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Medicine SHELF > Renal and GU > Flashcards

Renal and GU Flashcards

1
Q

What is the definition for acute kidney injury based open?

A

Rapid decline in renal function with an increase in serum creatinine level

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2
Q

What are the criteria for the RIFLE definition of acute kidney injury?

A

RISK: 1.5x Cr OR -25% GFR OR urine output <0.5 for 6h
INJURY: 2x Cr OR -50% GFR OR uo <0.5 for 12h
FAILURE: 3x Cr OR -75% GFR OR uo <0.5/24 or anuria 12h
LOSS: complete loss of kidney function requiring dialysis for >4wks
ESRD: dialysis >3mo

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3
Q

What are the most common clinical symptoms of acute kidney injury? Why?

A
  1. Weight gain
  2. Edema
    Both due positive water and sodium balance
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4
Q

What are some common causes of azotemia (increase in BUN, increased in Cr)?

A

BUN: catabolic drugs (steroids), GI/soft tissue bleeds due to RBC digestion and re-absorption of urea, dietary protein intake

Cr: increased muscle breakdown, various drugs. Baseline may vary with difference in muscle mass

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5
Q

What are the most common causes in morbidity in acute kidney injury?

A

Infection (75%)

Cardiorespiratory complications

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6
Q

What are (3) common causes of pre-renal acute kidney injury?

A
  1. Volume loss/sequestration
  2. Decreased cardiac output
  3. Hypotension
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7
Q

What are (4) common causes of intra-renal acute kidney injury?

A
  1. Glomerulonephritis
  2. Vascular disorder (small, large vessel)
  3. Interstitial disorder
  4. Acute tubular necrosis
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8
Q

What are the common causes of post-renal acute kidney injury?

A

Intrarenal: crystals, proteins
Extrarenal: pelvis/ureter, bladder/urethra

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9
Q

What physical exam parameters need to be evaluated daily to monitor for acute kidney injury progression?

A
  1. Daily weights, I/O
  2. BP
  3. Electrolytes
  4. Hb, Hct
  5. Infection signs
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10
Q

Presentation of a patient with signs of water depletion and CHF or cirrhosis would suggest acute kidney injury of which etiology?

A

Pre-renal

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11
Q

Presentation of a patient with signs of an allergic reaction (rash) would suggest acute kidney injury of which etiology?

A

Intra-renal: acute interstitial nephritis

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12
Q

Presentation of a patient with a suprapubic mass, BPH, or bladder dysfunction suggest acute kidney injury of which etiology?

A

Post-renal

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13
Q 
For a pre-renal cause of acute kidney injury, what would lab values for the following usually show?
UA
BUN:Cr ratio
FENa
Urine osmolality
Urine sodium
Urine sediment
A

UA: hyaline casts
BUN:Cr: >20:1 (GFR is decreased so filtration of metabolites is decreased, but tubules increase urea reabsorption to help reabsorb Na and H2O)
FENa: <1%
Urine osmolality: >500mOsm (tubular function is preserved so water is reabsorbed)
Urine sodium: <20 (tubular function is fine so electrolytes can be reabsorbed)
Urine sediment: scant (indicates lack of tubular damage)

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14
Q 
For a intra-renal cause of acute kidney injury, what would lab values for the following usually show?
UA
BUN:Cr ratio
FENa
Urine osmolality
Urine sodium
Urine sediment
A

UA: abnormal
BUN:Cr ratio: <20:1 (tubules cannot actively reabsorb urea since they are damaged)
FENa: >2-3% (Na not effectively reabsorbed)
Urine osmolality: 250-300mOsm (damage to tubules creates difficulty in concentrating urine)
Urine sodium: >40
Urine sediment: full, brownish pigment // granular casts with epithelial casts

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15
Q

What are some common causes of intrinsic renal damage?

