PANCE Prep- Nephro/Uro Flashcards

1
Q

Most active secretion happens in ___

Most reabsorption happens in ___

A

DCT

PCT

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2
Q

If serum glucose rises about ___, it reaches saturation and spills into the urine

A

180mg/dL

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3
Q

SE of loop diuretics

Site of action and most unique use

A
  1. *HypoK+, hypoCa++, hypoMg++
  2. HypoNa+ (less than thiazides)
  3. Hyperglycemia
  4. Hyperuricemia- caution in gout
  5. Ototoxicity
  6. Sulfa allergy
  7. Hypochloremic metabolic alkalosis

Thick ascending loop of henle
Use: hyperCa++

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4
Q

SE of thiazide diuretics

Site of action and most unique use

A
  1. *HypoNa+ (more than loop diuretics)
  2. HyperCa++
  3. HypoK+
  4. Hyperglycemia
  5. Hyperuricemia- caution in gout
  6. Sulfa allergy

DCT
Use: nephrogenic DI

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5
Q

SE of K+ sparing diuretics

Site of action and most unique use

A
  1. HyperK+
  2. Metabolic acidosis
  3. gynecomastia (w/ spironolactone)

Collecting ducts/tubules- inhibits aldosterone
Use: CHF and hyperaldosteronism

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6
Q

SE of Mannitol

Site of action and most unique use

A
  1. Pulmonary edema

PCT
Use: intracranial HTN/shock

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7
Q

SE of acetazolamide

Site of action and most unique use

A
  1. hyperchloremia metabolic acidosis
  2. kidney stones

PCT
Use: intracranial HTN and Glaucoma*

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8
Q

What hormones affect kidney absorptions and secretion?

A
  1. PTH- increases phosphate excretion in PCT and Ca++ resportion in DCT
  2. Angiotensin II- increases Na/H20 resportion in PCT
  3. Aldosterone- increases Na resorption in Collecting ducts/tubules
  4. ADH- inhibits H20 resportion
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9
Q

Diagnostic Components of Nephrotic Syndrome

A
  1. Proteinuria (>3.5g/day on 24hr urine or 3-4+ on dip, UA shows “OVAL FAT BODIES “MALTESE CROSS SHAPED)
  2. Hypoalbuminemia (<3.4g.dl)
  3. Hyperlipidemia
  4. Edema (often periorbital in kids)- worse in AM
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10
Q

80% of nephrotic syndrome in children is due to ___.

Dx and Tx?

A

Minimal change disease
-etiologies: idiopathic, allergies, viral infection

DX: podocyte damage on electron microscope, loss of neg. charge of glomerular basement membrane

TX: prednisone

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11
Q

MC cause of focal segmental glomerulosclerosis (FSGS)

TX?

A
  1. HTN esp. in AA

tx: Corticosteroids/prednisone

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12
Q

Clinical manifestations of acute glomerulonephritis (AGN)

Dx and tx?

A
  1. HTN
  2. Hematuria*** (RBC casts and “cola-colored urine)
  3. Dependent edema (periorbital in kids)
  4. Proteinuria
  5. Azotemia (nitrogen in urine)
  6. fever
  7. Oliguria (decreased UOP)

DX: hematuria (RBC casts), proteinuria, high specific gravity
**Renal biopsy is GOLD STANDARD

TX: usually self-limited
-Rapidly progressive AGN or severe: corticosteroids + Cyclophosphamide

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13
Q

Causes of acute glomerulonephritis

A
  1. IgA Nephropathy (Berger’s Disease)- MC cause in adults worldwide (young males s/p URI or GI infection)
  2. Post infection- GABHS
  3. Membranoproliferative
  4. Rapidly progressive glomerulonephritis
  5. Goodpastures’s Disease
  6. Vasculitis/ Wegener’s
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14
Q

Dx and Tx of IgA Nephropathy (Berger’s Disease)

A

DX: IgA mesangial deposits on immunostaining

TX: ACEI +/- Corticosteroids

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15
Q

Nephrotic vs Nephritic Syndrome

A

Nephrotic:

  1. increased urinary protein loss
  2. Proteinuria, HYPOALBUMINEMIA, EDEMA**, HYPERLIPIDEMIA
  3. UA: FATTY CASTS, OVAL FAT BODIES “Maltese cross”
  4. Biopsy: HYPOcellular

