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Clin med 3 - GU and Nephro > AKI, CKD > Flashcards

AKI, CKD Flashcards

1
Q

KDIGO AKI GUIDELINE

stage 1

stage 2

stage 3

A

•Preferred definition for AKI based on 3 stages consisting of ONLY Cr and Urine Output

•Stage 1

  • Increase Cr 1.5-1.9 baseline or
  • decreased UO

•Stage 2

  • Increase Cr 2-2.9X baseline or
  • UO 12 hrs

•Stage 3

  • Increase Cr 3X baseline or
  • Cr >4 or UO reduction 24hrs or anuria >12hrs
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2
Q

FeNa VS FeUrea or FeUA

A

FeNa: not accurate if pt is on diuretics w/in 24hrs

•FeNa < 1% = pre-renal azotemia

•FeNa >1% = intrinsic renal failure

•FeNa >4% = post-renal failure

FeUA: NOT influenced by diuretics

•FEUrea < 35% or FEUA < 9-10 % = prerenal

•FEUrea > 50% or FEUA > 10-12 % = ATN

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3
Q
  • FeNa < 1% =
  • FeNa >1% =
  • FeNa >4% =
A
  • FeNa < 1% = pre-renal azotemia
  • FeNa >1% = intrinsic renal failure
  • FeNa >4% = post-renal failure
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4
Q

Prerenal inury causes?

A

Hypovolemia

↓ cardiac output

↓ effective circulating volume

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5
Q

Prerenal Injury labs

Volume depletion

Decreased CO/Effective arterial volume

Urine output

A

Volume depletion

•Hemoconcentration: ↑ H/H, albumin, calcium

•↑ Na, BUN, Cr

Decreased CO/Effective arterial volume

•Edema

•↓ Na, Albumin

Urine output

•Oliguria (<500ml/d) or anuria (<100ml/day)**

  • High specific gravity (>1.015)
  • Normal sediment or hyaline casts
  • Low Urine Na (<20mEq/L)
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6
Q

tx prerenal dz due to DEC CO effectivenes

A

↓ CO/Effective circulating volume

Optimize cardiac performance carefully

  • •Diuretics (volume overloaded) -high dose IV
  • •Nitrates
  • •Dobutamine
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7
Q

3 categores of intersitial AKI

A

Glomerular

  • PSG
  • IgA Nephropathy
  • Nephrotic syndrome /Minimal change
  • Polycystic kidney Dz

Tubules & Interstitium

  • Acute Tubular Necrosis
  • Acute Interstitial Nephropathy

Vascular

  • Renal Artery Obstruction – vasculitis
  • Renal Vein obstruction
  • Microangiopathy – TTP, HUS, DIC
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8
Q

si/sx of Vascular intersitial AKI

A

FeNa >1% intrinsic renal failure

LE rash: livedo reticularis

urine eosinophils

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9
Q

postrenal AKI can be defined as

A

↑BUN and Cr from obstruction to urine flow in ureters, bladder or urethra (anuric & <5% of ARF

  • BOO (ex. BPH, prostate cancer)
  • Neurogenic bladder
  • Malignancy (ex. ovarian, cervical, retroperitoneal)
  • Pregnancy

Meds (Acyclovir, methotrexate, sulfa drugs

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10
Q

Polycystic Kidney Dz etiology

A

Autosomal dominant genetic disorder

  • cyst formation
  • enlargement of the kidney (and other organs ie. Pancreas, liver, spleen)
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11
Q

si/sx Polycystic Kidney Dz

A

Diffuse pain -abdomen, flank, back

  • •Enlargement of cysts
  • •Hemorrhage into cyst or perinephric hematoma
  • •Infectious – UTI, pyelonephritis, abscess, infected cyst
  • •Nephrolithiasis (20-30%)

HTN

+/- palpable flank mass

+/- hepatomegaly

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12
Q

Tx Polycystic Kidney Dz

A

BP management (ex. ACEI/ARB) =slow progression of dz

Pain management: AVOID NSAIDs

Nephrectomy / Surgical cyst decompression

Monitor & manage recurrent infections: UTI/Cysts

Hematuria: may need transfusion!!!