A

Tubular disease: ischemia, nephrotoxins
Glomerular disease: Goodpasture, GPA, PSGN, lupus
Vascular disease: renal artery occlusion, TTP, HUS
Interstitial disease: allergic interstitial nephritis (usually due to hypersensitivity medication)

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16
Q

What are some common nephrotoxins that may lead to intrinsic renal disease?

A

Antibiotics (aminoglycosides, vancomycin)
NSAIDs
Poisons
Myoglobinuria (muscle damage, rhabdomyalysis)
Hemoglobinuria (from hemolysis)
Chemo drugs (cisplatin)
Kappa, Gamma light chains (multiple myeloma)

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17
Q

What are the (3) basic tests to evaluate for post-renal kidney failure?

A
  1. Physical exam - palpate the bladder
  2. US - look for obstruction, hydronephrosis
  3. Catheter - look for large volume of urine
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18
Q

What are the (3) phases of acute tubular necrosis?

A
  1. Oliguric phase - azotemia and uremia (10-14d)
  2. Diuretic phase - fluid overload (due to retained solutes), or osmotic diuresis, or tubular damage
  3. Recovery phase
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19
Q

What lab tests are indicated in the diagnosis of acute kidney injury?

A 
Blood tests: BUN:Cr, e-, albumin, CBCd
Urinanalysis: protein, microscopic sediment
Urine chemistry: osmolality, FENa
Urine culture/sensitivities
Renal US: obstruction
CT abdomen, pelvis: if US abnormal
Renal arteriography: RA occlusion
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20
Q 
What do the following findings in urine microscopy indicate about the etiology of kidney damage?
Crystals
Micro-organisms
Granular casts
Hyaline casts
RBC casts
WBC casts
Fatty casts
A

Crystals: stones
Micro-organisms: infection, nonpathogenic colonization
Granular casts: “muddy brown,” seen in ATN due to degeneration of cells and protein aggregates
Hyaline casts: “empty,” prerenal injury
RBC casts: glomerular disease
WBC casts: renal parenchymal inflammation
Fatty casts: nephrotic syndrome

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21
Q

What intrinsic renal disease is suspected if the UA results show “muddy brown” casts, renal tubular cells/casts, granular casts, with trace protein and no blood?

A

Acute tubular necrosis

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22
Q

What intrinsic renal disease is suspected if the UA results show dysmorphic RBC, RBC casts, WBC casts, fatty casts, with high protein and blood content?

A

Acute glomerulonephritis

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23
Q

What intrinsic renal disease is suspected if the UA results show RBCs, WBCs, WBC casts, eosinophils, with mild protein and blood?

A

Acute interstitial nephritis

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24
Q

What are (4) common complications of acute kidney injury and how are they treated?

A
  1. ECF volume expansion w/pulmonary edema // treat with diuretic (furosemide)
  2. E- abnormalities (hyperK, metabolic acidosis // NaHCO2, hypoCa, hypoNa, hyperPO4, hyperurecimia)
  3. Uremia
  4. Infection
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25
Q

What are the indications for urgent dialysis in acute kidney injury?

A 
Acidosis
Electrolytes
Intoxications
Overload in volume
Uremia
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26
Q

What fluid replacement is given normally? What if acidemia is present?

A

Usually normal saline

If acidemia, use lactated ringers due to risk of hyperCl

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27
Q

Why does radiographic contract cause ATN? How can it be prevented?

A

Contrast dye causes afferent arteriole spasms; can pre-treat with saline hydration

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28
Q

What measurements define chronic kidney disease?

A

GFR <60, or structural/functional abnormalities for >3 months

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29
Q

What are the (2) main causes of CKD? What are some other causes?

A
  1. Diabetes (30%)
  2. HTN (25%)
  3. Chronic glomerulonephritis
  4. Interstitial nephritis, PCKD, obstructive uropathy
  5. Prolonged AKI leading to CKD
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30
Q

What is the most common clinical measure of GFR?