Nephritic: via inflammation

  1. increased urinary protein loss AND RBC loss
  2. Proteinuria, HTN, AZOTEMIA, OLIGURIA, HEMATURIA (RBC CASTS), FEVER, FLANK PAIN
  3. UA: Hematuria, RBC casts
  4. Biopsy: HYPERcellular, crescent shaped in RPGN
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16
Q

RIFLE Criteria for AKI

and phases of AKI

A

Risk, Injury, Failure:, Loss and ESRD

Phases: Oliguric (maintenance)–> diuretic–> recovery

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17
Q

Hallmark of Intrinsic AKI: ____

Causes of intrinsic AKI:

A

hallmark: CELLULAR CAST FORMATION

Causes:

  1. **Acute tubular Necrosis (ATN): prolong ischemia/hypovolemia vs nephrotoxic
    - aminoglycosides, contrast dye, gout crystals, rhabdomylolysis, MM (Bence-Jones)
  2. Acute tubulointerstital nephritis (AIN): inflammatory or allergic response
    - PCN, NSAIDS, sulfa drugs, infections, autoimmune/idiopathic
  3. Glomerular (AGN)
  4. Vascular
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18
Q

Dx and TX:

  1. Acute tubular necrosis
  2. Acute tubulointerstital nephritis
A
  1. ATN
    DX: UA: epithelial cell cast and Muddy brown cast*
    TX: remove offending agent, IVF (recovers in 7-21 days)
  2. AIN
    DX: UA: WBC casts are pathognomonic*, EOSINOPHILIA, increases serum IgE
    TX: remove offending agent (recovers in 1 yr)
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19
Q

What are the following casts seen in?

  1. RBC casts
  2. Muddy brown casts
  3. WBC casts
  4. Waxy casts
  5. Hyaline casts:
A
  1. RBC casts- AGN or vasculitis
  2. Muddy brown casts- ATN
  3. WBC casts- AIN or pyelonephritis
  4. Waxy casts- (narrow) CHRONIC ATN or (broad) ESRD*
  5. Hyaline casts: nonspecific
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20
Q

Describe the urine Na+ and specific gravity in prerenal AKI and ATN AKI

A

Prerenal: LOW urine Na+ and HIGH specific gravity

ATN: HIGH urine Na+ and LOW specific gravity

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21
Q

DX:

  • Abdominal/flank pain, palpable flank mass, HTN, hematuria,
  • CERBRAL “berry” aneurysm, hepatic cysts, MVP, colonic diverticula
A

Adult Polycystic Kidney Disease (AD disorder)

DX: renal US

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22
Q

What can cause Hyper and hypo-phosphatemia

A

Hyper: causes muscle weakness/flaccid paralysis

  1. Renal failure (MC)
  2. Primary HypoPTH
  3. Vit. D. INTOX

Hypo: causes soft tissue calcifications

  1. Primary HyperPTH
  2. Refeeding
  3. Antacids
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23
Q

Causes of Chronic kidney disease

*first presenting sx/ single best predictor of disease progression

A
  1. DM (MC)
  2. HTN (2nd MC)
  3. Glomerulonephritis

1st: proteinuria- microalbumuria
**Best to test w/ SPOT U.Albumin/U. Creatinine ratio
(use spot over 24hr)

*metabolic acidosis seen later on

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24
Q

What are the 2 most important modifiable risk factors for CKD

A
  1. HTN (goal <140/90 w/ ACEI)
  2. proteinuria- restrict protein in diet (w/ ACEI)

*goal HgbA1c <6.5%

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25
Q

Complications of CKD

A
  1. Anemia of chronic disease (normochromic, normocytic)
    * TX: oral FeSO4+/- EPO or Darbepoetin-alpha
  2. Coagulopathy- platelet dysfunction, increased bleeding
  3. Osteodystrophy (bone and prox. muscle pain and pathologic fx)
    - Osteitis fibrosis Cystica- periosteal erosions (“salt and pepper on skull xray”)
    - Increased PO4 and HYPOCALEMEMIA
    - LOW Vit. D (cannot be produced by kidney) and High PTH
26
Q

When is dialysis indicated for CKD

A

GFR = 10mL/min or serum creatinine >/= 8mg/dL

27
Q

What is SIADH and its etiologies?