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13
Q

definition and causes of Acute Interstitial Nephritis

A

allergic reaction to medication

  • •Antibiotics: B-lactams, sulfonamides, vancomycin, erythromycin, rifampin
  • •Acyclovir
  • •NSAIDS (either direct toxicity or allergy)
  • •Anticonvulsants: Phenytoin, valproate, carbamazepine

Post-infectious

Autoimmune

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14
Q

si/sx of Acute Interstitial Nephritis

A

After recent new drug exposure

Fever

Skin rash

Peripheral eosinophilia

Oliguria

more commonly, patients are found incidentally to have rising serum creatinine after initiation of new med

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15
Q

WBC casts & Hematuria

Dz?

Tx

A

Acute Interstitial Nephritis

D/c of offending agent: reversal of renal injury

Glucocorticoid therapy: accelerate renal recovery

  • •6 week taper prednisone or
  • •IV methylprednisolone pulse 3 days)
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16
Q

Potential Nephrotoxins that cause ATN

A
  • NSAIDs
  • Chemotherapeutic agents
  • Aminoglycosides
  • Amphotericin
  • Vancomycin
  • Radiocontrast dye (GFR 30 rad cutoff)
  • Poison (ethylene glycol, heavy metals)
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17
Q

UA - Pigmented granular casts (muddy-brown casts)

electrolyte changes?

A

Acute Tubular Necrosis (ATN

Serum hyperkalemia

Serum hyperphosphatemia

Serum hyperuricemia

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18
Q

Tx Acute Tubular Necrosis (ATN

A

Aggressive volume replacement– hydrate (If nephrotoxic agent, volume depletion)

Oliguria present and extracellular-volume normalized:

  • • consider loop-diuretic high dose (100-200mg Lasix) to improve urine output

Protein restriction

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19
Q

Cola colored urine (blood degraded/hematuria/RBC casts)

Edema

Hypertension (salt & fluid retention)

Dx

A

Post-strep glomerulonephritis

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20
Q

dx Post-strep glomerulonephritis

A

+ throat, skin culture for strep A

•Elevated titers of abs to strep products

•(+) Anti-streptolysin (ASO)*

UA: Hematuria – RBC casts

•Proteinuria

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21
Q

(-) strep A antibody test

Urine red or coca cola 1-2 days s/p onset

Dx & Tx

A

IgA Nephropathy

ACE-/ARB, Steroids

Dialysis

Renal transplant

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22
Q

Heavy proteinuria (>3.5g/24hr)

Hypoalbuminemia (<3 g/dL)

Peripheral edema

A

Nephrotic Syndrome: adult

minimal change: children

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23
Q

dx minimal chanhe histology?

A

Light microscopy is normal on renal bx

Histology - diffuse effacement of the epithelial cell foot processes on electron microscopy

Hypoalbuminemia

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24
Q

tx minimal change

A

Prednisone

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25
Q

name uurine sediment that correlated w/ dz

A
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26
Q

define CKD

A

Progressive loss of renal function that persists for more than 3 months

Commonly irreversible

Usually caused by long-term diseases such as DM, HTN

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27
Q

pathophys of CKD

A
  1. 1.Underlying etiology causes Adaptive hyperfiltration and nephron damage
  2. 2.In response to any damage the kidney - kidney ↑ filtration rate to normal undamaged nephrons (Hyperfiltration)
  3. 3.Hyperfiltration over time = glomerular hypertrophy, distortion of the glomerular architecture, sclerosis and l_oss of remaining nephrons_
  4. 4.Manifested by proteinuria and progressive renal failure
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28
Q

RAAS and AII impact on CKD

A

RAAS and AII activated trying to maintain GFR w/ resultant hyperfiltration however…