A

Cr clearance

31
Q 
What are the clinical symptoms of CKD?
Neurologic
CV
GI
Hematologic
Endocrine/metabolic
A

Neurologic: lethargy, somnolence, confusion, peripheral neuropathy, uremic seizures, weakness, asterixis, hyperreflexia, restless legs, hypoCa sx (lethargy, confusion, tetany)
CV: HTN (2/2 Na+H2O retention - decreased GFR leads to increased RAAS, BP), CHF (volume overload, anemia), pericarditis (uremia)
GI: (usually due to uremia) n/v, anorexia
Hematologic: normocytic normochromic (2/2 EPO deficiency), bleeding (2/2 platelet dysfunction due to uremia)
Endocrine/metabolic: hyperPO4, hypoCa, hyperPTH leading to renal osteodystrophy, CaPO4 crystals causing calciphylaxis (irreversible)

32
Q

What is the prognosis of CKD if small kidneys are seen on renal US?

A

Chronic renal insufficiency with small chance of recovery

33
Q

What (10) factors does a treatment plan for CKD need to include?

A
  1. Diet: low protein, low salt, restrict K, Ph, Mg
  2. ACEi - slows proteinuria, but may lead to hyperK
  3. BP control
  4. Glycemic control
  5. Smoking cessation
  6. Correct e-
  7. Anemia - (+) EPO
  8. Pulmonary edema (diuresis, dialyze if needed)
  9. Pruritis - capsaicin cream, cholestyramine, UV light
  10. Dialysis
34
Q

What is the only cure for CKD?

A

Transplant

35
Q

What are the two types of dialysis available?

A

Hemodialysis

Peritoneal dialysis

36
Q

What are the absolute indications for dialysis? (Hint: there is a mnemonic)

A 
A: acidosis
E: electrolyte abnormalities
I: intoxication
O: overload, volume
U: uremia
37
Q

What are the symptoms of uremia?

A

Neurological: lethargy/deterioration in MS, encephalopathy, seizures
CV: pericarditis
GI: nausea, vomiting

38
Q

What are the benefits and risks of hemodialysis?

A

Benefits: more efficient with high flow rates that shorten dialysis time, can be initiated quickly with temporary catheter sites
Risks: dissimilar to natural kidney function, rapid volume exchange may cause HPN leading to rapid shift of fluid from ECF into cells, hypoOsm due to solute removal, requires vascular access

39
Q

What are alternatives to traditional hemodialysis? When are they used?

A

CAVHD: continuous arteriovenous HD
CVVHD: continuous venovenous HD
- used in hemodynamically unstable patients (i.e. ICU patients with AKI)

40
Q

What are the benefits and risks of peritoneal hemodialysis?

A

Benefits: mimics natural kidney function since it is continuous, patients can do it themselves
Risks: high Glu may cause hyperGly and hyperTG, peritonitis, requires patients to take responsibility for use, abdominal distention

41
Q

Although dialysis can replace some kidney function, what properties of the kidney can it not replace?

A

Kidneys’ synthetic functions: EPO production, vitamin D activation

42
Q

What is “first-use syndrome” in relation to hemodialysis?

A

Reaction to using a new dialysis machine leading to chest pain, back pain, and rarely, anaphylaxis

43
Q

What MSK syndrome may arise due to hemodialysis use? Why?

A

BL Carpal Tunnel Syndrome: hemodialysis-associated amyloidosis of B2-microglobulin in bones and joints

44
Q

What is the laboratory cutoff for proteinuria?

A

> 150mg/protein/24h

45
Q

What are the (3) main categories of proteinuria? Why do they occur? What are some causes of each?

A
  1. Glomerular: increased permeability may lead to nephrotic syndrome; loss may be more severe than other causes of proteinuria (causes: glomerular nephritis)
  2. Tubular: decreased reabsorption of small proteins; kidney damage is less severe since nephrotoxicity of proteins is usually less (SCD, UTO, interstitial nephritis)
  3. Overflow: increased production overwhelms kidney ability to reabsorb (multiple myeloma - Bence Jones protein, rhabdomyolysis - myoglobin)
46
Q

What are some other causes of proteinuria not directly related to kidney pathology?

