amboss 7/1 renal Flashcards

1
Q

what type of cast is found in nephrotic syndrome

A

fatty casts

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2
Q

pregnant women with pyelonephritis should be what

A

admitted and given IV cefotaxime

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3
Q

what is the treatment of choice for complicated pyelonephritis

A

IV ciprofloxacin 10-14 days`

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4
Q

what is the likely culprit organism for a UTI with an indwelling catheter and + LE. patient has a history of stones

A

proteus mirabilis

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5
Q

what else will you find with a proteus infection

A

alkalized urine pH >7

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6
Q

what is the most common cause of UTI

A

ascending infection

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7
Q

what is a contraindication for foley

A

suspected urethral injury

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8
Q

what is the preferred method for evaluating urethral injury

A

retrograde urethrogram

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9
Q

what is a characteristic finding of uric acid crystals

A

low urine pH (which is characteristic of calcium oxalate, cystine as well), radiolucent stones on Xray (cannot be seen),

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10
Q

what are bipyramidal crystals

A

calcium oxalate

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11
Q

what are hexagon shaped crystals in the urine

A

cystinuria

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12
Q

what stones form in alkaline pH

A

calcium phosphate and struvite stones

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13
Q

which stones are found on x ray

A

calcium phosphate and struvite stones

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14
Q

what is the treatment of choice for unilateral fibromuscular dysplasia

A

ramipril and percutaneous angioplasty without stent

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15
Q

what is the treatment of choice for a real stone larger than 10mm

A

lithotripsy

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16
Q

what is a relative contraindication to lithotripsy

A

obesity

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17
Q

what is the alternative to lithotripsy

A

ureterenoscopy

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18
Q

what is the proper treatment for a large stone obstructing the ureter causing hydroneophrosis with concomitant infection (UTI/pyelo)

A

nephrostomy tube to decompress the ureter

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19
Q

what is the cause of analgesic nephropathy

A

Prostacyclins enhance renal blood flow by dilating renal capillaries, most prominently in the medulla of the kidney. By inhibiting prostacyclin production, nonsteroidal anti-inflammatory drugs (NSAIDs) decrease renal blood flow. After prolonged exposure to analgesics, especially analgesics used in combination, as is the case here, patients develop renal papillary necrosis and subsequent analgesic nephropathy (chronic kidney disease).

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20
Q

what is the presentation of analgesic nephropahty

A

features of kidney dysfunction: fatigue, anemia, uremia, and elevated creatinine. He also has sterile pyuria (WBCs in the urine with negative cultures) and ultrasonography shows changes associated with chronic kidney disease. Along with these findings, his long-term use of naproxen and the aspirin-caffeine combination

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21
Q

what are the characterstics to watch out for in renal cell carcinoma vs bladder cancer

A

signs of increased renin production –facial plethora, hypertension, blurry vision, signs of polycythemia

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22
Q

Patients with hematuria should generally be evaluated for

A

urinary tract infections (urinalysis, urine culture), kidney function (creatinine, BUN), and glomerular disease (urine microscopy). Furthermore, patients > 35 years or with risk factors for urothelial malignancy regardless of age should undergo cystoscopy to evaluate the lower urinary tract and CT urography to evaluate the upper urinary tract.

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23
Q

where does blood that presents initially in the stream of urine and then becomes normal before the stream ends typically originate from

A

the urethra

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24
Q

where does blood that presents throughout the stream or terminal blood come from in the urinary system

A

the bladder or above

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25
Q

what is the presentation of prerenal AKI

A

BUN/Cr > 20, oliguria, azotemia, decreased urine sodium (in response to the prerenal AKI)

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26
Q

what causes an increased risk of ascending bacterial infections during pregnancy

A

Increased levels of progesterone result in ureteral smooth muscle relaxation and ureteral dilation. Pressure exerted by the expanding uterus contributes to ureteral dilation. Ureteral dilation can increase urinary stasis and ureterovesical reflux, leading to higher rates of ascending bacterial infections.

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27
Q

One of the most commonly used polychemotherapy regimens for high-grade non-Hodgkin lymphoma is…

A

CHOP (a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone).

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28
Q

what is a SE of CHOP (a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone).

A

Hemorrhagic cystitis, which presents with lower urinary tract symptoms and hematuria, is a common complication of cyclophosphamide therapy.