↑ Pore size in GM by AII = increasing protein leak across the glomerular basement membrane

Consequence of repeated and continued activation of the RAAS = Microalbuminuria/Proteinuria - toxic to the tubules

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29
Q

define azotemia and how it rekates to uremic syndrome

A

Uremic Syndrome: clinical manifestations of uremia / advanced renal failure (stage 5)

  • Symptomatic manifestations associated with Azotemia

Azotemia = the accumulation of urea and other nitrogenous compounds and toxins caused by the decline in renal function

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30
Q

define CKD stages

Stage 1

Stage 2

Stage 3

Stage 4

Stage 5

A

Stage 1: GFR ≥ 90

Stage 2: GFR 60-89

Stage 3: GFR 30-59

Stage 4: GFR 15-29

Stage 5: GFR <15 or dialysis

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31
Q

CKD maging modality of choice

A

Renal US (consider other imaging) – imaging modality of choice

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32
Q

CKD When to Refer to Nephrology?

A
  • GFR < 30ml/min (CKD Stages 4 and 5)
  • Rapidly progressive CKD
  • Poorly controlled HTN despite 4 agents
  • Rare or genetic causes Suspected renal artery stenosis
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33
Q

si/sx stage 4 CKD

A

•Difficult to control HTN: large dose loop diuretics

  • Difficult to control edema
  • Hyperkalemia
  • Uremia
34
Q

labs in CKD

A

↑ BUN , Creatinine

Hyperkalemia, & phosphatemia

Hypocalcemia

Proteinuria – RBC/ & WBC cast in urine

35
Q

causes of ESRD

leading cause?

A

DM - leading Cause**

Diabetic Nephropathy

HTN

HTN Nephropathy

36
Q

DM pathophys in CKD

A
  1. Damages vessels in the kidney
  2. Elevated blood glucose rises beyond kidneys capacity to reabsorb glucose
  3. Glucose remains concentrated in the fluid, raising its osmotic pressure and causing more water to be carried out, increasing urine volume = prerenal hypovolemia and RAAS activation
37
Q

DM Tx

A

Primary prevention

  • Tight glucose control
  • Diet/exercise

•*BP control <130/80 - delays the onset of microalbuminuria

38
Q

Diabetic nephropathy

First sign –

Most common co-morbidity –

A

First sign – microalbuminuria

Most common co-morbidity –hypertension

39
Q

tx diabteic nephrop

A

ACEI/ARB’s – ALL patients even if normotensive

  • •renal protective qualities – inhibits angiotensin
  • •If need another BP lowering med Loop Diuretic – + a second agent to aide in BP control

fluid overload avoid sodium

Smoking cessation & Protein restriction

Treat c_hronic metabolic acidosi_s w/ bicarbonate

40
Q

CKD is a risk factor for _____ disease

A

CKD is a risk factor for cardiovascular disease

41
Q

Second leading cause of ESRD

A

HTN accelerates the progression of CKD

Controlling BP slows down ↓GFR

•Inhibiting RAAS is effective in lowering BP and ↓ microalbuminuria

42
Q

HTN Nephropathy is defined as

A

proteinuria and hypertension

43
Q

tx HTN Nephropathy

A

CKD Stages 1-3 w/ proteinuria: ACEI/ARB

  • ↓ progression of CKD & ↓ mortality/morbidity in HF

ACEI: Monitor serum creatinine & potassium concentration

  • •prior to initiation
  • •within 2 weeks of starting the drug
  • •and within 2 weeks after an increases in dose

Stage 4 & 5 require nephron consult before initiating ACEI/ARB

44
Q

when initating an ACEI it is important to monitor?

tiumeline?

A

Monitor serum creatinine & potassium concentration

  • •prior to initiation
  • •within 2 weeks of starting the drug
  • •and within 2 weeks after an increases in dose
45
Q

what changes do we expect to see in pt when initiating ACEI?

whendo we d/c?