A

increased ADH–> hypoNa and free water retention
***ISOVOLEMIC, Hypotonic, hyponatremia

Etiologies:
1. Stroke (MC), head trauma, post-op
2. Small cell lung CA
3. Meds: narcotics, anticonvulsants, Carbamazepine, IV cyclophosphamide, antidepressants (TCA/SSRIs), hydrochlorothiazide, ectasy
"AC-CANE"
28
Q

Tx of SIADH

A
  1. H20 restriction*
  2. Demelocycline (inhibits ADH)
  3. IV HYPERTONIC saline w/ furosemide
29
Q

Etiologies of diabetes inspidius

A
  1. Central- decreased ADH production (MC)
  2. Nephrogenic- partial/complete insensitivity to ADH

*Large amounts of dilute urine (polyuria, polydipsia, nocturia, HYPERNATREMIA)

30
Q

DX and TX DI

A

DX:

  1. fluid deprivation test- continues to produce dilute urine
  2. Desmopressin (ADH) stimulation test
    - Central DI- reduction in UOP
    - Nephrogenic- no change

TX:

  1. Central DI: Desmopressin/DDAVP or carbamazepine
  2. Nephrogenic: HCTZ, restrict Na+ and protein in diet

*if sx–> hypotonic fluid (oral is best)

31
Q

The following conditions will cause what type of HypoNA+?

  1. CHF
  2. SIADH
  3. HyperTG or Hyperproteinemia
  4. Hyperglycemia or mannitol infusion
  5. Cirrhosis
  6. Nephrotic Syndrome
A
  1. CHF: HYPERvolemic hypoNa+
  2. SIADH: Iso/eu+olemic hypoNa+
  3. HyperTG or Hyperproteinemia: Isotonic HypoNa+
  4. Hyperglycemia or mannitol infusion: Hypertonic hypoNa+
  5. Cirrhosis: HYPERvolemic hypoNa+
  6. Nephrotic Syndrome: HYPERvolemic hypoNa+

*HYPOTONIC HYPONA+ IS CLINICALLY SIGNIFICANT (volume depletion)

32
Q

What values go into calculating serum Osm?

A

2x [Na+] + glucose/18 + [BUN]/2.8

33
Q

Etiologies, lab findings, and EKG findings for Hypo and Hyper- Mg++

A

Hypo:

  1. etiologies: malabsportion, ETOHics, PPIs, Loop/thiazide diuretics
  2. Labs: HypoMg, HypoK, HypoCa++ (increased DTRs), low PTH
  3. EKG: Prolonged QT and PR interval, Torsades

Hyper:

  1. etiologies: renal insuff./AKI/CKD, lithium
  2. Labs: HyperMg, HyperK+, HyperCa++ (decreased DTRs)
  3. EKG: Prolonged QT and PR interval, Hyper K- peaked T waves, short QR, wide QRS
34
Q

EKG changes with Hypo and Hyper- K+

and TX

A

Hypo:
EKG: Flat T waves, prominent U waves
**ASSOCIATED risk with increased risk of Digoxin toxicity
TX: K+ replacement- tx hypoMg++ if present

Hyper:
EKG: Peaked T waves, flat P waves, short QR, wide QRS
TX: IV Calcium gluconate- stabilizes cardiac membranes
-Insulin w/ glucose (shifts K+ intracellularly)
-Kayexalate
-B2agonists

35
Q

Epididymitis is usually caused by: ____

Orchitis is usually caused by: ___

A

Epididymitis: bacterial, >35y/o and kids: enteric organism (E. coli or Klebsiella), if <35y/o: Chlamydia*, gonorrhea

Orchitis: viral, Mumps**

36
Q

DX and TX:

  • gradual onset of scrotal pain, erythema, swelling, +/- fever
  • Positive Prehn’s sign: relief of pain w/ elevation of affected scrotum
  • Positive/normal cremasteric reflex
A

Epididymitis and Orchitis

DX: scrotal US: enlarged epididymis, increased testicular blood flow*
UA: pyuria/bacteriuria

TX: bed rest, elevate scrotum, cool compresses, NSAIDS

  • Acute epididymitis s/s C and GN: Doxycycline + Ceftriaxone
  • Acute epididymitis >35y/o: Fluoroquinolones, or cephalexin or amox for kids
37
Q

DX and TX:

  • abrupt onset of scrotal, inguinal or lower abdominal pain (usually <6hr), N/V
  • Negative Prehns sign: no relief of pain w/ elevation of affected scrotum
  • Negative cremasteric reflex
  • Blue dot sign at upper pole
A

Testicular torsion
DX: testicular doppler US

TX: Detorsion and orchiopexy within 6 HOURS!

