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clin med II, exam 3 > CKD, nephrotic > Flashcards

CKD, nephrotic Flashcards

1
Q

What are the two leading causes of kidney disease

A
  • HTN
  • Diabetes
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2
Q

who is at risk for CKD

A
  • diabetes
  • HTN
  • cardiovascular disease
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3
Q

when is someone in kidney failure

A
  • GFR < 15
  • signs and symptoms of uremia
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4
Q

Define chronic kidney disease

A
  • kidney damage or decreased kidney function for 3 or more months
  1. GFR < 60 mL/min
  2. Evidence of kidney damage
    • albuminuria: urine albumin-creatinine ratio > or = 30 mg/g
    • abnormal imaging tests
    • abnormal urinary sediment
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5
Q

what is the best marker of kidney function

A

GFR

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6
Q

classify CKD into stages based on declining GFR

A
  • Stage 1: GFR > 90 with persistent albuminuria
  • Stage 2: GFR 60-89 with persistent albuminuria
  • Stage 3: GFR 30-59
  • Stage 4: GFR 15-29
  • Stage 5: GFR < 15 or dialysis
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7
Q

Normal to mildly increased albuminuria Stage 1 will have what ACR (urine albumin to creatinine ratio) and protein dipstick

A
  • ACR < 30
  • protein dipstick: neg to trace
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8
Q

Moderately increased albuminuria Stage 2 will have what ACR (urine albumin to creatinine ratio) and protein dipstick

A
  • ACR: 30-300
  • Protein dipstick: trace to 1+
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9
Q

severely increased albuminuria Stage 3 will have what ACR (urine albumin to creatinine ratio) and protein dipstick

A
  • ACR: > 300
  • protein dipstick: >1+
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10
Q

progressive nephron and GFR loss leads to abnormalities in production and metabolism of what hormones

A
  • erythropoietin
  • calcitriol (active form of vit D)
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11
Q

patients who are at risk for developing CKD should be screened for

A
  • urine albumin-to-creatinine ratio
  • serum creatinine to estimate GFR (eGFR)
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12
Q

What is uremic syndrome? What are some critical symptoms

A
  • profound disease in GFR < 5-10
  • build up of metabolic waste products
  • critical symptoms
    • pericarditis
    • sz
    • encephalopathy
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13
Q

what kidney size on renal US implies CKD

A

< 10 cm

  • kidney normally 10-12 cm
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14
Q

How can ARB/ACE-I be helpful in patients with kidney disease

A
  • renoprotective
  • helpful in slowing progressive of CKD
  • decrease albuminuria
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15
Q

How can ARB/ACE-I be harmful in patients with kidney disease

A
  • exacerbation of renal failure
  • hyperkalemia
  • contraindicated in bilateral renal artery stenosis
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16
Q

Patients who have proteinuric CKD should be treated more aggressively. What is the target BP in patients with proteinuria and those without proteinuria.

A
  • CKD, no proteinuria: < or = 140/90
  • CKD, + proteinuria: < or = 130/80
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17
Q

How can CKD lead to mineral and bone disorder (CKD-MBD)

A
  • CKD -> hypocalcemic, hyperphosphatemia and low vit D ->
    • secondary hyperparathyroidism
    • renal osteodystrophy
      • abnormalities in bone turnover
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18
Q

list some complications of CKD

A
  • cardiovascular disease
  • HTN
  • anemia
  • mineral and bone disorders
  • hyperkalemia
  • metabolic acidosis
  • uremia
  • fluid and salt retention
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19
Q

What are the two types of renal replacement therapy

A
  • for patients with kidney failure (ESRD)
  1. dialysis
    • hemodialysis
    • peritoneal dialysis
  2. kidney transplant
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20
Q

At what GFR is dialysis considered

A

GFR < 30

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21
Q

When is chronic dialysis indicated

A
  1. Uremia (pericarditis, encephalopathy)
  2. Fluid overload unresponsive to diuretics
  3. HTN- med resistant
  4. Refractory acidosis, hyperkalemia, and hyperphosphatemia
  5. Progressive deterioration in nutritional status
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22
Q

Describe the process of hemodialysis

A
  • requires a constant flow of blood along one side of a semipermeable membrane with a cleansing solution, or a dialysate, along the other
    • removal of unwanted substances from blood while adding back needed components
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23
Q

Complications of hemodialysis

A
  • hypotension
  • dialysis disequilibrium syndrome
    • HA, N/V, lethargy
  • arrhythmias
  • clotting/bleeding
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24
Q

In peritoneal dialysis, what is the dialyzer

A

the peritoneal membrane

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25
Q

explain the process of peritoneal dialysis

A
  • dialysate is instilled into peritoneal cavity via indwelling catheter
  • peritoneal membrane acts as partially permeable membrane
  • diffusion and osmosis drive waste products and excess fluid through peritoneum into dialysate until reaches equilibrium
  • dialysate is drained
  • *3-4 x/day
26
Q

complications of peritoneal dialysis

A
  • peritonitis
  • exit site infection
  • poor dialysate drainage
27
Q

what is the treatment of choice for ESRD

A

kidney transplant

28
Q

When do you refer a patient with CKD to a nephrologist

A
  • GFR < 30
  • refer to
    • manage complications
      • EPO therapy
      • bone and mineral metabolism abnormalities
      • resistant HTN
    • prep for dialysis
    • transplant eval
29
Q