A

•Expect worsening creatinine or ↓ GFR -

  • if values stabilized after initial rise - continue
  • (if they do not stabilize d/c & consult nephro)

•Contribution to hyperkalemia, >6.0mmol/L - stop any other harmful drugs, ↓ or hold potassium retaining diuretics, ↓ loop diuretic dosage

46
Q

Lowering BP Goals in a patient with CKD and HTN =

A

<130/80

47
Q

Most common primary malignant renal tumor in childhood

A

Wilms Tumor

Arises from primitive metanephric blastema: Sporadic or hereditary

•Genetics: loss of function mutations of tumor suppression & transcription genes à WT1 suppression gene, Chrom 11

48
Q

Wilms tumor Associated Disorders

A

GU: cryptorchidism, hypospadias

Isolated hemihypertrophy

Sporadic aniridia u

10% assoc w/ congenital malformation syndromes: WAGR:

  • •Wilms tumor
  • •Aniridia
  • •GU abnormalities
  • •Retardation, Intellectual disability

Beckwith-Wiedeman syndrome

Denys-Drash syndrome

49
Q

most common si/sx of wilms tumor

A

asymptomatic abdominal mass (gentle Wilms tumor are fragile)

  • Smooth & firm
  • Well demarcated
  • Rarely crosses midline
50
Q

imaging for wilms tumor

A

Abdominal U/S w/ Doppler:

  • Confirms mass arises from kidney
  • Evaluates contra- kidney
  • Doppler

Contrast CT for ALL renal tumors:

•Chest, Abdomen– pelvis CT: metastases evaluation

51
Q

tx wilms tumor

low risk w/ unitumor

most pts

high risk

A

Radical nephrectomy & LN sampling

Depending on staging/risk stratification:

Very low risk pts w/ uni- tumor=

  • Nephrectomy w/out chemo-/radiation

Most pts: Nephrectomy & Chemo-

High risk pts: Nephrectomy & Chemo- & Radiation

52
Q

staging wilms tumor

1-5

A

Stage I – tumor limited to Kidney and is completely excised

Stage II – Tumor extends beyond the kidney but is completely excised

Stage III – Residual tumor confined to the abdomen

Stage IV – presence of metastases

Stage V – Bilateral renal involvement at the time of diagnosis

53
Q

Renal Artery Stenosis caused by

pathophys

A

Atherosclerotic disease - ostial & proximal renal arterial segments

  • More common, elderly, CV risk factors

Fibromuscular dysplasia -middle & distal renal arterial segments

  • Younger pts <50, more common in females

Pathophys:

  1. Narrowing of renal arteries
  2. Kidney hypoperfusion
  3. Renovascular hypertension & ischemic nephropathy
  4. Renal failure
54
Q

most common si/sxs w/ renal artery stenosis is?

A

HTN

  • •Onset of HTN 50 y <30y or >50 y
  • •Severe or Refractory HTN
  • •Resistance to antihypertensive therapy
  • •Moderate-Severe HTN in pts w/ recurrent episodes of flash Pulmonary edema
  • •Nο FHx of HTN
55
Q

renal a. stenosis Imaging gold standard

A

Renal angiography

•Done after positive screening test

56
Q

tx Renal Artery Stenosis

Atherosclerotic disease s

Fibromuscular dysplasia

A

Atherosclerotic Disease: Goals:

Control BP, Stabilize renal function, ↓ CV complications

Medical therapy : 1st line: ACEIor ARBs

  • •Monitor Cre, GRF for first wks à If ⬆ Cre: D/C
  • •Suggests bi- RAS, RAS in Uni- functional kidney, or RAS in allograft if kidney transplant recipient

Angioplasty +/- stenting

Surgical bypass

Fibromuscular Dysplasia: Medical therapy alone usually not advised

Percutaneous transluminal angioplasty: Often curative

57
Q

types of kisney stones

common causes

A

calcium stones (Ca oxalate > Ca phosphate)

15% struvite (magnesium ammonium phosphate)