38
Q

Who is at risk for cryptorchidism

complications?
Tx?

A

Risk: premature infants, low birth weight (MC on RIGHT SIDE**)

Complications:

  1. testicular CA (in both testes)
  2. subfertility
  3. testicular torsion

TX: Orchiopexy as early as 6 months (ideally before 1 y/o)

39
Q

Types of testicular CA

A

MC 15-40y/o- MC on right side

  1. Germinal cell tumor (97%)- usually malignant
    - Seminoma *MC- Simple (lack tumor markers), sensitive (to radiation), Slow growing, stepwise spread
    - Nonseminomatous (increased AFP, BhCG and RADIOresistance
  2. Nongerminal cell tumors
    - Leydig
    - Sertoli
40
Q

MC cause of painless scrotal swelling

A

Hydrocele

if communicating: swelling worse w/ valsalva

TX: self-limiting or repair if persists beyond 1 y/o or communicating

41
Q

Cystic testicular mass, “bag of worms” superior to testicle, dilation worsens when patient is upright or w/ valsalva

A

Varicocele (MC on LEFT SIDE)

*MC surgically corrected cause of male infertility

42
Q

MC causes of cystitis and pyelo

TX

A

E. coli
Staph. saprophyticus in sexually active women

TX:
Phenazopyridine- no longer than 48 hrs (riske of methmoglobinuria, hemolytic anemia

  1. Uncomplicated: Nitrofurantoin, Fluoroquinolone (Cipro, Bactrim-DS)
  2. Complicated cystitis (prior tx failure or males): Fluoroquinolone PO or IV, Aminoglycoside
  3. Pregnancy: Amoxicillin or nitrofurantoin
  4. Pyelo: Fluoroquinolone PO or IV, Aminoglycoside
43
Q

Urine culture must show how much growth for it to be a positive UTI

A

Women: >/= 10^5 (100,000)
Males: >/= 10^2-4 + symptoms

44
Q

foreskin becomes trapped behind the corona of glans and forms a tight band, constricting penile tissue: ____

Inability to retract foreskin over the glans: ___

A

Paraphimosis- Urologic emergency!! tx is manual reduction +/- dorsal slit

Phimosis- tx is circumcision

45
Q

DX and TX Prostatitis

A

DX:

acute: equisitely tender, normal/hot, boggy prostate
chronic: NONtender, boggy prostate
1. UA/culture: + in acute
2. AVOID PROSTATIC MESSAGE in ACUTE prostatitis

TX:
Acute:
>35y/o (E. coli MC): fluoroquinolones or bactrim
<35 (C, G MC): Ceftriaxone + doxy

Chronic: fluoroquinolones or bactrim x6-12 wks
-Transurethral resection of the prostate (TURP) for refractory chronic

46
Q

DX and TX:

uniformly enlarged, firm, rubbery prostate with irritative sx or obstructive sx

A

DX: DRE, PSA

TX:

  1. observe: avoid antihistamines and anti-cholinergics
  2. 5-alpha reductase inhibitors (finasteride, duasteride)- reduces size but not immediate relief)
  3. alpha1 blocker (tamsulosin, doxazosin, terazosin)- relaxes smooth muscles- immediate relief
  4. TURP
47
Q

Risk factors for prostate CA

A
  1. high fat diet, obesity, AA, adenocarcinoma*

***back/bone pain (increase incidence of METS to bones)

48
Q

MC type of bladder CA and risk factors for bladder CA

A
Transitional cell (TCC)
**highest recurrance rates of call cancers

RF: smoking (MC), occupational exposure to dyes, rubbers or leather, age >40, white males, Cyclophosphamide, pioglitazone

49
Q

DX and TX:

hematuria, flank/abdominal pain, palpable mass, weight loss, L-sided varicocele, HTN, hyperCalcemia

A

Renal cell carcinoma
RF: smoking, dialysis, HTN, obesity, males

DX: CT scan usually first test

TX: radical nephrectomy

50
Q

Nephroblastoma is MC in ______
presents as ____
DX and TX?