Name some interventions to delay progression of CKD

A
  • ACE-I, ARB
  • BP control
  • glycemic control
  • protein resistriction
30
Q

What characteristics are associated with chronic tubulointerstitial disorders

A
  1. interstitial chronic inflammation
  2. intersititial fibrosis
  3. tubular atrophy
31
Q

What characteristics are essential to diagnosis of chronic tubulointerstitial disorders

A
  • kidney size small and contracted
  • decreased urinary concentrating ability
  • hypercholermic metabolic acidosis
  • reduced GFR
32
Q

What are the most common causes of chronic tubulointerstitial disorders

A
  • obstructive uropathy
  • reflux nephropathy
33
Q

What causes obstructive uropathy

A
  • prolonged obstruction of urinary tract
  • obstruction -> decrease in renal blood flow, GFR and impaired tubular function
    • stones
    • bladder outlet obstruction
    • carcinoma of cervix, colon, or bladder
34
Q

what imaging modality would you get to assess for obstructive uropathy

A
  • US
    • detect mass lesions
    • hydroureter
    • hydronephrosis
35
Q

What are common causes of reflex nephropathy

A
  1. vesicoureteral reflux (VUR): urologic abnormality in childhood
  2. hx of recurrent UTI -> scarring is associated with intrarenal reflux
  • typically goes unnoticed until early adulthood
36
Q

Ingestion of what medications can cause analgesic nephropathy? What is the minumum dose they have to take

A
  • Aspirin and NSAIDs
  • ingestions of at least 1g/day for 3 years
37
Q

clinical presentation

  • hematuria
  • mild proteinuria
  • polyuria ( inability to concentrate urine due to tubular damage)
  • anemia
A

analgesic nephropathy

38
Q

What are three common general findings of all chronic tubulointerstitial disorders

A
  • polyuria
    • inability to concentrate urine secondary to tubular damage
  • hyperkalemia
    • decreased GFR
    • distal tubules become resistant to aldosterone
  • UA is nonspecific
    • proteinuria ( < 2 g/d), broad waxy casts
39
Q

Define Nephrotic syndrome

A
  • Noninflammatory damage to glomerular capillary wall (podocyte and glomerular basement membrane)
40
Q

Nephrotic syndrome is characterized by what 5 things

A
  • Heavy Proteinuria: > 3.5 g/d
  • Hypoalbuminemia
  • Edema
  • Hyperlipidemia
  • Lipiduria
41
Q

What are the three primary disease that cause Nephrotic syndrome

A
  1. Minimal change disease
  2. Membranous Nephropathy
  3. Focal Segmental Glomerulosclerosis
42
Q

What are the two secondary diseases that cause Nephrotic syndrome

A
  1. diabetic nephropathy
  2. amyloidosis
43
Q

What are complications Nephrotic syndrome

A
  • Hypercoagulability -> thrombosis
  • Vit D deficiency and hypocalcemia
  • infection
  • malnutrition
  • anemia
44
Q

what would you characteristically see in urine microscopy in a patient with Nephrotic syndrome

A
  • oval fat body: represents lipiduria
45
Q

What is initial diagnostic imaging modality for Nephrotic syndrome

A

renal US

46
Q

What is the most common cause of proteinuric renal disease in children

A

Minimal change disease

47
Q

cause of Minimal change disease

A

idiopathic (80-90%)

48
Q

what is Minimal change disease

A
  • injury to glomerular epithelial foot processes (podocyte)
49
Q

tx of Minimal change disease

A
  • Predinose
    • often treated empirically without biopsy
    • progression to ESRD is rare
50
Q

Causes of Membranous Nephropathy

A
  • idiopathic
  • secondary
    • autoimmune, infection, malignancy
  • seen in all ethnic and racial groups and in both sexes
51
Q

What histopathology is seen with Membranous Nephropathy

A
  • diffuse thickening of the GBM in the absence of significant hypercellularity/glomerular inflammation
52
Q

tx of Membranous Nephropathy and Focal Segmental Glomerulosclerosis

A
  • supportive
  • +/- immunosuppresive medication
53
Q

What is Focal Segmental Glomerulosclerosis

A
  • renal pattern of injury resulting from damage to podocytes
  • Glomerulosclerosis = hardening -> scarring
54
Q

Focal Segmental Glomerulosclerosis normally affects what patient population

A
  • african american
  • M >F
55
Q

how is Focal Segmental Glomerulosclerosis diagnosed

A
  • diagnosis is established definitively with biopsy
    • segmental solidification of glomerular tuft
    • injury to podocyte -> collapse of glomerular capillaries -> scarring
56
Q

Diabetic Nephropathy presents with what clinical syndrome

A
  • persistent albuminuria
  • progressive CKD
  • +/- retinopathy
57
Q

peak incidence of Diabetic Nephropathy

A

persons who have had diabetes for 10-20 years

58
Q

how does diabetes lead to Diabetic Nephropathy

A
  • long standing hyperglycemia -> development of albuminuria
59
Q

tx of Diabetic Nephropathy

A
  • strict glycemic control
  • BP control
  • ACE-I/ARB
  • dialysis and transplant when indicated
60
Q

What is Amyloidosis

A
  • extracellular deposition of an abnormally folded protein (amyloid)
61
Q

how does amyloidosis lead to nephrotic syndrome

A

glomeruli are filled with amorphous deposits -> proteinuria and decreased GFR

62
Q

how is amyloidosis diagnosed

A
  • serum and urine protein electrophoresis

clin med II, exam 3 (6 decks)

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