  • •Uncommon UTI organisms

5% uric acid – radiolucent (cannot see on CT)

  • •Gout, hyperuricosuria

1-3% cystine: radiolucent (usu faintly radio-opaque)

58
Q

Si/ Sx Nephrolithiasis

A

Renal colic begins suddenly & waxes and wanes lasting 20-60 mins

Severe unilateral flank pain– radiating to groin/testicle/labia (T10-S4 dermatome)

Pacing, Rocking, Writhing, Constant movement unable to find position of comfort (contrast to peritonitis)

59
Q

dx of choice for stones

what do we see on this modality

A

NCCT of abdomen + pelvis: identifies all stone types in all location (uric acid, pure cystine and certain drug stones not seen)

  • Ureteral dilatation
  • Collecting system dilatation
  • Perinephric stranding
  • Periureteric stranding
  • Nephromegaly
  • “Rim sign”
60
Q

imaging modality uses for stones

KUB:

IVP:

US:

A

KUB: NOT radiolucent stones

IVP: info about the stone

  • •size, location, radiodensity
  • •and degree of obstruction.

US: Detects indirect signs of obstruction:

  • •Procedure of choice for patients who should avoid radiation
  • • children, pregnant women and woman in childbearing age.
61
Q

Stone imaging of choice for patients who should avoid radiation

A

US •children, pregnant women and woman in childbearing age.

62
Q

first line analgesic w/ stones

A

NSAID ketorolac FIRST LINE)

63
Q

meds for d/c pts w/ stones

A

give strainer and bring in stone for analysis

Cocktail of medications

  • Diclofenac 50mg po bid
  • Valium 2mg po QID prn
  • Tamsulosin 10mg qd
  • Oxycodone 5-10mg q4-6hr prn
64
Q

defien Staghorn Calculi

most common pathogen?

A

Upper urinary tract stones involve the renal pelvis and extend into at least 2 calyces (struvite stone)

  • •Always assoc w/ infection - Urease-producing bacteria
  • •Pro_teus species (most common)_
  • •Staphylococcus species, Klebsiella species, Providencia species, and Pseudomonas species
65
Q

dx & Tx Staghorn Calculi:

A

Rarely present as colic type stones, no pain!!

•Medical tx not enough - Suppressive antibiotic therapy or Urease inhibitors (acetohydroxamic acid)

•PNL surgical tx of choice followed by PNL & ESWL combination

66
Q

Med Expulsion Therapy for stones

A

Tamsulosin – Med Expulsion Therapy

•assoc 65% greater likelihood passage >5mm distal stones

67
Q

imaging study for hydronephrosis & renal stones

A

US

68
Q

Surgical Options for Stones

A

Extracorporeal shock wave lithotripsy

Ureteroscopy

Percutaneous nephrostolithotomy

Percutaneous Nephrostomy

Open nephrostomy

69
Q

Indications for Surgery of stones

CI??

A

Uncomplicated stone <10mm not passed in 4-6 wks

  • Symptomatic stones w/o other etiology for pain
  • >10mm stones
  • Pregnancy and failed observation
  • Pediatric and failed MET

Contraindications:

  • Active UTI untreated
  • Coagulopathy
  • Pregnancy
70
Q

tx of choice in pts w/ stones who ned FAST decompression

  • Septic or hemodynamically unstable
  • Significant comorbidity
  • Stone unlikely to be able to be bypassed with stent
A

Percutaneous Nephrostomy:

Small tube through flank into renal pelvis for decompression (FASTEST)

•Bridge to surgery

71
Q

surgical options for stones:

proximal stones

mid and distal ureteral stones

stones >2cm and proximal collecting system

A

proximal stones: Extracorporeal shock wave lithotripsy

mid and distal ureteral stones: Ureteroscopy

stones >2cm and proximal collecting system: Percutaneous nephrostolithotomy

72
Q

most common si/sx Bladder Cancer

A

Painless Hematuria (80-90%) **

73
Q

types of bladder cancer

RF??