A
  • kids w/in 1st 5 yrs of life
  • painless, palpable abdominal mass, hematuria, HTN, anemia
  • DX: abdominal US (best initial), CT w / contrast or MRI
  • TX: nephrectomy followed by chemo
  • 80-90% cure rate
51
Q

types of kidney stones and their cause

A
  1. Calcium oxalate (MC)- increased protein, salt- inhibits Ca resorption
  2. Uric acid- high protein, increased purines
  3. Struvite stones (Mg ammonium phosphate)- may form staghorn calculi due to urea-splitting organisms (proteus, Klebsiella, psueudomonas, Serratia, enterobacter)
  4. Cystine (genetic)
52
Q

kidney stone w/ urine pH >7.2 (alkaline) is mostly likely ___

A

associated w/ struvite stones

53
Q

DX and TX kidney stones

A

DX:

  1. Noncontrast CT abd/pelvis (MC initial test)
  2. Renal US- look for hydronephrosis
  3. KUB radiograph: only for calcium and struvite stones
  4. Intravenous pyelography- Gold standard

TX:
<5mm in diameter: 80% chance of sponatenous passage
-IVF, analgesic, antiemetics, tamsulosin)

> 7mm: Extracorpeal shock wave lithotripsy

  1. Uretoscopy +/- stent- immediate relief for high risk
  2. percutaneous nephrlithotomy- large stones or struvite
54
Q

Flaccid penile state is achieved by ____ stimulation

Erected penile state is achieved by ____ stimulation

A
flaccid= sympathetic stimulation
erected= parasympathetic stimulation
55
Q

Types of priapism and etiologies

A

Ischemic/low flow (MC): decreased venous outlfow
Nonischemic/high flow: increased arterial flow

Etiologies:

  1. idiopathic (MC)
  2. sickle cell
56
Q

TX of low-flow and high-flow priapism

A

low-flow:

  1. phenylephrine*
  2. Terbutaline
  3. needle aspiration (esp. if >4hrs)
  4. shunt surgery

high-flow:
1. observation

57
Q

MC causes of urethritis TX?

A

gonococcal- abrupt–> TX: ceftriaxone or azithro
non-gonoccal-chlamydia- 5-8 days –> TX: azithro or doxy

DX: nucleic acid amplification for both

58
Q

Infant neonatal conjuncvitits (ophthalmia neonatorium)
Presents:
-2-5 DOL: ____ TX?
-5-7 DOL: ___ TX?

A

2-5 DOL: gonococcal- erythromycin ointment- risk for blindness otherwise

5-7 DOL: chlamydia: azithro

59
Q

DX and TX of renovascular hypertension (renal artery stenosis)

A

DX: CT or MRA
-renal arteriography is gold standard*

TX: angioplasty w/ stent- definitive
-ACEI/ARBs- however CI if bilateral stenosis or solitary kidney

60
Q

TX of enuresis

A
  1. Behavioral- motivation, education, reassurance
  2. Enuresis alarm- use if failed behavioral tx
  3. Desmopressin (DDAVP)- best for short-term use
  4. TCA (ex. Imipramine)- use if failed above
61
Q

What type of urinary incontinence and cause?

  1. from sneezing, coughing, laughing
  2. nocturia*, frequency, small volume voids
  3. Small volume voids, frequency, dribbling, increased post-void residual >200
A
  1. Stress incontinence (increased intra-abdominal pressure, laxity of pelvic floor muscles ie child birth)
  2. Urge incontinence (detrusor muscle overactivity, overactive bladder)
  3. Overflow incontinence (decreased detrusor muscle activity/atony, underactive bladder)
62
Q

TX

  1. Stress incontinence
  2. Urge incontinence
  3. Overflow incontinence
A
  1. stress- pelvic floor exercises, alpha agonists (midodrine,
    pseudoephedrine) , surgery, devices, estrogen
  2. Urge- bladder training, anticholinergics (oxybutynin, tolterodine), TCA (imipramine), Miragegron (B3 agonist-relaxant), surgical, diet
  3. Overflow- intermittent/indwelling cath*, cholinergics (bethanacol), BPH (alpha-1 blockers: tamsulosin)