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29
Q

what is the treatment for CHOP induced hemorrhagic cystitis

A

mercaptoethane sulfonate –by deactivating acrolein and by increasing the urinary excretion of cysteine, a free radical scavenger. Adequate hydration and frequent voiding are further important measures to prevent hemorrhagic cystitis.

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30
Q

what is the work up for a child with recurrent UTI

A

voiding cystourethrography

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31
Q

what test is suggestive of cysteinuria

A

urine nitroprusside test

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32
Q

what are the findings for minimal change disease on light microscopy

A

No changes

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33
Q

what are the findings for minimal change disease on electron microscopy

A

effacement of foot processes of the podocytes

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34
Q

what are the findings for minimal change disease

A

proteinuria, edema, hypoalbuminuria, (nephrotic syndrome).

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35
Q

what does linear deposition of antiGBM antibiodies indicate

A

good pastures

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36
Q

what does deposits of IgG and C3 at the glomerular basement membrane indicate

A

membranoproliferative glomerulonephropathy

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37
Q

what does subepithelial dense deposits indicate on EM

A

spike and dome appearance; membranous

membranous nephropathy looks like thicken glomerular basement membrane.

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38
Q

is membranous nephropathy found in children

A

no.

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39
Q

what does mesangial proliferation indicate

A

IgA nephropathy

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40
Q

what else, other than deposits of IgG and C3 at the glomerular basement membrane can indicate membranoproliferative glomerulonephropathy

A

Splitting of the glomerular basement membrane (which results in a tram-track appearance)

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41
Q

what is associated with membranous nephropathy

A

caused by immune complex deposition (associated with systemic lupus erythematosus, hepatitis B, or hepatitis C) or by overactivation of the alternative complement pathway.
more likely to occur in asian or Korean people

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42
Q

what are the imaging findings for post strep glomerulonephritis

A

Light microscopy: glomeruli appear enlarged and hypercellular (infiltration of monocytes and polymorphonuclear cells)
Immunofluorescent microscopy: granular deposits (IgG, IgM, C3 complement), which create a “lumpy-bumpy” appearance (starry sky pattern)

sub epithelial complex deposition

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43
Q

what is the presentation of IgA nephropathy

A

second to third decade of life with recurrent episodes of gross hematuria usually during or immediately following infection

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44
Q

what is the mechanism of IgA nephropathy

A

Between episodes of flares, patients typically have asymptomatic urinary abnormalities such as microhematuria. The most likely explanation for these findings is an increased number of defective circulating IgA antibodies, the synthesis of which is triggered by mucosal infections (e.g., pharyngitis).

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45
Q

does hypertension occur with minimal change disease

A

no.

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46
Q

what are complement levels in minimal change

A

normal

47
Q

what does nephrotic syndrome with hypertension, reduced complement associated with Hep B infection

A

membraneous nephropathy.

48
Q

who gets minimal change

A

children less than 5

49
Q

what is the presentation of renal tubular acidosis type I

A

Type 1 renal tubular acidosis is associated with decreased activity of the H+/K+ ATPase antiporter on the apical surface of intercalated cell, which reabsorbs K+ and secretes H+ into the lumen of the tubule. This subsequently results in hypokalemia and hyperchloremic metabolic acidosis with urine that cannot be acidified to a pH < 5.5.

50
Q

how do patients with RTA1 present

A

in a hyperchloremic, hypokalemic, metabolic acidosis with a urine pH of > 5.5

51
Q

what is potter sequence

A

craniofacial abnormalities, clubbed feet, and pulmonary hypoplasia.

52
Q

what is a good prophylactic agent for postcoital UTI

A

Bactrim or nitrofurantoin, cephalexin, a fluoroquinolone,

53
Q

postcoital treatment for UTI agent

A

amoxicillin clavulanate

54
Q

what is urge incontinence

A

from increased detrusor muscle activity, which causes involuntary detrusor muscle contraction and urinary tenesmus that lead to a sudden release of urine.

55
Q

what is the treatment for urge incontinence

A

Anticholinergic agents (e.g., oxybutynin) can help treat this condition by decreasing detrusor muscle tone.

56
Q

what is overflow incontinence

A

Overflow incontinence (due to detrusor under-activity or bladder outlet obstruction) results in increased urine bladder volumes. Patients with overflow incontinence usually have continuous urinary leakage or dribbling (not sudden episodes of urinary loss), and post-void residual urine volumes would be increased.