A 
UTI
Fever
Heavy exertion/stress
CHF
Pregnancy
Orthostatic proteinuria
47
Q

What are the (3) key features of nephrotic syndrome? Why does it occur?

A
  1. Proteinuria : glomerular, tubular, overload, other
  2. HypoALB: hepatic production cannot keep up with losses
  3. HyperLPD: increased hepatic LDL/VLDL production due to increase in attempt to produce albumin
48
Q

Why is there an increased risk in infection with nephrotic syndrome? Infections caused by which organism are most prominent?

A

Loss of immunoglobulins as part of small protein loss; pneumococcal

49
Q

When urine dipstick analysis is used for diagnosis of proteinuria, what is one limitation of what it tests for?

A

Specific to albumin, so proteinuria due to globulin loss (like multiple myeloma) may be missed

50
Q

After UA confirms the presence of protein, what test is indicated next?

A

24h urine collection to determine significance of protein loss

51
Q

What may be the earliest sign of diabetic nephropathy but overt signs and symptoms may be seen?

A

Microalbuminuria

52
Q

What immunologic tests may be indicated when determining the etiology of proteinuria?

A 
ANA: lupus
Anti-glomerular BM: Goodpasture
Hepatitis serology: MN, MPGN
Antistreptococcal AB: PSGN
Complement levels
Cryoglobulin studies
53
Q

What is an essential medication in treating diabetics with HTN who show symptomatic proteinuria? Why?

A

ACEi - decrease urinary albumin loss

54
Q

What does microscopic hematuria suggest about the etiology of bleeding? What about gross hematuria?

A

Microscopic: more likely glomerular in origin
Gross: nonglomerular or urologic

55
Q

What is the assumption when gross painless hematuria is reported?

A

Assume bladder or kidney cancer until proven otherwise

56
Q

What are common causes of hematuria in the following locations?
Intrarenal
Ureter
Lower urinary tract (bladder, urethra, prostate)
Other

A

Intrarenal: tumor, infection, stones, trauma, glomerular dz, IgA nephropathy, strenuous exercise, fever, PCKD, cysts, SCD, analgesic induced, renal papillary necrosis
Ureter: tumor, infection, stones, trauma, stricture
Lower urinary tract (bladder, urethra, prostate): tumor, infection, stones, trauma, BPH, chronic irritation
Other: systemic diseases (SLE, HSP, rheumatic fever, GPA, HUS, GP, PAN), bleedign disorders, medications

57
Q

What medications may lead to hematuria?

A

Cyclophosphamide
Anticoagulants
Salicylates
Sulfonamides

58
Q

What test has 90%+ sensitivity in detecting hematuria?

A

Urine dipstick

59
Q

When evaluating hematuria, what is the next step after UA shows normal-shaped RBCs, no casts, no proteinuria, with NEG UCx? What happens if the next evaluation is NEG?

A

Evaluate for coagulopathy

If neg, do KUB to check for stones

60
Q

What evaluating hematuria, what is the next step if UA shows pyuria with a POS UCx?

A

Treat UTI and reevaluate

61
Q

When evaluating hematuria, what is the next step after UA shows dysmorphic RBCs, RBC casts, or proteinuria?

A

Evaluate for intrinsic renal disease with serology, 24h urina, GFR, renal bx

62
Q

What is the next step after sending a urine specimen for cytology if the suspicion for malignancy is high?

