Step Up - Renal Flashcards

1
Q

Provide a framework for characterizing AKIs and provide the etiologies within each category (3).

A

1) Prerenal (40-80%)
a) Volume loss or sequestration
b) Low CO
c) Hypotension
2) Postrenal (5-15%)
a) Intrarenal - crystals, protein
b) Extrarenal - pelvis, ureter, bladder, urethra involvement
3) Renal (10-30%)
a) GN
b) Vascular disorder - small or large vessel
c) Interstitial disorder
d) Acute tubular necrosis

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2
Q

Why should NSAIDs and ACEi be avoided in patients with decreased renal perfusion (prerenal AKI)?

A

1) NSAIDs - constrict afferent arteriole
2) ACEi - efferent arteriole vasodilation
- both further reduce renal blood flow
- prerenal insult can become ATN if ischemia persists

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3
Q

With respect to prerenal AKI, comment on anticipated findings/values on urinalysis, BUN/Cr ratio, FeNa, Urine Osmo, Urine Sodium

A

1) Urinalysis - bland, hyaline casts
2) BUN/Cr - >20:1
3) FeNa less than 1%
4) Urine Osmo >500 mOsm
5) Urine Na less than 20
- adequate resorption

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4
Q

With respect to intrinsice AKI, comment on anticipated findings/values on urinalysis, BUN/Cr ratio, FeNa, Urine Osmo, Urine Sodium

A

1) Urinalysis - abnormal
2) BUN/Cr - less than 20:1
3) FeNa - 2-3%
4) Urine Osmo 250-300 mOsm
5) Urine Na >40
- impaired resorption

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5
Q

Describe the cells/casts seen in prerenal, intrarenal (ATN, GN, AIN), and postrenal urinalysis. Comment on the presence and amount of protein and blood seen.

A

1) Prerenal - benign U/A (few hyaline casts), no blood or protein
2) ATN - muddy brown casts, granular casts, trace protein, no blood
3) GN - RBC casts, fatty casts, 4+ protein, 3+ blood
4) AIN - WBC casts, eosinophils, 1+ protein, 2+ blood
5) Postrenal - Benign U/A, no blood or protein

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6
Q

What are the 3 most common causes of Chronic Kidney Disease?

A

1) DM
2) HTN
3) Chronic GN
- Any AKI can lead to CKD if prolonged or treatment not provided

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7
Q

Comment of the electrolyte disturbances and acid/base disturbance seen in Chronic Kidney Disease (K, Mg, Ca, Phos). Why does each one exist?

A

1) hyperkalemia - decreased urinary secretion
2) hypermagnesemia - decreased urinary loss
3) Hyperphosphatemia - decreased renal clearnace
4) Hypocalcemia - due to decrease vit D production. Leads to hyperparathyroidism and possible hypercalcemia and renal osteodystrophy
5) Metabolic Acidosis - due to decreased renal H clearance and ammonia production

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8
Q

What are the absolute indications for dialysis in ESRD (hint: AEIOU)?

A
A - acidosis (signnificant)
E - Electrolytes (high K)
I - Intoxicants (methynol, lithium)
O - Overload (hypervolemia not managed otherwise)
U - Uremia SSx (ex. pericarditis)
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9
Q

Define proteinuria. What are the features of nephrotic syndrome (5)?

A

1) Proteinuria - >150mg/day
2) Nephrotic syndrome
a) Urine protein > 3.5g/day
b) Hypoalbuminemia - increase loss, causes edema
c) Edema - caused by hypoalbuminemia and hyperaldosteronism
d) Hyperlipidemia - high synthesis of LDL and VLDL (due to liver albumin production rate)
e) Hypercoagulable state - loss of anticoagulants in urine

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10
Q

Contrast nephritic and nephrotic syndrome in terms of there presentations.

A
  • both can be present in a GN
    1) Nephritic - hematuria, azotemia, mild proteinuria, HTN, edema
    2) Nephrotic - high proteinuria, hypoalbuminemia, hyperlipidemia, edema, hypercoagulable state and increased infection risk.
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11
Q

Briefly list and describe the primary glomerular disorders (GNs) (5).

