brain stem + cord above T6 (including C-spine)
After spinal shock: Detrusor overactivity + detrusor external sphincter dyssynergia (DESD) + Smooth muscle sphincter dyssynergia (DISD) + autonomic dysreflexia
93
Autonomic dysreflexia
Afferent stimuli below T6 (bladder distention) in patient with injury above T6 --> massive reflex sympathetic discharge --> vasoconstriction, HTN, reflex bradycardia, flushing, HA, diaphoresis
94
Complete lesion between T6 and S2
After spinal shock: Absent sensation + DO + DESD + smooth muscle sphincter synergy DESD arises because the normal pathways for supraspinal centers to inhibit external sphincter contraction during voiding has been disrupted Intact sacral nerve arcs (can be assessed by presence of bulbocavernosus reflex) are required for DESD
95
Detrusor External Sphincter Dyssynergia
Involuntary rise in EMG activity (EUS contraction) during an involuntary DO contraction, narrowing of the membranous urethra, which can lead to incomplete bladder emptying and risk to upper tracts Further neurological evaluation is warranted (i.e. MS) Sacral nerve arcs must be present to have DESD, intact bulbocavernosus reflex indicates the presence of sacral nerve arcs (only 70% of women have this reflex, 30% do not) Sphincterotomy is a historical option for a patient with DESD (new hydro or on UDS) and inability/refusal to CIC. Actual DESD is only possible in the setting of a spinal cord lesion; a patient may have pelvic floor dysfunction with symptoms that sound like DESD - the most likely UDS finding for such a patient is a low peak flow rate --> try PFPT or SNM
96
Cauda Equina (Horse's Tail): L2-S5 spinal nerve bundle
STARTS at L1 vertebra, typically a/w spinal pathology (disc herniation) in the L4-S2 region injury Typically presents with lumbar spinal pain a/w bladder and bowel incontinence Nerve compression --> impairment of parasympathetic motor and sensory fibers to the bladder and pelvic floor (bulbocavernosus reflex absent) +/- impairment of pudendal nerve fibers innervating the external sphincter - UDS shows detrusor areflexia, normal compliance +/- denervation potentials from external sphincter - NSGY emergency to decompress nerve
97
Lesions at or distal to sacral cord
Detrusor areflexia and denervation potentials on EMG Below S2: (after spinal shock) persistent detrusor areflexia +/- decreased compliance +/- open smooth sphincter +/- residual resting sphincter
98
The cremasteric artery is a branch of the...
...inferior epigastric artery (from external iliac)
99
The vasal artery is a branch of the...
...superior vesical artery (a branch of the anterior trunk of the internal iliac)
100
Inferior hypogastric plexus injury (after LAR or APR or TAH)
Denervation of bladder +/- sphincter mechanisms --> areflexia (pelvic nerve damage) + fixed external sphincter tone (pudendal nerve innervation of external sphincter is disrupted) --> increased outlet resistance --> areflexic poorly compliant bladder --> UDS shows decreased compliance, incompetent bladder neck, fixed EUS, detrusor underactivity
101
SCI in T11 - L2 may damage sympathetic supply to bladder and impair tonic outlet resistance...
Crede maneuver may allow patient to overcome remaining outlet resistance and void
102
Quinolones side effects
(ciprofloxacin, levofloxacin, etc) Inhibit DNA gyrase May cause false positive on opiate screen Risk of tendon rupture Affect metabolism of theophylline (tx asthma/COPD), caffeine
103
Painful necrotic penile ulcer + painful inguinal LAD
Gram-negative coccobacilli (haemophilus ducreyi) Chancroid Tx with Azithromycin (1g PO)
104
Gonorrhea treatment
Single dose IM ceftriaxone
105
Chlamydia treatment
10 days PO doxycycline
106
Non-gonoccocal urethritis
think chlamydia or ureaplasma treat with two weeks PO doxycycline vs. single dose azithromycin
107
Alpha-blocker most likely to cause retrograde ejaculation? Least likely?
Most = Silodosin Least = Alfuzosin
108
Prostatitis is characterized into 4 syndromes
Category I: ABP, MC due to E. Coli II: Chronic bacterial prostatitis - rUTI due to same organism, mc E. Coli, enterococcus or another gram - III: Chronic prostatitis/pelvic pain syndrome. Type A = inflammatory with WBCs, Type B = non-inflammatory, no WBCs IV: Asymptomatic inflammatory prostatitis - incidental Dx on TRUS Bx for elevated PSA
109
Male urethral blood supply
Internal iliac --> internal pudendal --> branches into (from ventral to dorsal) BCD B = bulbourethral (artery of bulb of penis) C = cavernosal (deep artery of penis) D = dorsal penile arteries (also supplies most of blood flow to glans penis)
110
How is baseline flaccidity maintained?
Tonic contraction of penile vascular smooth muscle via norepinephrine release from postganglionic sympathetic nerves
111
How is an erection achieved?
Parasympathetic stimulation Release of NO from non-adrenergic, non-cholinergic nerves NOx binds guanylyl cyclase Increases cGMP (cGMP is broken down by PDE5) + protein kinase Opens K+ channels and closes Ca++ channels Decreases intracellular Ca++ Ca++ dissociates from Calmodulin Relaxation of penile arterial smooth muscle and increased arterial blood flow PGE1 also increases conversion of ATP to cAMP by adenylate cyclase Decreases intracellular Ca++ Ca++ dissociates from Calmodulin Relaxation of penile arterial smooth muscle
112
Detumescence?
PDE5 breaks down cGMP so smooth muscle relaxation is reversed + PIP3 pathway increased intracellular Ca++ cavernosal SM contraction increased intracorporeal pressure slow decrease in pressure as reopening of venous channels occurs with resumption of baseline arterial flow Rapid decrease in intracorporal pressure Flaccidity
113
After complete suprasacral SCI, reflexogenic (but not psychogenic) erections are generally preserved
Sacral SCI eliminates reflexogenic erections but may not eliminate psychogenic
114
Painless, slowly growing ulcers without lymphadenopathy
Granuloma inguinale (klebsiella granulomatosis) Azithromycin 1g PO weekly for 3 weeks Doxycycline for 3 weeks Treat partners within 60 days
115
NLUTD: Low Risk - Stratification - Further workup - Surveillance
Lesion is suprapontine (CVA, Parkinson's, brain tumor, TBI, CP) or distal to cord (disk disease, s/p pelvic surgery, DM) Spontaneously voiding with low PVR No rUTIs No bladder stones Normal/stable renal function and upper tract imaging Synergistic voiding on UDS Further workup and surveillance not indicated Reevaluate ID new problems arise (autonomic dysreflexia, UTIs, stones, upper urinary tract or renal function deterioration)