57
Q

Stress incontinence

A

can result from decreased pelvic floor muscle tone in which the urethra and bladder neck cannot completely close against the anterior vaginal wall. As a result, increases in intra-abdominal pressure (e.g., coughing, sneezing, lifting) force urine through an incompletely closed urethra.

58
Q

what is the cause of stress incontanence

A

urethral hyper mobility

59
Q

what is the first line surgical intervention for stress incontinence and when is it used

A

A urethral sling is the first-line surgical procedure for stress incontinence if conservative therapy, consisting of pelvic floor muscle exercises (Kegel exercises), lifestyle changes (e.g., weight loss, alcohol cessation), and use of continence pessaries have failed. The sling is inserted via vaginal approach and supports and partially compresses the urethral lumen, thereby decreasing or stopping urinary leakage when intraabdominal pressure increases

60
Q

rapidly progressive glomerulonephritis presents how

A

with crescent formation and hematuria with proteinuria

61
Q

what is the treatment for RPGN

A

methylprednisolone

62
Q

what is the cause of incontinence in NPH

A

inability to suppress voiding caused by underlying compression of the periventricular white matter tract

63
Q

what is the presentation of nephrogenic DI

A

hypernatremia, high ADH, with low urine osmolarity

presents with polyuria, polydipsia, nocturia, dehydration

64
Q

what is nephritic syndrome

A

this is glomerular capillary change that causes proteinuria, hmaturia, oliguria, azotemia and salt retention. this results in swelling of the periphery, hypertension and intravascular volume expansion

65
Q

what is allergic interstitial nephritis

A

rash and kidney pain. there will be eosinophilia on urinalysis

66
Q

what can cause allergic interstitial nephritis

A

PPIs, such as pantropazole rifampin

cephalosporins, NSAIDs,

67
Q

what kidney diseases/disorders does lupus cause

A

causes membranous nephropathy. thickening of the capillary loops through immune complex deposition.
subepithelial spike and dome appearance

lupus also can cause membranoproliferative glomerulonephritis which causes microhematuria and elevated creatinine

68
Q

what are the immune complexes in membranous nephropahty caused by lupus

A

IgG and C3

69
Q

what is hypercellular glomeruli associated with

A

PSGN

70
Q

what is another cause of membraneous nephropathy

A

lung cancer/solid malignancy
Deposition of antibodies between podocytes and the basal membrane causes thickening of glomerular capillary loops and basal membrane, which in turn leads to nephrotic syndrome.

71
Q

who gets focal segmental glomerulosclerosis

A

heroin abuse, obesity, sickle cell disease, and HIV infection

72
Q

what is the course of FSGS

A

ESRD

73
Q

what is the presentation of acute interstitial nephritis

A

fever, rash, bloody urine, eosinophils in urine

74
Q

what are the characteristics of diabetic kidney

A

Nodular glomerulosclerosis with Kimmelstiel-Wilson nodules is pathognomonic of diabetic nephropathy, even though diffuse glomerulosclerosis is the most common finding. Early antihypertensive treatment, e.g., with ACE inhibitors, can delay the progression of diabetic nephropathy.

75
Q

what is common in people with sickle cell trait

A

renal papillary ischemia/necrosis

76
Q

what is scleroderma renal crisis

A

severe hypertension and features of acute renal failure, such as increased creatinine, oliguria/anuria, vomiting, and fluid overload (as evident from pedal edema, dyspnea, jugular venous distention, an S3 gallop, pulmonary edema, and pleural effusion).

77
Q

what is the pathophysiology of myeloma kidney

A

immunoglobulin light chains or Bence Jones protein

78
Q

what is required for the diagnosis of multiple myeloma

A

bone marrow biopsy

79
Q

what are hepatic cysts characteristic for

A

polycystic kidney disease

80
Q

what should autosomal dominant polycystic kidney disease really be called

A

polycystic renal-hepatic-ACOM disease.

81
Q

what are other findings in ADPKD

A

mitral valve prolapse, kidney, hepatic, testicular, spleen, ovary, and pancreatic cysts

82
Q

what is IgA neprhopathy

A

renal glomerular damage caused by IgA deposition in the mesangium of the renal glomeruli

83
Q

what is the treatment for bladder cancer with muscle wall involvement but no local invasion or lymph node

A

radical cystectomy with ileoconduit and cisplatin

84
Q

what is the treatment for uncomplicated pyelonephritis

A

7 days of fluoroquininolone outpatient

85
Q

Detrusor sphincter dyssynergia is

A

commonly seen in patients with multiple sclerosis or spinal cord injury. In patients with detrusor sphincter dyssynergia, involuntary contractions of the detrusor muscle press small amounts of urine against the contracted sphincter muscle.