A
  • GN tx: steroids and cytotoxic agents
    1) Minimal change disease - nephrotic syndrome, pediatric population, fusion of foot processes on EM.
    2) Focal segmental glomerulosclerosis - poor prognosis, progressive
    3) Membranous glomerulonephritis - Nephrotic syndrome, thick glomerular capillary walls, prognosis fair-good.
    4) IgA nephropathy - hematuria, linked to URTI, IgA and C3 deposition on EM, prognosis good.
    5) Hereditary nephritis - inheriteded disease with variable penetrance, no Tx.
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12
Q

Briefly discuss 3 secondary glomerular disorders (GNs)

A

1) Membranoproliferative - Infectious etiology (Hep C/B, syphilis, lupus). Poor prognosis
2) Poststreptococcal GN - nephritic syndrome, pediatric population, self-limited
3) Goodpasture Syndrome - IgG antiglomerular basement membrane antibody, biopsy shows linear immunofluorescence pattern, Tx: plasmapheresis

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13
Q

What are the causes of acute interstitial nephritis (4)? What are the clinical features (3)? How is it treated (3)?

A

1) Causes: allergic reaction to medication, infection, collagen vascular disease (sarcoidosis), autoimmune (SLE, sjogren)
2) Features: AKI, rash/fever/eosinophilia, pyuria/hematuria
3) Tx: stop offending agent, steroids, treat infection

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14
Q

Describe type 1 renal tubular acidosis, what abnormalities are noted (4)?

A

1) Deficit: inability to secrete H at the distal tubule
2) Impact:
- hypokalemia
- renal stone/nephrocalcinosis
- rickets/osteomalacia
- hypokalemic, hypercholermic nonanion gap metabolic acidosis

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15
Q

Describe type 2 renal tubular acidosis, what abnormalities are noted (3)?

A

1) Deficit: inability to resorb HCO3 at proximal tubule
2) Impact:
- loss of K and Na
- hypokalemic, hyperchloremic nonAG met. acidosis
- No stones

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16
Q

Describe type 4 renal tubular acidosis, what abnormalities are noted (3)?

A

1) Deficit: hypoaldosteronism or renal resistance to aldosterone
2) Impact:
- Decrease Na absorption (distal tube)
- decreased H and K excretion (distal tube)
- hyperkalemia, acidic urine
- No stones

17
Q

What is the major complication of ADPKD? What are some clinical features (5)? How is it diagnosed and treated?

A

1) 50% enter ESRD by 60s
2) Features: hematuria, abdo pain, HTN, palpable kidneys, intracerebral berry aneurysms, recurrent infection
3) Dx: U/S, CT, MRI
4) drain cysts if symptoatic, treat infections and HTN.

18
Q

What are the clinical features of ARPKD (5)? How is it diagnosed? How is it treated/

A

1) Features: hepatic involvement (always), large size kidneys, HTN, pulmonary hypoplasia (neonate), oligohydramnios with Potter syndrome (neonate)
2) Dx: prenatal U/S
3) Tx: none. kidney transplant. Manage respiratory issues. Can be fatal in neonatal period.

19
Q

What are the cause of renal artery stenosis (2)? What are the clinical features (3)? How is it diagnosed? How is it treated (3)?

A

1) Causes: atherosclerosis, fibromuscular dysplasia
2) Features: refractory HTN, low renal function, abdominal bruit
3) Dx: Imaging - renal arteriogram, MRA, contrast CT, Doppler U/S
4) Tx: renal angioplasty, bypass graft, conservative mgmt with meds (ACEi, CCB).

20
Q

What are the types of renal stones, list in order of most to least common (4)?

A

1) Calcium stones
2) uric acid stones - precipitated in acidic urine, not seen on Xray
3) Struvite stone (staghorn) - associated with recurrent UTIs, precipitated by alkaline urine
4) Cystine stones - genetic predisposition (cystinuria)
- stones >1cm do not pass spontaneously

21
Q

Discuss the indications for transrectal ultrasound (TRUS) with biopsy in prostate cancer work-up wrt PSA values and DRE findings.

A

1) If PSA > 4.0ng/ml, do TRUS with biopsy

2) If DRE abnormal, do TRUS with biopsy

22
Q

How is prostate cancer treated in: localized disease, locally invasive disease, metastatic disease?

A

1) Localized disease - watchful waiting in elderly, otherwise radical prostatectomy (curative)
2) Locally Invasive - radiation plus androgen deprivation (not curative)
3) Metastatic - androgen reduction (orchiectomy, antiandrogens, LH, GnRH antagonists) (not curative)

23
Q

What are the types of cells found in testicular cancers (4)?

A

1) Germ cell tumors (95%)
- Seminomas (35%) - highly treatable
- Nonseminomatous (65%) - embryonal carcinoma, choriocarcinoma, teratoma, yolk sac carcinoma
2) Non-Germ cell tumors (5%) - typ. benign
- Leydig cells
- Sertoli cells

24
Q

What are the tumor markers in testicular cancer (2)?

A
  • BHCG

- AFP