A

Transitional cell carcinoma : 90% of bladder Ca

  • Can arise anywhere in the urinary tract, including the renal pelvis, ureter, bladder, and urethra

Squamous cell carcinoma: Up to 7%

Adenocarcinoma: Rare

Risk Factors:

Cigarette smoking**

Chronic urinary inflammation (SC injury & chronic catheter)

Occupational exposures** à organic chemicals, rubber, paint, paper production, and dye industries have increased risks of urothelial cancers.

74
Q

bladder cancer dx standard

A

Cystoscopy: Diagnostic standard w/ bx

75
Q

tx of bladder cancer

Non-muscle invasive

Muscle-Invasive disease (

A

Non-muscle invasive (Ta,T1,CIS):

Endoscopic TURBT w/ electrocautery or laser fulguration

Radical cystectomy

Immunotherapy and chemotherapy: Intravesical instillation of BCG (Bacillus-Calmette Guerin) vaccine

Muscle-Invasive disease (T2 and Greater)

Neoadjuvant chemotherapy before radical cystectomy (MVAC)

  • Methotrexate • Vincristine • Adriamycin • Cisplatin

Radical cystectomy w/ regional LN dissection: Tx of choice*******

Radiation therapy (T2-3)

76
Q

Renal Cell Carcinoma most common si/sx

A

Hematuria (+/-painless)

Weight loss, Fever, Night sweats, Malaise

L sided varicocele à obstruction of the testicular v. Supraclavicular LN

CLASSIC TRIAD

  1. flank pain
  2. Hematuria
  3. flank mass (10%)
77
Q

RCC occurs frquently w/

A

Frequent occurrence w/ paraneoplastic syndromes

78
Q

RCC diagnostic method of choice

A

CT w/ contrast :

79
Q

Tx RCC
Localized dz

Locally advanced dz

disseminated

A

Localized dz: neohrectomy

T1a <4cm - partial nephrectomy

T1b-T2 radical nephrectomy (recurrent 2-3%)

Locally advanced dz: venous tumor thrombus à Dx w/ MRI

Radical nephrectomy, LN dissection & IVC thrombectomy

disseminated

Palliative radical nephrectomy: to relieve sx

Chemo & Radiation therapy: chemo & radioresistant tumor

Biologic response modifiers: IL-2 & Interferon alpha

Multikinase-inhibitor, VEGF inhibitor treatment

80
Q

Indications of venous tumor thrombus

A
  • lower extremity edema
  • isolated right-sided varicocele or one that does not collapse with recumbency
  • dilated superficial abdominal veins
  • pulmonary embolism
  • right atrial mass
  • nonfunction of the involved kidney
81
Q

Bladder Cancer Staging

A
  • TA Noninvasive papillary tumor
  • Tis Carcinoma in situ flat tumor

•T1 - in wedge subepithelial conn. tissue

•T2 Tumor in wedge muscle

  • •T2a tumor in superficial m, inner half
  • •T2b tumor in deep muscle, outer half

•T3: through the muscle layer of the bladder & into adipose

•T4: spread beyond the adipose to nearby organs or structures

  • •T4a: spread to the stroma of the prostate (in men), or uterus /vagina
  • •T4b: spread to the pelvic or abd wall
82
Q

RCC Staging (1-IV)

A

•Stage I:—Tumor is c_onfined within the kidney_ parenchyma

  • •Ia: <4cm
  • •Ib: 4-7cm

•Stage II:—Tumor (>7cm) involves the perinephric fat but is confined within Gerota’s fascia

•Stage IIIA:—Tumor i_nvolves the main renal vein or inferior vena cava_

•Stage IIIB:—Tumor i_nvolves regional LNs_

•Stage IIIC:—Tumor involves both local vessels & regional LNs

•Stage IVA:—Tumor involves adjacent organs other than the adrenal (colon, pancreas, etc).

•Stage IVB:—Distant metastases

Clin med 3 - GU and Nephro (3 decks)

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