A

Cystoscopy, especially if patient is 40+ with RF for bladder cancer

63
Q 
Regarding nephrotic syndrome:
Pathophysiology?
Causes?
Lab findings?
Clinical symptoms?
A

Pathophysiology: increased glomerular permeability
Causes: MG (mc), DM, SLE, infection, drugs, GN
Lab findings: urine protein >3.5g/d, hypoalbuminemia, HLD, fatty casts in urine
Clinical symptoms: edema, hypercoagulable state, increased infection risk

64
Q 
Regarding nephritic syndrome:
Pathophysiology?
Causes?
Lab findings?
Clinical symptoms?
A

Pathophysiology: inflammation of glomeruli
Causes: PSGN (mc), any cause of GN
Lab findings: hematuria, AKI (azotemia, oliguria), mild proteinuria
Clinical symptoms: HTN, edema

65
Q 
What is the most common cause of nephrotic syndrome? What population is is more common in? 
Pathophysiology? 
Microscopy findings? 
Prognosis? 
Treatment?
A

Minimal change disease, seen in children (asso w/Hodgkins and NHGD lymphoma)
Pathophys: systemic T-cell dysfuction
Light microscopy: nothing
Electron microscopy: fusion/effacement of foot processes
Good prognosis
Treat with steroids

66
Q 
Pathophysiology of focal segmental glomerulosclerosis?
Population?
Clinical symptoms?
Prognosis?
Treatment?
A

Path: Histopathologic lesions with multiple causes
Pop: 25% of nephrotic syndrome, common in blacks
Sx: hematuria, HTN
Prognosis: poor; renal insufficiency in 5-10 yrs, ESRD
Tx: controversial - cytotoxic agents, steroids, immunosuppressive agents, ACE/ARBs

67
Q 
Pathophysiology of membranous glomerularnephritis?
Population?
Clinical symptoms?
Prognosis?
Treatment?
A

Path: thickened capillary walls, idiopathic (mc), infections (HCV, HBV, syphilis, malaria), drugs (gold, captopril, penicillamine), malignancy, lupus
Pop: Non-diabetic adults
Prognosis: fair to good, remission (40%), renal failure (33%)
Tx: n/a, steroid resistant

68
Q 
What is the most common cause of glomerular hematuria?
Cause?
Clinical symptoms?
Microscopy findings?
Prognosis?
Treatment?
A

IgA Nephropathy (Berger disease)
Path: URTI
Sx: asx recurrent hematuria/mild proteinuria; gross hematuria 1-3d after URTI; normal renal function
E- Microscopy: mesangial IgA and C3 deposition
Prognosis: good, preserved renal function, renal ins (25%)
Tx: n/a, steroids unproven

69
Q

What is hereditary nephritis?
Clinical symptoms?
Treatment?

A

???
Sx: hematuria, pyuria, proteinuria, high-frequency hearing loss without deafness, progressive renal failure
Tx: n/a

70
Q 
What is the most common cause of nephritic syndrome?
Pathophysiology?
Clinical symptoms?
What marker may be elevated?
Prognosis?
Treatment?
A

Post-streptococcal GN
Path: occurs 10-14d after infection with GAS (B-hemolytic) of URT or skin
Sx: hematuria, edema, HTN, low complement levels, proteinuria
Marker: ASO
Prognosis: self-limited w/great prognosis, may RPGN
Tx: supportive (HTN, diuretics), steroids if severe case, abx unproven

71
Q 
What is the classic triad seen in goodpasture syndrome?
Clinical symptoms?
What occurs prior to kidney disease?
Biopsy findings?
Treatment?
A

Proliferative GN (crescentic), pulmonary hemorrhage, IgG antoglomerular BM-AB
Sx: rapidly progressive renal failure, hemoptysis, cough, dyspnea
Prior: lung disease precedes kidney disease by days-weeks
Biopsy: linear immunofluorescence pattern
Tx: plasmapheresis to remove circulating anti-IgG AB, cyclophosphomide, steroids may decrease new AB

72
Q

What are HIV nephropathy:
Clinical symptoms?
Histopathology?
Treatment?

A

Sx: proteinuria, edema, hematuria
Histo: ~collapsing form of FSGS
Tx: prednisone, ACEi, antiretroviral tx

73
Q

What are some other causes of secondary glomerular disorders not covered yet?

A 
Diabetic nephropathy
HTN nephropathy
Lupus
Dysproteinemias
SCD Nephropathy
GPA
PAN

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