86
Q

what is a devstating consequence of pyelonephritis

A

renal papillary necrosis

87
Q

what amyloid is produced from RA or inflammatory processes

A

amyloid A

88
Q

what are 5 alpha reductase inhibitors used for

A

BPH.

89
Q

what is consequence of using 5 alpha reductase inhibitors for BPH

A

reduces symptoms and PSA levels

90
Q

what are the recommendations for PSA screening

A

should be discussed if there is mild symmetrical enlargement and the person is 50

91
Q

what is the effect of losartan on vessel tone, renin actiivty, sodium excretion, levels of aldosterone

A

blocking of angiotensin II receptors leads to an increase in urinary sodium excretion, decreased vessel tone, and lower levels of aldosterone. The combination of these effects lowers blood pressure. Due to a loss of negative feedback regulation, treatment with sartans typically leads to increased renin levels and increased renin activity, which in turn leads to increased levels of angiotensin II.

92
Q

what is a complication of crohns disease

A

Malabsorption of fatty acids due to deficiency in bile acids is common in patients with Crohn disease (and/or short bowel syndrome) and likely explains this patient’s nephrolithiasis. In the intestinal lumen, undigested fatty acids chelate calcium, which would normally bind oxalate and lead to its excretion in the feces. Patients with Crohn disease often have pathologically increased luminal oxalate and increased oxalate absorption. After entering the serum, oxalate is excreted in the urine (hyperoxaluria), where it binds calcium and forms calcium oxalate stones.

93
Q

what are uric acid stones treated with

A

potassium citrate

94
Q

what can exacerbate uric acid stones

A

probenecid

95
Q

how does posterior urethral tear present

A

high riding prostate, blood at the meatus, urge to void but cant,

96
Q

lymphogranuloma venereum is what and presents how

A

Chlamydia trachomatis are responsible for this STI, which has an increasing incidence among men who have sex with men. Further manifestations are systemic symptoms such as fever, malaise, chills, and/or myalgia. notorious for pustules and granuloma with painless lesion/ulcer

97
Q

what is the treatment for HPV condylomata acuminata

A

curettage or laser surgery or electrocoagulation

98
Q

painless vascular lesions and the absence of inguinal lymphadenopathy are suggestive of

A

granuloma inguinale, which is caused by Klebsiella granulomatis.

99
Q

what is the treatment for Klebsiella granulomatis.

A

azithromycin

100
Q

what is the test to confirm the diagnosis of primary syphilis

A

dark field microscopy

101
Q

treatment for C. trachomatis epididymitis

A

involves ceftriaxone and doxycycline.

102
Q

what is the most common cause of epidimititis from 15-35

A

Neisseria gonorrhoeae and Chlamydia trachomatis.

103
Q

common cause of epididymitis in prepubertal boys, males > 35 years,

A

Escherichia coli

and men who are the insertive partner during anal intercourse.

104
Q

what is an alternative treatment for chlamydia

A

doxycycline

105
Q

what is the first thing to do with testicular pain

A

ultrasound to rule out torsion

106
Q

is the standard of care for treating non-seminomas in all stages.

A

Adjuvant chemotherapy with cisplatin, etoposide, and bleomycin (BEP regimen) The patient has signs of advanced non-seminoma with metastases to his liver and increased tumor markers (stage IIIC). In addition to the radical inguinal orchiectomy, he would likely require 4 cycles of this regimen due to the advanced nature of his cancer.

107
Q

increased serum β-hCG concentration, and often produce large amounts of α-fetoprotein.

A

A yolk sac tumor

108
Q

mild increase in serum β-hCG (typically < 100 mIU/mL) but no alpha fetal protein

A

seminoma

109
Q

large amounts of beta-HCG

A

choriocarcinoma

110
Q

when does spontaneous testicular descent occur

A

by 4-6 months it is unlikely to happen

111
Q

does a varicocele increase the risk of testicular torsion

A

no.

112
Q

Risk factors for testicular torsion include

A

testicular tumors, testicles with a horizontal lie, undescended testes, a spermatic cord with a long intrascrotal portion, and extension of the tunica vaginalis over the proximal spermatic cord (bell-clapper anatomical variant).

113
Q

what can leydig tumors do?

A

produce sex hormones